Ignet

Gene Information

Gene symbol: GAL

Gene name: galanin/GMAP prepropeptide

HGNC ID: 4114

Synonyms: GMAP, GAL-GMAP, GLNN

Related Genes

#	Gene Symbol	Number of hits
1	ACE	1 hits
2	ADCY10	1 hits
3	ADCY7	1 hits
4	ADCYAP1	1 hits
5	AGRP	1 hits
6	AKR1B1	1 hits
7	APLP2	1 hits
8	AVP	1 hits
9	BRD2	1 hits
10	CALCA	1 hits
11	CARTPT	1 hits
12	CASP10	1 hits
13	CCK	1 hits
14	CRH	1 hits
15	FADD	1 hits
16	GALP	1 hits
17	GAP43	1 hits
18	GAST	1 hits
19	GCG	1 hits
20	GHRH	1 hits
21	GHRL	1 hits
22	GIP	1 hits
23	GNAO1	1 hits
24	GPI	1 hits
25	GRP	1 hits
26	HBB	1 hits
27	HSPA1A	1 hits
28	HSPB1	1 hits
29	IDDM4	1 hits
30	INS	1 hits
31	JUN	1 hits
32	LEP	1 hits
33	MLN	1 hits
34	MYH14	1 hits
35	MYLK	1 hits
36	NAGLU	1 hits
37	NMB	1 hits
38	NOS1	1 hits
39	NPY	1 hits
40	NTRK2	1 hits
41	NTRK3	1 hits
42	NTS	1 hits
43	PDYN	1 hits
44	PMCH	1 hits
45	POMC	1 hits
46	PPY	1 hits
47	PRKAR2A	1 hits
48	PYY	1 hits
49	S100A12	1 hits
50	SCG5	1 hits
51	SERPINE2	1 hits
52	SLC2A4	1 hits
53	SNAP25	1 hits
54	SON	1 hits
55	SST	1 hits
56	SUCLG1	1 hits
57	SYP	1 hits
58	TAC1	1 hits
59	TH	1 hits
60	TRH	1 hits
61	TSC22D3	1 hits
62	VIP	1 hits

Related Sentences

#	PMID	Sentence
1	1283731	Galanin inhibits tolbutamide-stimulated insulin secretion in the perfused pig pancreas.
2	1283731	The neuropeptide galanin is known to inhibit insulin secretion in a variety of species.
3	1283731	We found that at this dose level, galanin did not affect insulin secretion stimulated by glucose alone.
4	1283731	In contrast, galanin clearly suppressed tolbutamide-stimulated insulin secretion.
5	1283731	Hence, we conclude that galanin has a weak influence on insulin secretion in the pig pancreas, being unable to inhibit glucose-stimulated insulin secretion at the dose level of 100 nmol/l.
6	1283731	However, when active, galanin clearly inhibits insulin secretion also in the pig pancreas.
7	1283731	Galanin inhibits tolbutamide-stimulated insulin secretion in the perfused pig pancreas.
8	1283731	The neuropeptide galanin is known to inhibit insulin secretion in a variety of species.
9	1283731	We found that at this dose level, galanin did not affect insulin secretion stimulated by glucose alone.
10	1283731	In contrast, galanin clearly suppressed tolbutamide-stimulated insulin secretion.
11	1283731	Hence, we conclude that galanin has a weak influence on insulin secretion in the pig pancreas, being unable to inhibit glucose-stimulated insulin secretion at the dose level of 100 nmol/l.
12	1283731	However, when active, galanin clearly inhibits insulin secretion also in the pig pancreas.
13	1283731	Galanin inhibits tolbutamide-stimulated insulin secretion in the perfused pig pancreas.
14	1283731	The neuropeptide galanin is known to inhibit insulin secretion in a variety of species.
15	1283731	We found that at this dose level, galanin did not affect insulin secretion stimulated by glucose alone.
16	1283731	In contrast, galanin clearly suppressed tolbutamide-stimulated insulin secretion.
17	1283731	Hence, we conclude that galanin has a weak influence on insulin secretion in the pig pancreas, being unable to inhibit glucose-stimulated insulin secretion at the dose level of 100 nmol/l.
18	1283731	However, when active, galanin clearly inhibits insulin secretion also in the pig pancreas.
19	1283731	Galanin inhibits tolbutamide-stimulated insulin secretion in the perfused pig pancreas.
20	1283731	The neuropeptide galanin is known to inhibit insulin secretion in a variety of species.
21	1283731	We found that at this dose level, galanin did not affect insulin secretion stimulated by glucose alone.
22	1283731	In contrast, galanin clearly suppressed tolbutamide-stimulated insulin secretion.
23	1283731	Hence, we conclude that galanin has a weak influence on insulin secretion in the pig pancreas, being unable to inhibit glucose-stimulated insulin secretion at the dose level of 100 nmol/l.
24	1283731	However, when active, galanin clearly inhibits insulin secretion also in the pig pancreas.
25	1283731	Galanin inhibits tolbutamide-stimulated insulin secretion in the perfused pig pancreas.
26	1283731	The neuropeptide galanin is known to inhibit insulin secretion in a variety of species.
27	1283731	We found that at this dose level, galanin did not affect insulin secretion stimulated by glucose alone.
28	1283731	In contrast, galanin clearly suppressed tolbutamide-stimulated insulin secretion.
29	1283731	Hence, we conclude that galanin has a weak influence on insulin secretion in the pig pancreas, being unable to inhibit glucose-stimulated insulin secretion at the dose level of 100 nmol/l.
30	1283731	However, when active, galanin clearly inhibits insulin secretion also in the pig pancreas.
31	1283731	Galanin inhibits tolbutamide-stimulated insulin secretion in the perfused pig pancreas.
32	1283731	The neuropeptide galanin is known to inhibit insulin secretion in a variety of species.
33	1283731	We found that at this dose level, galanin did not affect insulin secretion stimulated by glucose alone.
34	1283731	In contrast, galanin clearly suppressed tolbutamide-stimulated insulin secretion.
35	1283731	Hence, we conclude that galanin has a weak influence on insulin secretion in the pig pancreas, being unable to inhibit glucose-stimulated insulin secretion at the dose level of 100 nmol/l.
36	1283731	However, when active, galanin clearly inhibits insulin secretion also in the pig pancreas.
37	1285360	The changes in plasma gastrin-releasing peptide (GRP), arginine vasopressin (AVP), neuropeptide Y (NPY), corticotropin releasing hormone (CRH), galanin, ACTH, cortisol, delta sleep-inducing peptide (DSIP), adrenaline, noradrenaline and pancreatic polypeptide (PP) were measured after 5 and 15 minutes of acute insulin-induced moderate hypoglycaemia (2.0 mmol/l) in 10 patients with Type 1 diabetes mellitus with no autonomic neuropathy and in 10 healthy subjects.
38	1285360	No group differences or changes in mean plasma concentrations were found for galanin, DSIP and CRH.
39	1285360	The changes in plasma gastrin-releasing peptide (GRP), arginine vasopressin (AVP), neuropeptide Y (NPY), corticotropin releasing hormone (CRH), galanin, ACTH, cortisol, delta sleep-inducing peptide (DSIP), adrenaline, noradrenaline and pancreatic polypeptide (PP) were measured after 5 and 15 minutes of acute insulin-induced moderate hypoglycaemia (2.0 mmol/l) in 10 patients with Type 1 diabetes mellitus with no autonomic neuropathy and in 10 healthy subjects.
40	1285360	No group differences or changes in mean plasma concentrations were found for galanin, DSIP and CRH.
41	1370155	Sequence of human galanin and its inhibition of glucose-stimulated insulin secretion from RIN cells.
42	1370155	Human galanin was synthesized, and its bioactivity was compared with porcine and rat galanin based on inhibition of insulin release from a glucose-responsive rat insulinoma (RIN) cell line.
43	1370155	Human galanin inhibited glucose-stimulated insulin secretion in a dose-dependent manner in RIN cells.
44	1370155	Sequence of human galanin and its inhibition of glucose-stimulated insulin secretion from RIN cells.
45	1370155	Human galanin was synthesized, and its bioactivity was compared with porcine and rat galanin based on inhibition of insulin release from a glucose-responsive rat insulinoma (RIN) cell line.
46	1370155	Human galanin inhibited glucose-stimulated insulin secretion in a dose-dependent manner in RIN cells.
47	1370155	Sequence of human galanin and its inhibition of glucose-stimulated insulin secretion from RIN cells.
48	1370155	Human galanin was synthesized, and its bioactivity was compared with porcine and rat galanin based on inhibition of insulin release from a glucose-responsive rat insulinoma (RIN) cell line.
49	1370155	Human galanin inhibited glucose-stimulated insulin secretion in a dose-dependent manner in RIN cells.
50	1374311	Plasma neuropeptide Y (NPY) and galanin before and during exercise in type 1 diabetic patients with autonomic dysfunction.
51	1374311	Plasma neuropeptide Y (NPY), plasma galanin and plasma catecholamines were determined before and during an ergometer exercise test in 11 type 1 diabetic patients (age 19-36 years, mean 30; duration of diabetes 2-18 years, mean 9) with autonomic dysfunction and in 13 age-matched healthy controls (age 24-36 years, mean 29).
52	1374311	Before exercise, plasma NPY (100 +/- 6 pmol/l vs 144 +/- 7 pmol/l; P less than 0.001) and plasma galanin (54 +/- 3 pmol/l vs 77 +/- 5 pmol/l; P less than 0.005) were significantly lower in patients than in controls.
53	1374311	During exercise, plasma NPY, plasma adrenaline, and plasma noradrenaline increased in patients and controls while galanin only increased in patients.
54	1374311	Plasma neuropeptide Y (NPY) and galanin before and during exercise in type 1 diabetic patients with autonomic dysfunction.
55	1374311	Plasma neuropeptide Y (NPY), plasma galanin and plasma catecholamines were determined before and during an ergometer exercise test in 11 type 1 diabetic patients (age 19-36 years, mean 30; duration of diabetes 2-18 years, mean 9) with autonomic dysfunction and in 13 age-matched healthy controls (age 24-36 years, mean 29).
56	1374311	Before exercise, plasma NPY (100 +/- 6 pmol/l vs 144 +/- 7 pmol/l; P less than 0.001) and plasma galanin (54 +/- 3 pmol/l vs 77 +/- 5 pmol/l; P less than 0.005) were significantly lower in patients than in controls.
57	1374311	During exercise, plasma NPY, plasma adrenaline, and plasma noradrenaline increased in patients and controls while galanin only increased in patients.
58	1374311	Plasma neuropeptide Y (NPY) and galanin before and during exercise in type 1 diabetic patients with autonomic dysfunction.
59	1374311	Plasma neuropeptide Y (NPY), plasma galanin and plasma catecholamines were determined before and during an ergometer exercise test in 11 type 1 diabetic patients (age 19-36 years, mean 30; duration of diabetes 2-18 years, mean 9) with autonomic dysfunction and in 13 age-matched healthy controls (age 24-36 years, mean 29).
60	1374311	Before exercise, plasma NPY (100 +/- 6 pmol/l vs 144 +/- 7 pmol/l; P less than 0.001) and plasma galanin (54 +/- 3 pmol/l vs 77 +/- 5 pmol/l; P less than 0.005) were significantly lower in patients than in controls.
61	1374311	During exercise, plasma NPY, plasma adrenaline, and plasma noradrenaline increased in patients and controls while galanin only increased in patients.
62	1374311	Plasma neuropeptide Y (NPY) and galanin before and during exercise in type 1 diabetic patients with autonomic dysfunction.
63	1374311	Plasma neuropeptide Y (NPY), plasma galanin and plasma catecholamines were determined before and during an ergometer exercise test in 11 type 1 diabetic patients (age 19-36 years, mean 30; duration of diabetes 2-18 years, mean 9) with autonomic dysfunction and in 13 age-matched healthy controls (age 24-36 years, mean 29).
64	1374311	Before exercise, plasma NPY (100 +/- 6 pmol/l vs 144 +/- 7 pmol/l; P less than 0.001) and plasma galanin (54 +/- 3 pmol/l vs 77 +/- 5 pmol/l; P less than 0.005) were significantly lower in patients than in controls.
65	1374311	During exercise, plasma NPY, plasma adrenaline, and plasma noradrenaline increased in patients and controls while galanin only increased in patients.
66	1380870	Dynamics of 7B2 and galanin expression in solitary magnocellular hypothalamic vasopressin neurons of the homozygous Brattleboro rat.
67	1380870	The phenotypic expression of coexisting peptides in mutant magnocellular VP cells shows a differential pattern. 7B2 is one of the peptides which is not detectable, whereas there is a clear galanin expression.
68	1380870	Here we report the presence of 7B2 and galanin in these heterozygous cells, which suggests that for the expression of 7B2, but not for that of galanin, the relative amount of mutant VP precursor must be diminished.
69	1380870	Dynamics of 7B2 and galanin expression in solitary magnocellular hypothalamic vasopressin neurons of the homozygous Brattleboro rat.
70	1380870	The phenotypic expression of coexisting peptides in mutant magnocellular VP cells shows a differential pattern. 7B2 is one of the peptides which is not detectable, whereas there is a clear galanin expression.
71	1380870	Here we report the presence of 7B2 and galanin in these heterozygous cells, which suggests that for the expression of 7B2, but not for that of galanin, the relative amount of mutant VP precursor must be diminished.
72	1380870	Dynamics of 7B2 and galanin expression in solitary magnocellular hypothalamic vasopressin neurons of the homozygous Brattleboro rat.
73	1380870	The phenotypic expression of coexisting peptides in mutant magnocellular VP cells shows a differential pattern. 7B2 is one of the peptides which is not detectable, whereas there is a clear galanin expression.
74	1380870	Here we report the presence of 7B2 and galanin in these heterozygous cells, which suggests that for the expression of 7B2, but not for that of galanin, the relative amount of mutant VP precursor must be diminished.
75	1381831	We measured hyothalamic NPY and NPY mRNA, along with galanin, neurotensin, and somatostatin in chow-fed rats and in rats with dietary obesity, and examined the effect of dexfenfluramine on these peptides in this model.
76	1381831	Hypothalami were dissected into medial and lateral blocks, and NPY, galanin, neurotensin, and somatostatin were measured by radioimmunoassay.
77	1381831	We measured hyothalamic NPY and NPY mRNA, along with galanin, neurotensin, and somatostatin in chow-fed rats and in rats with dietary obesity, and examined the effect of dexfenfluramine on these peptides in this model.
78	1381831	Hypothalami were dissected into medial and lateral blocks, and NPY, galanin, neurotensin, and somatostatin were measured by radioimmunoassay.
79	1691431	Marked sex differences in lean control mice were found at 3 weeks of age in pancreatic Met-enkephalin-LI and galanin-LI (with two- to threefold higher content in males).
80	1691431	Low pancreatic content (50% to 70% lower than in control mice) of galanin-LI, Met-enkephalin-LI and Leu-enkephalin-LI was associated with hyperinsulinemia in male B6 ob/ob and db/db mice at 3 weeks of age, though not in B6 db/db females and not in BKs db/db mice of either sex.
81	1691431	Marked sex differences in lean control mice were found at 3 weeks of age in pancreatic Met-enkephalin-LI and galanin-LI (with two- to threefold higher content in males).
82	1691431	Low pancreatic content (50% to 70% lower than in control mice) of galanin-LI, Met-enkephalin-LI and Leu-enkephalin-LI was associated with hyperinsulinemia in male B6 ob/ob and db/db mice at 3 weeks of age, though not in B6 db/db females and not in BKs db/db mice of either sex.
83	1695589	Inhibition of insulin and somatostatin secretion and stimulation of glucagon release by homologous galanin in perfused rat pancreas.
84	1695589	Thus, we investigated the influence of synthetic rat galanin (50 nM) on unstimulated insulin, glucagon, and somatostatin release and on the responses of these hormones to arginine (10 mM), glucose (16.6 mM), and vasoactive intestinal polypeptide (VIP; 1 nM) in a homologous animal model, the perfused rat pancreas.
85	1695589	Infusion of rat galanin reduced unstimulated insulin release (approximately 60%, P less than 0.01) and the insulin responses to arginine (approximately 30%, P less than 0.025), glucose (100%, P less than 0.01), and VIP (approximately 80%, P less than 0.025).
86	1695589	Galanin also inhibited unstimulated somatostatin secretion (approximately 15%, P less than 0.05) and virtually abolished the somatostatin output evoked by arginine, glucose, and VIP.
87	1695589	Pig galanin inhibited the insulin output elicited by arginine (approximately 45%, P less than 0.05) but did not affect the somatostatin and glucagon responses to the aminogenic stimulus.
88	1695589	In conclusion, the opposite effects of galanin on insulin and glucagon secretion favor the concept of galanin as a diabetogenic agent.
89	1695589	Galanin also behaves as a potent inhibitor of somatostatin release.
90	1695589	Inhibition of insulin and somatostatin secretion and stimulation of glucagon release by homologous galanin in perfused rat pancreas.
91	1695589	Thus, we investigated the influence of synthetic rat galanin (50 nM) on unstimulated insulin, glucagon, and somatostatin release and on the responses of these hormones to arginine (10 mM), glucose (16.6 mM), and vasoactive intestinal polypeptide (VIP; 1 nM) in a homologous animal model, the perfused rat pancreas.
92	1695589	Infusion of rat galanin reduced unstimulated insulin release (approximately 60%, P less than 0.01) and the insulin responses to arginine (approximately 30%, P less than 0.025), glucose (100%, P less than 0.01), and VIP (approximately 80%, P less than 0.025).
93	1695589	Galanin also inhibited unstimulated somatostatin secretion (approximately 15%, P less than 0.05) and virtually abolished the somatostatin output evoked by arginine, glucose, and VIP.
94	1695589	Pig galanin inhibited the insulin output elicited by arginine (approximately 45%, P less than 0.05) but did not affect the somatostatin and glucagon responses to the aminogenic stimulus.
95	1695589	In conclusion, the opposite effects of galanin on insulin and glucagon secretion favor the concept of galanin as a diabetogenic agent.
96	1695589	Galanin also behaves as a potent inhibitor of somatostatin release.
97	1695589	Inhibition of insulin and somatostatin secretion and stimulation of glucagon release by homologous galanin in perfused rat pancreas.
98	1695589	Thus, we investigated the influence of synthetic rat galanin (50 nM) on unstimulated insulin, glucagon, and somatostatin release and on the responses of these hormones to arginine (10 mM), glucose (16.6 mM), and vasoactive intestinal polypeptide (VIP; 1 nM) in a homologous animal model, the perfused rat pancreas.
99	1695589	Infusion of rat galanin reduced unstimulated insulin release (approximately 60%, P less than 0.01) and the insulin responses to arginine (approximately 30%, P less than 0.025), glucose (100%, P less than 0.01), and VIP (approximately 80%, P less than 0.025).
100	1695589	Galanin also inhibited unstimulated somatostatin secretion (approximately 15%, P less than 0.05) and virtually abolished the somatostatin output evoked by arginine, glucose, and VIP.
101	1695589	Pig galanin inhibited the insulin output elicited by arginine (approximately 45%, P less than 0.05) but did not affect the somatostatin and glucagon responses to the aminogenic stimulus.
102	1695589	In conclusion, the opposite effects of galanin on insulin and glucagon secretion favor the concept of galanin as a diabetogenic agent.
103	1695589	Galanin also behaves as a potent inhibitor of somatostatin release.
104	1695589	Inhibition of insulin and somatostatin secretion and stimulation of glucagon release by homologous galanin in perfused rat pancreas.
105	1695589	Thus, we investigated the influence of synthetic rat galanin (50 nM) on unstimulated insulin, glucagon, and somatostatin release and on the responses of these hormones to arginine (10 mM), glucose (16.6 mM), and vasoactive intestinal polypeptide (VIP; 1 nM) in a homologous animal model, the perfused rat pancreas.
106	1695589	Infusion of rat galanin reduced unstimulated insulin release (approximately 60%, P less than 0.01) and the insulin responses to arginine (approximately 30%, P less than 0.025), glucose (100%, P less than 0.01), and VIP (approximately 80%, P less than 0.025).
107	1695589	Galanin also inhibited unstimulated somatostatin secretion (approximately 15%, P less than 0.05) and virtually abolished the somatostatin output evoked by arginine, glucose, and VIP.
108	1695589	Pig galanin inhibited the insulin output elicited by arginine (approximately 45%, P less than 0.05) but did not affect the somatostatin and glucagon responses to the aminogenic stimulus.
109	1695589	In conclusion, the opposite effects of galanin on insulin and glucagon secretion favor the concept of galanin as a diabetogenic agent.
110	1695589	Galanin also behaves as a potent inhibitor of somatostatin release.
111	1695589	Inhibition of insulin and somatostatin secretion and stimulation of glucagon release by homologous galanin in perfused rat pancreas.
112	1695589	Thus, we investigated the influence of synthetic rat galanin (50 nM) on unstimulated insulin, glucagon, and somatostatin release and on the responses of these hormones to arginine (10 mM), glucose (16.6 mM), and vasoactive intestinal polypeptide (VIP; 1 nM) in a homologous animal model, the perfused rat pancreas.
113	1695589	Infusion of rat galanin reduced unstimulated insulin release (approximately 60%, P less than 0.01) and the insulin responses to arginine (approximately 30%, P less than 0.025), glucose (100%, P less than 0.01), and VIP (approximately 80%, P less than 0.025).
114	1695589	Galanin also inhibited unstimulated somatostatin secretion (approximately 15%, P less than 0.05) and virtually abolished the somatostatin output evoked by arginine, glucose, and VIP.
115	1695589	Pig galanin inhibited the insulin output elicited by arginine (approximately 45%, P less than 0.05) but did not affect the somatostatin and glucagon responses to the aminogenic stimulus.
116	1695589	In conclusion, the opposite effects of galanin on insulin and glucagon secretion favor the concept of galanin as a diabetogenic agent.
117	1695589	Galanin also behaves as a potent inhibitor of somatostatin release.
118	1695589	Inhibition of insulin and somatostatin secretion and stimulation of glucagon release by homologous galanin in perfused rat pancreas.
119	1695589	Thus, we investigated the influence of synthetic rat galanin (50 nM) on unstimulated insulin, glucagon, and somatostatin release and on the responses of these hormones to arginine (10 mM), glucose (16.6 mM), and vasoactive intestinal polypeptide (VIP; 1 nM) in a homologous animal model, the perfused rat pancreas.
120	1695589	Infusion of rat galanin reduced unstimulated insulin release (approximately 60%, P less than 0.01) and the insulin responses to arginine (approximately 30%, P less than 0.025), glucose (100%, P less than 0.01), and VIP (approximately 80%, P less than 0.025).
121	1695589	Galanin also inhibited unstimulated somatostatin secretion (approximately 15%, P less than 0.05) and virtually abolished the somatostatin output evoked by arginine, glucose, and VIP.
122	1695589	Pig galanin inhibited the insulin output elicited by arginine (approximately 45%, P less than 0.05) but did not affect the somatostatin and glucagon responses to the aminogenic stimulus.
123	1695589	In conclusion, the opposite effects of galanin on insulin and glucagon secretion favor the concept of galanin as a diabetogenic agent.
124	1695589	Galanin also behaves as a potent inhibitor of somatostatin release.
125	1695589	Inhibition of insulin and somatostatin secretion and stimulation of glucagon release by homologous galanin in perfused rat pancreas.
126	1695589	Thus, we investigated the influence of synthetic rat galanin (50 nM) on unstimulated insulin, glucagon, and somatostatin release and on the responses of these hormones to arginine (10 mM), glucose (16.6 mM), and vasoactive intestinal polypeptide (VIP; 1 nM) in a homologous animal model, the perfused rat pancreas.
127	1695589	Infusion of rat galanin reduced unstimulated insulin release (approximately 60%, P less than 0.01) and the insulin responses to arginine (approximately 30%, P less than 0.025), glucose (100%, P less than 0.01), and VIP (approximately 80%, P less than 0.025).
128	1695589	Galanin also inhibited unstimulated somatostatin secretion (approximately 15%, P less than 0.05) and virtually abolished the somatostatin output evoked by arginine, glucose, and VIP.
129	1695589	Pig galanin inhibited the insulin output elicited by arginine (approximately 45%, P less than 0.05) but did not affect the somatostatin and glucagon responses to the aminogenic stimulus.
130	1695589	In conclusion, the opposite effects of galanin on insulin and glucagon secretion favor the concept of galanin as a diabetogenic agent.
131	1695589	Galanin also behaves as a potent inhibitor of somatostatin release.
132	1701038	Colchicine treatment alone resulted in appearance of galanin-, dynorphin-, cholecystokinin-, [Leu]enkephalin- and thyrotropin-releasing hormone-positive cells.
133	1701038	When salt-loaded rats received colchicine, corticotropin-releasing factor- and peptide histidine-isoleucine-like immunoreactivity in addition increased, whereas galanin- and dynorphin-like immunoreactivity markedly decreased.
134	1701038	The Brattleboro rats resembled untreated rats, except their lack of vasopressin-like immunoreactivity, the marked increase in tyrosine hydroxylase-like immunoreactivity, and smaller increase in galanin- and dynorphin-like immunoreactivity.
135	1701038	Addition of colchicine to Brattleboro rats resulted in some distinct further changes in that dynorphin-like immunoreactivity decreased in some neurons and that [Leu]enkephalin-, corticotropin-releasing factor- and peptide histidine-isoleucine-like immunoreactivity increased substantially.
136	1701038	However, a marked difference in immunoreactive [Leu]enkephalin levels was observed with no difference in dynorphin-like immunoreactivity, and opposite changes in galanin-like immunoreactivity.
137	1701038	Vasopressin-containing neurons primarily express tyrosine hydroxylase, galanin, dynorphin, [Leu]enkephalin and peptide histidine-isoleucine, and to a minor extent cholecystokinin and thyrotropin-releasing hormone.
138	1701038	Oxytocin-containing neurons mainly have cholecystokinin and corticotropin-releasing factor, and to a minor extent galanin, dynorphin, [Leu]enkephalin and thyrotropin-releasing hormone.
139	1701038	Colchicine treatment alone resulted in appearance of galanin-, dynorphin-, cholecystokinin-, [Leu]enkephalin- and thyrotropin-releasing hormone-positive cells.
140	1701038	When salt-loaded rats received colchicine, corticotropin-releasing factor- and peptide histidine-isoleucine-like immunoreactivity in addition increased, whereas galanin- and dynorphin-like immunoreactivity markedly decreased.
141	1701038	The Brattleboro rats resembled untreated rats, except their lack of vasopressin-like immunoreactivity, the marked increase in tyrosine hydroxylase-like immunoreactivity, and smaller increase in galanin- and dynorphin-like immunoreactivity.
142	1701038	Addition of colchicine to Brattleboro rats resulted in some distinct further changes in that dynorphin-like immunoreactivity decreased in some neurons and that [Leu]enkephalin-, corticotropin-releasing factor- and peptide histidine-isoleucine-like immunoreactivity increased substantially.
143	1701038	However, a marked difference in immunoreactive [Leu]enkephalin levels was observed with no difference in dynorphin-like immunoreactivity, and opposite changes in galanin-like immunoreactivity.
144	1701038	Vasopressin-containing neurons primarily express tyrosine hydroxylase, galanin, dynorphin, [Leu]enkephalin and peptide histidine-isoleucine, and to a minor extent cholecystokinin and thyrotropin-releasing hormone.
145	1701038	Oxytocin-containing neurons mainly have cholecystokinin and corticotropin-releasing factor, and to a minor extent galanin, dynorphin, [Leu]enkephalin and thyrotropin-releasing hormone.
146	1701038	Colchicine treatment alone resulted in appearance of galanin-, dynorphin-, cholecystokinin-, [Leu]enkephalin- and thyrotropin-releasing hormone-positive cells.
147	1701038	When salt-loaded rats received colchicine, corticotropin-releasing factor- and peptide histidine-isoleucine-like immunoreactivity in addition increased, whereas galanin- and dynorphin-like immunoreactivity markedly decreased.
148	1701038	The Brattleboro rats resembled untreated rats, except their lack of vasopressin-like immunoreactivity, the marked increase in tyrosine hydroxylase-like immunoreactivity, and smaller increase in galanin- and dynorphin-like immunoreactivity.
149	1701038	Addition of colchicine to Brattleboro rats resulted in some distinct further changes in that dynorphin-like immunoreactivity decreased in some neurons and that [Leu]enkephalin-, corticotropin-releasing factor- and peptide histidine-isoleucine-like immunoreactivity increased substantially.
150	1701038	However, a marked difference in immunoreactive [Leu]enkephalin levels was observed with no difference in dynorphin-like immunoreactivity, and opposite changes in galanin-like immunoreactivity.
151	1701038	Vasopressin-containing neurons primarily express tyrosine hydroxylase, galanin, dynorphin, [Leu]enkephalin and peptide histidine-isoleucine, and to a minor extent cholecystokinin and thyrotropin-releasing hormone.
152	1701038	Oxytocin-containing neurons mainly have cholecystokinin and corticotropin-releasing factor, and to a minor extent galanin, dynorphin, [Leu]enkephalin and thyrotropin-releasing hormone.
153	1701038	Colchicine treatment alone resulted in appearance of galanin-, dynorphin-, cholecystokinin-, [Leu]enkephalin- and thyrotropin-releasing hormone-positive cells.
154	1701038	When salt-loaded rats received colchicine, corticotropin-releasing factor- and peptide histidine-isoleucine-like immunoreactivity in addition increased, whereas galanin- and dynorphin-like immunoreactivity markedly decreased.
155	1701038	The Brattleboro rats resembled untreated rats, except their lack of vasopressin-like immunoreactivity, the marked increase in tyrosine hydroxylase-like immunoreactivity, and smaller increase in galanin- and dynorphin-like immunoreactivity.
156	1701038	Addition of colchicine to Brattleboro rats resulted in some distinct further changes in that dynorphin-like immunoreactivity decreased in some neurons and that [Leu]enkephalin-, corticotropin-releasing factor- and peptide histidine-isoleucine-like immunoreactivity increased substantially.
157	1701038	However, a marked difference in immunoreactive [Leu]enkephalin levels was observed with no difference in dynorphin-like immunoreactivity, and opposite changes in galanin-like immunoreactivity.
158	1701038	Vasopressin-containing neurons primarily express tyrosine hydroxylase, galanin, dynorphin, [Leu]enkephalin and peptide histidine-isoleucine, and to a minor extent cholecystokinin and thyrotropin-releasing hormone.
159	1701038	Oxytocin-containing neurons mainly have cholecystokinin and corticotropin-releasing factor, and to a minor extent galanin, dynorphin, [Leu]enkephalin and thyrotropin-releasing hormone.
160	1701038	Colchicine treatment alone resulted in appearance of galanin-, dynorphin-, cholecystokinin-, [Leu]enkephalin- and thyrotropin-releasing hormone-positive cells.
161	1701038	When salt-loaded rats received colchicine, corticotropin-releasing factor- and peptide histidine-isoleucine-like immunoreactivity in addition increased, whereas galanin- and dynorphin-like immunoreactivity markedly decreased.
162	1701038	The Brattleboro rats resembled untreated rats, except their lack of vasopressin-like immunoreactivity, the marked increase in tyrosine hydroxylase-like immunoreactivity, and smaller increase in galanin- and dynorphin-like immunoreactivity.
163	1701038	Addition of colchicine to Brattleboro rats resulted in some distinct further changes in that dynorphin-like immunoreactivity decreased in some neurons and that [Leu]enkephalin-, corticotropin-releasing factor- and peptide histidine-isoleucine-like immunoreactivity increased substantially.
164	1701038	However, a marked difference in immunoreactive [Leu]enkephalin levels was observed with no difference in dynorphin-like immunoreactivity, and opposite changes in galanin-like immunoreactivity.
165	1701038	Vasopressin-containing neurons primarily express tyrosine hydroxylase, galanin, dynorphin, [Leu]enkephalin and peptide histidine-isoleucine, and to a minor extent cholecystokinin and thyrotropin-releasing hormone.
166	1701038	Oxytocin-containing neurons mainly have cholecystokinin and corticotropin-releasing factor, and to a minor extent galanin, dynorphin, [Leu]enkephalin and thyrotropin-releasing hormone.
167	1701038	Colchicine treatment alone resulted in appearance of galanin-, dynorphin-, cholecystokinin-, [Leu]enkephalin- and thyrotropin-releasing hormone-positive cells.
168	1701038	When salt-loaded rats received colchicine, corticotropin-releasing factor- and peptide histidine-isoleucine-like immunoreactivity in addition increased, whereas galanin- and dynorphin-like immunoreactivity markedly decreased.
169	1701038	The Brattleboro rats resembled untreated rats, except their lack of vasopressin-like immunoreactivity, the marked increase in tyrosine hydroxylase-like immunoreactivity, and smaller increase in galanin- and dynorphin-like immunoreactivity.
170	1701038	Addition of colchicine to Brattleboro rats resulted in some distinct further changes in that dynorphin-like immunoreactivity decreased in some neurons and that [Leu]enkephalin-, corticotropin-releasing factor- and peptide histidine-isoleucine-like immunoreactivity increased substantially.
171	1701038	However, a marked difference in immunoreactive [Leu]enkephalin levels was observed with no difference in dynorphin-like immunoreactivity, and opposite changes in galanin-like immunoreactivity.
172	1701038	Vasopressin-containing neurons primarily express tyrosine hydroxylase, galanin, dynorphin, [Leu]enkephalin and peptide histidine-isoleucine, and to a minor extent cholecystokinin and thyrotropin-releasing hormone.
173	1701038	Oxytocin-containing neurons mainly have cholecystokinin and corticotropin-releasing factor, and to a minor extent galanin, dynorphin, [Leu]enkephalin and thyrotropin-releasing hormone.
174	1718802	Galanin, an inhibitor of insulin secretion in pancreatic beta-cells, exerts its multiple effects through mechanisms that are sensitive to pertussis toxin (PTX).
175	1718802	Antibody AS, which selectively recognizes Gi alpha 1 and Gi alpha 2, decreased tracer galanin binding to membranes at concentrations where there were no effects of other antibodies specifically directed against Gi alpha 3 or G alpha o.
176	1718802	Galanin, an inhibitor of insulin secretion in pancreatic beta-cells, exerts its multiple effects through mechanisms that are sensitive to pertussis toxin (PTX).
177	1718802	Antibody AS, which selectively recognizes Gi alpha 1 and Gi alpha 2, decreased tracer galanin binding to membranes at concentrations where there were no effects of other antibodies specifically directed against Gi alpha 3 or G alpha o.
178	1720364	In female cp/cp rats, central hypothalamic levels of neuropeptide Y (NPY), neurotensin, somatostatin and substance P were significantly lower (p less than 0.02) than in lean female controls.
179	1720364	The other 4 peptides examined (bombesin, calcitonin gene-related peptide, neuromedin B and vasoactive intestinal peptide) did not differ significantly between cp/cp and lean females, either fed freely or food-restricted.
180	1720364	NPY and galanin are powerful and specific central appetite stimulants, whereas neurotensin, substance P and somatostatin inhibit feeding when injected centrally.
181	1943736	Hypothalamic tissue levels of nine regulatory peptides (bombesin, calcitonin gene-related peptide [CGRP], galanin, neuromedin B, neuropeptide Y [NPY], neurotensin, somatostatin, substance P, and vasoactive intestinal peptide [VIP]) were compared in Aston obese diabetic (ob/ob) and lean (+/?)
182	2262048	The neuropeptides examined were vasoactive intestinal peptide, neuropeptide Y, substance P. calcitonin gene-related peptide, galanin and somatostatin.
183	2262048	Substance P and calcitonin gene-related peptide which are colocalized in a proportion of the somatostatin neurons were unaffected.
184	2457528	The nonadrenergic component may be mediated by the 29-amino acid peptide galanin in that this neuropeptide meets several of the criteria necessary to be considered a sympathetic neurotransmitter in the endocrine pancreas. 1) Galanin administration inhibits basal insulin and somatostatin secretion and stimulates basal glucagon secretion from the pancreas, qualitatively reproducing the effects of sympathetic nerve stimulation.
185	2457528	The quantity released is sufficient to reproduce sympathetic nerve stimulation-induced effects on insulin secretion and to contribute to the neural effects on somatostatin and glucagon release. 4) Whether interference with galanin action or release reduces the islet response to sympathetic nerve stimulation remains to be determined.
186	2457528	If galanin is a sympathetic neurotransmitter in the endocrine pancreas, it may contribute to the inhibition of insulin secretion that occurs during stress and thereby to the hyperglycemic response.
187	2457528	Moreover, the local presence of this potent beta-cell inhibitor in the islet leads to speculation on galanin's contribution to the impairment of insulin secretion that occurs in non-insulin-dependent diabetes mellitus and therefore on the potential utility of a galanin antagonist in the treatment of this disease.
188	2457528	The nonadrenergic component may be mediated by the 29-amino acid peptide galanin in that this neuropeptide meets several of the criteria necessary to be considered a sympathetic neurotransmitter in the endocrine pancreas. 1) Galanin administration inhibits basal insulin and somatostatin secretion and stimulates basal glucagon secretion from the pancreas, qualitatively reproducing the effects of sympathetic nerve stimulation.
189	2457528	The quantity released is sufficient to reproduce sympathetic nerve stimulation-induced effects on insulin secretion and to contribute to the neural effects on somatostatin and glucagon release. 4) Whether interference with galanin action or release reduces the islet response to sympathetic nerve stimulation remains to be determined.
190	2457528	If galanin is a sympathetic neurotransmitter in the endocrine pancreas, it may contribute to the inhibition of insulin secretion that occurs during stress and thereby to the hyperglycemic response.
191	2457528	Moreover, the local presence of this potent beta-cell inhibitor in the islet leads to speculation on galanin's contribution to the impairment of insulin secretion that occurs in non-insulin-dependent diabetes mellitus and therefore on the potential utility of a galanin antagonist in the treatment of this disease.
192	2457528	The nonadrenergic component may be mediated by the 29-amino acid peptide galanin in that this neuropeptide meets several of the criteria necessary to be considered a sympathetic neurotransmitter in the endocrine pancreas. 1) Galanin administration inhibits basal insulin and somatostatin secretion and stimulates basal glucagon secretion from the pancreas, qualitatively reproducing the effects of sympathetic nerve stimulation.
193	2457528	The quantity released is sufficient to reproduce sympathetic nerve stimulation-induced effects on insulin secretion and to contribute to the neural effects on somatostatin and glucagon release. 4) Whether interference with galanin action or release reduces the islet response to sympathetic nerve stimulation remains to be determined.
194	2457528	If galanin is a sympathetic neurotransmitter in the endocrine pancreas, it may contribute to the inhibition of insulin secretion that occurs during stress and thereby to the hyperglycemic response.
195	2457528	Moreover, the local presence of this potent beta-cell inhibitor in the islet leads to speculation on galanin's contribution to the impairment of insulin secretion that occurs in non-insulin-dependent diabetes mellitus and therefore on the potential utility of a galanin antagonist in the treatment of this disease.
196	2457528	The nonadrenergic component may be mediated by the 29-amino acid peptide galanin in that this neuropeptide meets several of the criteria necessary to be considered a sympathetic neurotransmitter in the endocrine pancreas. 1) Galanin administration inhibits basal insulin and somatostatin secretion and stimulates basal glucagon secretion from the pancreas, qualitatively reproducing the effects of sympathetic nerve stimulation.
197	2457528	The quantity released is sufficient to reproduce sympathetic nerve stimulation-induced effects on insulin secretion and to contribute to the neural effects on somatostatin and glucagon release. 4) Whether interference with galanin action or release reduces the islet response to sympathetic nerve stimulation remains to be determined.
198	2457528	If galanin is a sympathetic neurotransmitter in the endocrine pancreas, it may contribute to the inhibition of insulin secretion that occurs during stress and thereby to the hyperglycemic response.
199	2457528	Moreover, the local presence of this potent beta-cell inhibitor in the islet leads to speculation on galanin's contribution to the impairment of insulin secretion that occurs in non-insulin-dependent diabetes mellitus and therefore on the potential utility of a galanin antagonist in the treatment of this disease.
200	2457856	Galanin coexists with vasopressin in the normal rat hypothalamus and galanin's synthesis is increased in the Brattleboro (diabetes insipidus) rat.
201	2457856	Galanin is a peptide containing 29 amino acid residues, that is present in the median eminence, in the magnocellular neurons of the supraoptic (SON) and paraventricular nuclei (PVN) of the rat hypothalamus and in the posterior pituitary.
202	2457856	We report here that: (1) immunoreactivity for galanin (GAL) and vasopressin coexist in the SON of normal rats, (2) levels of mRNA encoding preprogalanin are markedly elevated in the PVN and SON of Brattleboro (diabetes insipidus) rats, as determined by in situ hybridization histochemistry but (3) levels of GAL-like immunoreactivity (GAL-LI) are significantly reduced in the posterior pituitary of these rats, as determined by radioimmunoassay.
203	2457856	Galanin coexists with vasopressin in the normal rat hypothalamus and galanin's synthesis is increased in the Brattleboro (diabetes insipidus) rat.
204	2457856	Galanin is a peptide containing 29 amino acid residues, that is present in the median eminence, in the magnocellular neurons of the supraoptic (SON) and paraventricular nuclei (PVN) of the rat hypothalamus and in the posterior pituitary.
205	2457856	We report here that: (1) immunoreactivity for galanin (GAL) and vasopressin coexist in the SON of normal rats, (2) levels of mRNA encoding preprogalanin are markedly elevated in the PVN and SON of Brattleboro (diabetes insipidus) rats, as determined by in situ hybridization histochemistry but (3) levels of GAL-like immunoreactivity (GAL-LI) are significantly reduced in the posterior pituitary of these rats, as determined by radioimmunoassay.
206	2457856	Galanin coexists with vasopressin in the normal rat hypothalamus and galanin's synthesis is increased in the Brattleboro (diabetes insipidus) rat.
207	2457856	Galanin is a peptide containing 29 amino acid residues, that is present in the median eminence, in the magnocellular neurons of the supraoptic (SON) and paraventricular nuclei (PVN) of the rat hypothalamus and in the posterior pituitary.
208	2457856	We report here that: (1) immunoreactivity for galanin (GAL) and vasopressin coexist in the SON of normal rats, (2) levels of mRNA encoding preprogalanin are markedly elevated in the PVN and SON of Brattleboro (diabetes insipidus) rats, as determined by in situ hybridization histochemistry but (3) levels of GAL-like immunoreactivity (GAL-LI) are significantly reduced in the posterior pituitary of these rats, as determined by radioimmunoassay.
209	2475378	The neuropeptide galanin inhibits glucose-stimulated insulin release in dogs and rodents and has been proposed as having a role in the control of insulin release in humans.
210	2475378	The results showed no effect of galanin infusion on plasma glucose or serum insulin, although a rise in serum growth hormone even in the face of the intravenous glucose load confirmed the potent growth hormone-stimulating effect of galanin.
211	2475378	The neuropeptide galanin inhibits glucose-stimulated insulin release in dogs and rodents and has been proposed as having a role in the control of insulin release in humans.
212	2475378	The results showed no effect of galanin infusion on plasma glucose or serum insulin, although a rise in serum growth hormone even in the face of the intravenous glucose load confirmed the potent growth hormone-stimulating effect of galanin.
213	2578419	Galanin inhibits insulin secretion and induces hyperglycemia in dogs.
214	2578419	Intravenous administration of galanin into fasted conscious dogs produced a dose-dependent hyperglycemia accompanied by decreases in plasma insulin levels, but with no elevation of plasma glucagon levels.
215	2578419	Galanin infusions produced greater parenteral glucose-induced rises in plasma glucose levels along with markedly blunted insulin responses compared with glucose and insulin responses to control glucose infusions.
216	2578419	Immediately after cessation of the galanin infusions, elevation of plasma insulin levels occurred in the basal state and after parenteral glucose loading.
217	2578419	These results suggest that galanin's hyperglycemic activity is predominantly mediated by a reversible inhibition of insulin secretion.
218	2578419	Galanin inhibits insulin secretion and induces hyperglycemia in dogs.
219	2578419	Intravenous administration of galanin into fasted conscious dogs produced a dose-dependent hyperglycemia accompanied by decreases in plasma insulin levels, but with no elevation of plasma glucagon levels.
220	2578419	Galanin infusions produced greater parenteral glucose-induced rises in plasma glucose levels along with markedly blunted insulin responses compared with glucose and insulin responses to control glucose infusions.
221	2578419	Immediately after cessation of the galanin infusions, elevation of plasma insulin levels occurred in the basal state and after parenteral glucose loading.
222	2578419	These results suggest that galanin's hyperglycemic activity is predominantly mediated by a reversible inhibition of insulin secretion.
223	2578419	Galanin inhibits insulin secretion and induces hyperglycemia in dogs.
224	2578419	Intravenous administration of galanin into fasted conscious dogs produced a dose-dependent hyperglycemia accompanied by decreases in plasma insulin levels, but with no elevation of plasma glucagon levels.
225	2578419	Galanin infusions produced greater parenteral glucose-induced rises in plasma glucose levels along with markedly blunted insulin responses compared with glucose and insulin responses to control glucose infusions.
226	2578419	Immediately after cessation of the galanin infusions, elevation of plasma insulin levels occurred in the basal state and after parenteral glucose loading.
227	2578419	These results suggest that galanin's hyperglycemic activity is predominantly mediated by a reversible inhibition of insulin secretion.
228	2578419	Galanin inhibits insulin secretion and induces hyperglycemia in dogs.
229	2578419	Intravenous administration of galanin into fasted conscious dogs produced a dose-dependent hyperglycemia accompanied by decreases in plasma insulin levels, but with no elevation of plasma glucagon levels.
230	2578419	Galanin infusions produced greater parenteral glucose-induced rises in plasma glucose levels along with markedly blunted insulin responses compared with glucose and insulin responses to control glucose infusions.
231	2578419	Immediately after cessation of the galanin infusions, elevation of plasma insulin levels occurred in the basal state and after parenteral glucose loading.
232	2578419	These results suggest that galanin's hyperglycemic activity is predominantly mediated by a reversible inhibition of insulin secretion.
233	2578419	Galanin inhibits insulin secretion and induces hyperglycemia in dogs.
234	2578419	Intravenous administration of galanin into fasted conscious dogs produced a dose-dependent hyperglycemia accompanied by decreases in plasma insulin levels, but with no elevation of plasma glucagon levels.
235	2578419	Galanin infusions produced greater parenteral glucose-induced rises in plasma glucose levels along with markedly blunted insulin responses compared with glucose and insulin responses to control glucose infusions.
236	2578419	Immediately after cessation of the galanin infusions, elevation of plasma insulin levels occurred in the basal state and after parenteral glucose loading.
237	2578419	These results suggest that galanin's hyperglycemic activity is predominantly mediated by a reversible inhibition of insulin secretion.
238	2873516	Urinary excretion of glycosaminoglycans (GAGS) and sialic acid (SA), as well as the activity of two renal enzymes related to glycoprotein metabolism, N-acetyl-beta-D-glucosaminidase (NAG) and beta-galactosidase (GAL), and two others unrelated to glycosaminoglycans and glycoprotein metabolism, gamma-glutamyltranspeptidase (gamma-Gt) and angiotensin-I-converting enzyme (ACE), were evaluated in 40 insulin-dependent diabetic patients with normal range albuminuria, 21 patients with mesangial glomerulonephritis, and 30 control subjects.
239	2873516	Diabetic and glomerulonephritic patients excreted a significantly higher amount of GAGS and SA, and showed greater NAG and GAL activities; gamma-Gt and ACE levels were within normal ranges.
240	2873516	No correlation could be demonstrated between diabetes duration and GAGS, SA, NAG and GAL findings.
241	2873516	Moreover, no correspondence between degree of metabolic control, as reflected by glycosylated hemoglobin (HbA1a-c) and GAGS, SA, NAG and GAL emerged.
242	2873516	Urinary excretion of glycosaminoglycans (GAGS) and sialic acid (SA), as well as the activity of two renal enzymes related to glycoprotein metabolism, N-acetyl-beta-D-glucosaminidase (NAG) and beta-galactosidase (GAL), and two others unrelated to glycosaminoglycans and glycoprotein metabolism, gamma-glutamyltranspeptidase (gamma-Gt) and angiotensin-I-converting enzyme (ACE), were evaluated in 40 insulin-dependent diabetic patients with normal range albuminuria, 21 patients with mesangial glomerulonephritis, and 30 control subjects.
243	2873516	Diabetic and glomerulonephritic patients excreted a significantly higher amount of GAGS and SA, and showed greater NAG and GAL activities; gamma-Gt and ACE levels were within normal ranges.
244	2873516	No correlation could be demonstrated between diabetes duration and GAGS, SA, NAG and GAL findings.
245	2873516	Moreover, no correspondence between degree of metabolic control, as reflected by glycosylated hemoglobin (HbA1a-c) and GAGS, SA, NAG and GAL emerged.
246	2873516	Urinary excretion of glycosaminoglycans (GAGS) and sialic acid (SA), as well as the activity of two renal enzymes related to glycoprotein metabolism, N-acetyl-beta-D-glucosaminidase (NAG) and beta-galactosidase (GAL), and two others unrelated to glycosaminoglycans and glycoprotein metabolism, gamma-glutamyltranspeptidase (gamma-Gt) and angiotensin-I-converting enzyme (ACE), were evaluated in 40 insulin-dependent diabetic patients with normal range albuminuria, 21 patients with mesangial glomerulonephritis, and 30 control subjects.
247	2873516	Diabetic and glomerulonephritic patients excreted a significantly higher amount of GAGS and SA, and showed greater NAG and GAL activities; gamma-Gt and ACE levels were within normal ranges.
248	2873516	No correlation could be demonstrated between diabetes duration and GAGS, SA, NAG and GAL findings.
249	2873516	Moreover, no correspondence between degree of metabolic control, as reflected by glycosylated hemoglobin (HbA1a-c) and GAGS, SA, NAG and GAL emerged.
250	2905691	Reduced hypothalamic somatostatin and neuropeptide Y concentrations in the spontaneously-diabetic Chinese hamster.
251	2905691	In the diabetic hamsters, hypothalamic concentrations of somatostatin and neuropeptide Y were significantly reduced by 25-30% below controls.
252	2905691	None of the other four peptides examined (bombesin, galanin, neurotensin and vasoactive intestinal peptide) differed significantly between the two groups.
253	2905691	Disturbances in neuropeptide Y (the most potent central appetite stimulant yet discovered) and in somatostatin could be related to hyperphagia, an early and possibly primary abnormality of the diabetic syndrome in the Chinese hamster.
254	3289997	Hypothalamic concentrations of the other six peptides examined (bombesin, galanin, neuromedin B, substance P, somatostatin, and vasoactive intestinal peptide) did not differ significantly between STZ-D and control groups at any time.
255	3537810	Using a chemical detection method, a search for previously unknown peptides that possess the C-terminal amide structure in extracts of brain and intestine was carried out and a number of novel neuropeptides and hormonal peptides, designated neuropeptide Y, PHI, peptide YY, galanin and neuropeptide K were isolated.
256	7505245	Inhibition of insulin secretion by galanin is pertussis toxin (PTX) sensitive, suggesting the activation of one or more heterotrimeric (alpha, beta, gamma) G-proteins (Gi/Go).
257	7505518	Galanin inhibits insulin secretion and has been proposed to function as a sympathetic neurotransmitter in the endocrine pancreas in some species, for example in the dog.
258	7526840	Inhibition of adenylate cyclase activity by galanin in rat insulinoma cells is mediated by the G-protein Gi3.
259	7526840	Galanin inhibits adenylate cyclase activity and insulin secretion and modulates ion channels in pancreatic beta-cells through pertussis-toxin-sensitive G-protein(s).
260	7526840	Antibodies directed against the C-terminal region of specific G-protein alpha-subunits were used to determine which G-protein(s) couple galanin receptors to inhibition of adenylate cyclase in the rat insulinoma cell line RINm5F.
261	7526840	Preincubation of membranes with EC antibody (anti-alpha i3) decreased the inhibition of forskolin-stimulated adenylate cyclase activity by galanin (100 nM) by 45% compared with control IgG (P < 0.05) whereas preincubation with AS (anti-alpha i1, alpha i2) or GO (anti-alpha o) antibodies had no significant effect.
262	7526840	Inhibition of adenylate cyclase activity by galanin was largely abolished in membranes from cells exposed to the oligodeoxynucleotide antisense to alpha i3, whereas all other oligodeoxynucleotides had no significant effect on this pathway.
263	7526840	These results suggest that Gi3 is the G protein that couples galanin receptors to inhibition of adenylate cyclase activity in RINm5F cells.
264	7526840	Inhibition of adenylate cyclase activity by galanin in rat insulinoma cells is mediated by the G-protein Gi3.
265	7526840	Galanin inhibits adenylate cyclase activity and insulin secretion and modulates ion channels in pancreatic beta-cells through pertussis-toxin-sensitive G-protein(s).
266	7526840	Antibodies directed against the C-terminal region of specific G-protein alpha-subunits were used to determine which G-protein(s) couple galanin receptors to inhibition of adenylate cyclase in the rat insulinoma cell line RINm5F.
267	7526840	Preincubation of membranes with EC antibody (anti-alpha i3) decreased the inhibition of forskolin-stimulated adenylate cyclase activity by galanin (100 nM) by 45% compared with control IgG (P < 0.05) whereas preincubation with AS (anti-alpha i1, alpha i2) or GO (anti-alpha o) antibodies had no significant effect.
268	7526840	Inhibition of adenylate cyclase activity by galanin was largely abolished in membranes from cells exposed to the oligodeoxynucleotide antisense to alpha i3, whereas all other oligodeoxynucleotides had no significant effect on this pathway.
269	7526840	These results suggest that Gi3 is the G protein that couples galanin receptors to inhibition of adenylate cyclase activity in RINm5F cells.
270	7526840	Inhibition of adenylate cyclase activity by galanin in rat insulinoma cells is mediated by the G-protein Gi3.
271	7526840	Galanin inhibits adenylate cyclase activity and insulin secretion and modulates ion channels in pancreatic beta-cells through pertussis-toxin-sensitive G-protein(s).
272	7526840	Antibodies directed against the C-terminal region of specific G-protein alpha-subunits were used to determine which G-protein(s) couple galanin receptors to inhibition of adenylate cyclase in the rat insulinoma cell line RINm5F.
273	7526840	Preincubation of membranes with EC antibody (anti-alpha i3) decreased the inhibition of forskolin-stimulated adenylate cyclase activity by galanin (100 nM) by 45% compared with control IgG (P < 0.05) whereas preincubation with AS (anti-alpha i1, alpha i2) or GO (anti-alpha o) antibodies had no significant effect.
274	7526840	Inhibition of adenylate cyclase activity by galanin was largely abolished in membranes from cells exposed to the oligodeoxynucleotide antisense to alpha i3, whereas all other oligodeoxynucleotides had no significant effect on this pathway.
275	7526840	These results suggest that Gi3 is the G protein that couples galanin receptors to inhibition of adenylate cyclase activity in RINm5F cells.
276	7526840	Inhibition of adenylate cyclase activity by galanin in rat insulinoma cells is mediated by the G-protein Gi3.
277	7526840	Galanin inhibits adenylate cyclase activity and insulin secretion and modulates ion channels in pancreatic beta-cells through pertussis-toxin-sensitive G-protein(s).
278	7526840	Antibodies directed against the C-terminal region of specific G-protein alpha-subunits were used to determine which G-protein(s) couple galanin receptors to inhibition of adenylate cyclase in the rat insulinoma cell line RINm5F.
279	7526840	Preincubation of membranes with EC antibody (anti-alpha i3) decreased the inhibition of forskolin-stimulated adenylate cyclase activity by galanin (100 nM) by 45% compared with control IgG (P < 0.05) whereas preincubation with AS (anti-alpha i1, alpha i2) or GO (anti-alpha o) antibodies had no significant effect.
280	7526840	Inhibition of adenylate cyclase activity by galanin was largely abolished in membranes from cells exposed to the oligodeoxynucleotide antisense to alpha i3, whereas all other oligodeoxynucleotides had no significant effect on this pathway.
281	7526840	These results suggest that Gi3 is the G protein that couples galanin receptors to inhibition of adenylate cyclase activity in RINm5F cells.
282	7526840	Inhibition of adenylate cyclase activity by galanin in rat insulinoma cells is mediated by the G-protein Gi3.
283	7526840	Galanin inhibits adenylate cyclase activity and insulin secretion and modulates ion channels in pancreatic beta-cells through pertussis-toxin-sensitive G-protein(s).
284	7526840	Antibodies directed against the C-terminal region of specific G-protein alpha-subunits were used to determine which G-protein(s) couple galanin receptors to inhibition of adenylate cyclase in the rat insulinoma cell line RINm5F.
285	7526840	Preincubation of membranes with EC antibody (anti-alpha i3) decreased the inhibition of forskolin-stimulated adenylate cyclase activity by galanin (100 nM) by 45% compared with control IgG (P < 0.05) whereas preincubation with AS (anti-alpha i1, alpha i2) or GO (anti-alpha o) antibodies had no significant effect.
286	7526840	Inhibition of adenylate cyclase activity by galanin was largely abolished in membranes from cells exposed to the oligodeoxynucleotide antisense to alpha i3, whereas all other oligodeoxynucleotides had no significant effect on this pathway.
287	7526840	These results suggest that Gi3 is the G protein that couples galanin receptors to inhibition of adenylate cyclase activity in RINm5F cells.
288	7526840	Inhibition of adenylate cyclase activity by galanin in rat insulinoma cells is mediated by the G-protein Gi3.
289	7526840	Galanin inhibits adenylate cyclase activity and insulin secretion and modulates ion channels in pancreatic beta-cells through pertussis-toxin-sensitive G-protein(s).
290	7526840	Antibodies directed against the C-terminal region of specific G-protein alpha-subunits were used to determine which G-protein(s) couple galanin receptors to inhibition of adenylate cyclase in the rat insulinoma cell line RINm5F.
291	7526840	Preincubation of membranes with EC antibody (anti-alpha i3) decreased the inhibition of forskolin-stimulated adenylate cyclase activity by galanin (100 nM) by 45% compared with control IgG (P < 0.05) whereas preincubation with AS (anti-alpha i1, alpha i2) or GO (anti-alpha o) antibodies had no significant effect.
292	7526840	Inhibition of adenylate cyclase activity by galanin was largely abolished in membranes from cells exposed to the oligodeoxynucleotide antisense to alpha i3, whereas all other oligodeoxynucleotides had no significant effect on this pathway.
293	7526840	These results suggest that Gi3 is the G protein that couples galanin receptors to inhibition of adenylate cyclase activity in RINm5F cells.
294	7535266	Gi2 and Gi3 proteins mediate the inhibition of adenylyl cyclase by galanin in the RINm5F cell.
295	7535266	Inhibition of adenylyl cyclase activity is one of at least four mechanisms by which the neuropeptide galanin inhibits insulin secretion from pancreatic beta-cells.
296	7535266	In a membrane preparation of the insulin-secreting cell line RINm5F, a maximally effective concentration of galanin inhibited forskolin-stimulated adenylyl cyclase activity by 30%.
297	7535266	Because galanin receptors interact with four G-proteins (Gi1, Gi2, Gi3, and Go1), any or all of these may inhibit adenylyl cyclase.
298	7535266	Therefore, to identify the G-protein(s) involved, antibodies raised against various G-protein alpha-subunits were used to block the inhibition of forskolin-stimulated adenylyl cyclase activity by galanin in RINm5F membrane preparations.
299	7535266	Antisera AS/7 and EC/2, specific for G alpha i1/alpha i2 and G alpha i3, respectively, were able to significantly attenuate the inhibitory effect of galanin, whereas antisera specific for Go proteins were not.
300	7535266	Thus, galanin inhibition of adenylyl cyclase activity in these cells is selectively mediated by two inhibitory G-proteins, Gi2 and Gi3.
301	7535266	Gi2 and Gi3 proteins mediate the inhibition of adenylyl cyclase by galanin in the RINm5F cell.
302	7535266	Inhibition of adenylyl cyclase activity is one of at least four mechanisms by which the neuropeptide galanin inhibits insulin secretion from pancreatic beta-cells.
303	7535266	In a membrane preparation of the insulin-secreting cell line RINm5F, a maximally effective concentration of galanin inhibited forskolin-stimulated adenylyl cyclase activity by 30%.
304	7535266	Because galanin receptors interact with four G-proteins (Gi1, Gi2, Gi3, and Go1), any or all of these may inhibit adenylyl cyclase.
305	7535266	Therefore, to identify the G-protein(s) involved, antibodies raised against various G-protein alpha-subunits were used to block the inhibition of forskolin-stimulated adenylyl cyclase activity by galanin in RINm5F membrane preparations.
306	7535266	Antisera AS/7 and EC/2, specific for G alpha i1/alpha i2 and G alpha i3, respectively, were able to significantly attenuate the inhibitory effect of galanin, whereas antisera specific for Go proteins were not.
307	7535266	Thus, galanin inhibition of adenylyl cyclase activity in these cells is selectively mediated by two inhibitory G-proteins, Gi2 and Gi3.
308	7535266	Gi2 and Gi3 proteins mediate the inhibition of adenylyl cyclase by galanin in the RINm5F cell.
309	7535266	Inhibition of adenylyl cyclase activity is one of at least four mechanisms by which the neuropeptide galanin inhibits insulin secretion from pancreatic beta-cells.
310	7535266	In a membrane preparation of the insulin-secreting cell line RINm5F, a maximally effective concentration of galanin inhibited forskolin-stimulated adenylyl cyclase activity by 30%.
311	7535266	Because galanin receptors interact with four G-proteins (Gi1, Gi2, Gi3, and Go1), any or all of these may inhibit adenylyl cyclase.
312	7535266	Therefore, to identify the G-protein(s) involved, antibodies raised against various G-protein alpha-subunits were used to block the inhibition of forskolin-stimulated adenylyl cyclase activity by galanin in RINm5F membrane preparations.
313	7535266	Antisera AS/7 and EC/2, specific for G alpha i1/alpha i2 and G alpha i3, respectively, were able to significantly attenuate the inhibitory effect of galanin, whereas antisera specific for Go proteins were not.
314	7535266	Thus, galanin inhibition of adenylyl cyclase activity in these cells is selectively mediated by two inhibitory G-proteins, Gi2 and Gi3.
315	7535266	Gi2 and Gi3 proteins mediate the inhibition of adenylyl cyclase by galanin in the RINm5F cell.
316	7535266	Inhibition of adenylyl cyclase activity is one of at least four mechanisms by which the neuropeptide galanin inhibits insulin secretion from pancreatic beta-cells.
317	7535266	In a membrane preparation of the insulin-secreting cell line RINm5F, a maximally effective concentration of galanin inhibited forskolin-stimulated adenylyl cyclase activity by 30%.
318	7535266	Because galanin receptors interact with four G-proteins (Gi1, Gi2, Gi3, and Go1), any or all of these may inhibit adenylyl cyclase.
319	7535266	Therefore, to identify the G-protein(s) involved, antibodies raised against various G-protein alpha-subunits were used to block the inhibition of forskolin-stimulated adenylyl cyclase activity by galanin in RINm5F membrane preparations.
320	7535266	Antisera AS/7 and EC/2, specific for G alpha i1/alpha i2 and G alpha i3, respectively, were able to significantly attenuate the inhibitory effect of galanin, whereas antisera specific for Go proteins were not.
321	7535266	Thus, galanin inhibition of adenylyl cyclase activity in these cells is selectively mediated by two inhibitory G-proteins, Gi2 and Gi3.
322	7535266	Gi2 and Gi3 proteins mediate the inhibition of adenylyl cyclase by galanin in the RINm5F cell.
323	7535266	Inhibition of adenylyl cyclase activity is one of at least four mechanisms by which the neuropeptide galanin inhibits insulin secretion from pancreatic beta-cells.
324	7535266	In a membrane preparation of the insulin-secreting cell line RINm5F, a maximally effective concentration of galanin inhibited forskolin-stimulated adenylyl cyclase activity by 30%.
325	7535266	Because galanin receptors interact with four G-proteins (Gi1, Gi2, Gi3, and Go1), any or all of these may inhibit adenylyl cyclase.
326	7535266	Therefore, to identify the G-protein(s) involved, antibodies raised against various G-protein alpha-subunits were used to block the inhibition of forskolin-stimulated adenylyl cyclase activity by galanin in RINm5F membrane preparations.
327	7535266	Antisera AS/7 and EC/2, specific for G alpha i1/alpha i2 and G alpha i3, respectively, were able to significantly attenuate the inhibitory effect of galanin, whereas antisera specific for Go proteins were not.
328	7535266	Thus, galanin inhibition of adenylyl cyclase activity in these cells is selectively mediated by two inhibitory G-proteins, Gi2 and Gi3.
329	7535266	Gi2 and Gi3 proteins mediate the inhibition of adenylyl cyclase by galanin in the RINm5F cell.
330	7535266	Inhibition of adenylyl cyclase activity is one of at least four mechanisms by which the neuropeptide galanin inhibits insulin secretion from pancreatic beta-cells.
331	7535266	In a membrane preparation of the insulin-secreting cell line RINm5F, a maximally effective concentration of galanin inhibited forskolin-stimulated adenylyl cyclase activity by 30%.
332	7535266	Because galanin receptors interact with four G-proteins (Gi1, Gi2, Gi3, and Go1), any or all of these may inhibit adenylyl cyclase.
333	7535266	Therefore, to identify the G-protein(s) involved, antibodies raised against various G-protein alpha-subunits were used to block the inhibition of forskolin-stimulated adenylyl cyclase activity by galanin in RINm5F membrane preparations.
334	7535266	Antisera AS/7 and EC/2, specific for G alpha i1/alpha i2 and G alpha i3, respectively, were able to significantly attenuate the inhibitory effect of galanin, whereas antisera specific for Go proteins were not.
335	7535266	Thus, galanin inhibition of adenylyl cyclase activity in these cells is selectively mediated by two inhibitory G-proteins, Gi2 and Gi3.
336	7535266	Gi2 and Gi3 proteins mediate the inhibition of adenylyl cyclase by galanin in the RINm5F cell.
337	7535266	Inhibition of adenylyl cyclase activity is one of at least four mechanisms by which the neuropeptide galanin inhibits insulin secretion from pancreatic beta-cells.
338	7535266	In a membrane preparation of the insulin-secreting cell line RINm5F, a maximally effective concentration of galanin inhibited forskolin-stimulated adenylyl cyclase activity by 30%.
339	7535266	Because galanin receptors interact with four G-proteins (Gi1, Gi2, Gi3, and Go1), any or all of these may inhibit adenylyl cyclase.
340	7535266	Therefore, to identify the G-protein(s) involved, antibodies raised against various G-protein alpha-subunits were used to block the inhibition of forskolin-stimulated adenylyl cyclase activity by galanin in RINm5F membrane preparations.
341	7535266	Antisera AS/7 and EC/2, specific for G alpha i1/alpha i2 and G alpha i3, respectively, were able to significantly attenuate the inhibitory effect of galanin, whereas antisera specific for Go proteins were not.
342	7535266	Thus, galanin inhibition of adenylyl cyclase activity in these cells is selectively mediated by two inhibitory G-proteins, Gi2 and Gi3.
343	7535425	The protein kinase A inhibitor, Rp-cAMPS, at 100 microM, completely inhibited the relaxant effect of an EC50 concentration of galanin (3 nM), but only inhibited that by VIP by 80% (p < 0.05).
344	7678403	Galanin stimulated the high-affinity GTPase, over the concentration range in which it inhibits stimulated insulin secretion, to a maximal rate 80% greater than the basal rate.
345	7689105	This study investigates the ability of two chimeric galanin analogs, [# 1-galantide = (M-15) = [galanin (1-13)-substance P(5-11)] and #2-M-35[galanin(1-13)bradykinin (2-9)], which were recently reported to function as galanin-receptor antagonists in the CNS, to interact with galanin receptors on rat jejunal muscle strips or dispersed smooth muscle cells from guinea pig stomach.
346	7689105	In dispersed smooth muscle cells, galanin, as well as each chimeric analog, caused muscle relaxation, whereas substance P and bradykinin both caused muscle contraction.
347	7796922	Both galanin and somatostatin inhibit insulin release from pancreatic beta-cells by opening KATP through the activation of G-protein.
348	7796922	Glucagon-like peptide-1[7-36], which stimulates insulin secretion by indirectly blocking KATP in beta-cells, shows antidiabetic effects in patients with non-insulin-dependent diabetes mellitus.
349	8637571	The hypothalamus plays a central role in the integrated regulation of energy homeostasis and body weight, and a number of hypothalamic neuropeptides, such as neuropeptide Y (ref. 1), galanin, CRH (ref. 3) and GLP-1 (ref. 4), have been implicated in the mediation of these effects.
350	8738309	Enteric neuropeptides in streptozotocin-diabetic rats; effects of insulin and aldose reductase inhibition.
351	8738309	The aim of the present study was to determine whether diabetes-induced changes in the distribution of enteric neuropeptides, could be prevented in 12-week streptozotocin-diabetic rats, by rigorous control of glycaemia, using daily adminstration of insulin, or an aldose reductase inhibitor (ponalrestat).
352	8738309	The pattern of distribution of nerve fibres and cell bodies, containing immunoreactive vasoactive intestinal polypeptide (VIP), galanin (GAL), calcitonin gene-related peptide (CGRP) and substance P was examined in the myenteric plexus of ileum from control, untreated diabetic, insulin-treated diabetic and aldose reductase inhibitor-treated diabetic rats.
353	8738309	The increase in VIP- and GAL-like immunoreactivity, seen in the myenteric plexus of untreated diabetic rat ileum, was not present in the myenteric plexus of ileum from insulin- and aldose reductase inhibitor-treated diabetic rats.
354	8738309	This was prevented by insulin treatment, but aldose reductase inhibitor treatment had no effect.
355	8738309	Generally, the similarity of effect of ponalrestat and insulin on VIP and galanin expression in this study supports a primary effect of insulin via glycaemic control.
356	8738309	The dissimilarity of the effect of the two treatments on CGRP expression may imply a neurotrophic effect of insulin, although there are certainly consequences of hyperglycaemia other than exaggerated flux through the polyol pathway.
357	8738309	Enteric neuropeptides in streptozotocin-diabetic rats; effects of insulin and aldose reductase inhibition.
358	8738309	The aim of the present study was to determine whether diabetes-induced changes in the distribution of enteric neuropeptides, could be prevented in 12-week streptozotocin-diabetic rats, by rigorous control of glycaemia, using daily adminstration of insulin, or an aldose reductase inhibitor (ponalrestat).
359	8738309	The pattern of distribution of nerve fibres and cell bodies, containing immunoreactive vasoactive intestinal polypeptide (VIP), galanin (GAL), calcitonin gene-related peptide (CGRP) and substance P was examined in the myenteric plexus of ileum from control, untreated diabetic, insulin-treated diabetic and aldose reductase inhibitor-treated diabetic rats.
360	8738309	The increase in VIP- and GAL-like immunoreactivity, seen in the myenteric plexus of untreated diabetic rat ileum, was not present in the myenteric plexus of ileum from insulin- and aldose reductase inhibitor-treated diabetic rats.
361	8738309	This was prevented by insulin treatment, but aldose reductase inhibitor treatment had no effect.
362	8738309	Generally, the similarity of effect of ponalrestat and insulin on VIP and galanin expression in this study supports a primary effect of insulin via glycaemic control.
363	8738309	The dissimilarity of the effect of the two treatments on CGRP expression may imply a neurotrophic effect of insulin, although there are certainly consequences of hyperglycaemia other than exaggerated flux through the polyol pathway.
364	8738309	Enteric neuropeptides in streptozotocin-diabetic rats; effects of insulin and aldose reductase inhibition.
365	8738309	The aim of the present study was to determine whether diabetes-induced changes in the distribution of enteric neuropeptides, could be prevented in 12-week streptozotocin-diabetic rats, by rigorous control of glycaemia, using daily adminstration of insulin, or an aldose reductase inhibitor (ponalrestat).
366	8738309	The pattern of distribution of nerve fibres and cell bodies, containing immunoreactive vasoactive intestinal polypeptide (VIP), galanin (GAL), calcitonin gene-related peptide (CGRP) and substance P was examined in the myenteric plexus of ileum from control, untreated diabetic, insulin-treated diabetic and aldose reductase inhibitor-treated diabetic rats.
367	8738309	The increase in VIP- and GAL-like immunoreactivity, seen in the myenteric plexus of untreated diabetic rat ileum, was not present in the myenteric plexus of ileum from insulin- and aldose reductase inhibitor-treated diabetic rats.
368	8738309	This was prevented by insulin treatment, but aldose reductase inhibitor treatment had no effect.
369	8738309	Generally, the similarity of effect of ponalrestat and insulin on VIP and galanin expression in this study supports a primary effect of insulin via glycaemic control.
370	8738309	The dissimilarity of the effect of the two treatments on CGRP expression may imply a neurotrophic effect of insulin, although there are certainly consequences of hyperglycaemia other than exaggerated flux through the polyol pathway.
371	8897861	Decreased glucose-induced cAMP and insulin release in islets of diabetic rats: reversal by IBMX, glucagon, GIP.
372	8897861	Somatostatin, prostaglandin E2, UK-14304, or galanin inhibited cAMP accumulation and insulin release to the same extent in both types of islets.
373	8897861	The addition of IBMX, glucagon, or gastric inhibitory polypeptide (GIP) to perifused islets of diabetic rats amplified their insulin response to glucose, and a clear biphasic pattern of the release was regained.
374	9032095	Activated receptors for galanin and norepinephrine, and for several other agonists, inhibit insulin release from pancreatic beta-cells via pertussis toxin-sensitive Gi- and Go-proteins and by acting on at least four cellular mechanisms.
375	9149292	Differential effects of baseline macronutrient preferences on macronutrient selection after galanin, NPY, and an overnight fast.
376	9149292	We investigated whether these individual preferences in macronutrient selection could be modified by an overnight fast or by two orexigenic peptides, galanin and neuropeptide Y (NPY), which may selectively stimulate fat and carbohydrate intake.
377	9149292	In counterbalanced tests conducted on separate days, saline, galanin, or NPY was infused into the paraventricular nucleus of the hypothalamus and 60-min food intake was measured.
378	9149292	These data demonstrate that baseline preferences for fat or carbohydrate are not significantly modified by galanin or NPY but that an overnight fast increases fat preference.
379	9149292	Differential effects of baseline macronutrient preferences on macronutrient selection after galanin, NPY, and an overnight fast.
380	9149292	We investigated whether these individual preferences in macronutrient selection could be modified by an overnight fast or by two orexigenic peptides, galanin and neuropeptide Y (NPY), which may selectively stimulate fat and carbohydrate intake.
381	9149292	In counterbalanced tests conducted on separate days, saline, galanin, or NPY was infused into the paraventricular nucleus of the hypothalamus and 60-min food intake was measured.
382	9149292	These data demonstrate that baseline preferences for fat or carbohydrate are not significantly modified by galanin or NPY but that an overnight fast increases fat preference.
383	9149292	Differential effects of baseline macronutrient preferences on macronutrient selection after galanin, NPY, and an overnight fast.
384	9149292	We investigated whether these individual preferences in macronutrient selection could be modified by an overnight fast or by two orexigenic peptides, galanin and neuropeptide Y (NPY), which may selectively stimulate fat and carbohydrate intake.
385	9149292	In counterbalanced tests conducted on separate days, saline, galanin, or NPY was infused into the paraventricular nucleus of the hypothalamus and 60-min food intake was measured.
386	9149292	These data demonstrate that baseline preferences for fat or carbohydrate are not significantly modified by galanin or NPY but that an overnight fast increases fat preference.
387	9149292	Differential effects of baseline macronutrient preferences on macronutrient selection after galanin, NPY, and an overnight fast.
388	9149292	We investigated whether these individual preferences in macronutrient selection could be modified by an overnight fast or by two orexigenic peptides, galanin and neuropeptide Y (NPY), which may selectively stimulate fat and carbohydrate intake.
389	9149292	In counterbalanced tests conducted on separate days, saline, galanin, or NPY was infused into the paraventricular nucleus of the hypothalamus and 60-min food intake was measured.
390	9149292	These data demonstrate that baseline preferences for fat or carbohydrate are not significantly modified by galanin or NPY but that an overnight fast increases fat preference.
391	9439531	Neuropeptide Y, galanin, and leptin release in obese women and in women with anorexia nervosa.
392	9439531	The study objective was to determine circulating levels of the appetite-controlling neuropeptides, neuropeptide Y (NPY), galanin, and leptin, in subjects with eating disorders.
393	9439531	Plasma NPY, galanin, and leptin concentrations were measured in peripheral blood samples with radioimmunoassay methods.
394	9439531	Plasma NPY and galanin concentrations in women with anorexia nervosa did not differ from the levels in the control group.
395	9439531	Our results indicate that inappropriate plasma concentrations of NPY, galanin, and leptin in obese women may be a consequence of their weight status, or could be one of many factors involved in the pathogenesis of obesity.
396	9439531	Neuropeptide Y, galanin, and leptin release in obese women and in women with anorexia nervosa.
397	9439531	The study objective was to determine circulating levels of the appetite-controlling neuropeptides, neuropeptide Y (NPY), galanin, and leptin, in subjects with eating disorders.
398	9439531	Plasma NPY, galanin, and leptin concentrations were measured in peripheral blood samples with radioimmunoassay methods.
399	9439531	Plasma NPY and galanin concentrations in women with anorexia nervosa did not differ from the levels in the control group.
400	9439531	Our results indicate that inappropriate plasma concentrations of NPY, galanin, and leptin in obese women may be a consequence of their weight status, or could be one of many factors involved in the pathogenesis of obesity.
401	9439531	Neuropeptide Y, galanin, and leptin release in obese women and in women with anorexia nervosa.
402	9439531	The study objective was to determine circulating levels of the appetite-controlling neuropeptides, neuropeptide Y (NPY), galanin, and leptin, in subjects with eating disorders.
403	9439531	Plasma NPY, galanin, and leptin concentrations were measured in peripheral blood samples with radioimmunoassay methods.
404	9439531	Plasma NPY and galanin concentrations in women with anorexia nervosa did not differ from the levels in the control group.
405	9439531	Our results indicate that inappropriate plasma concentrations of NPY, galanin, and leptin in obese women may be a consequence of their weight status, or could be one of many factors involved in the pathogenesis of obesity.
406	9439531	Neuropeptide Y, galanin, and leptin release in obese women and in women with anorexia nervosa.
407	9439531	The study objective was to determine circulating levels of the appetite-controlling neuropeptides, neuropeptide Y (NPY), galanin, and leptin, in subjects with eating disorders.
408	9439531	Plasma NPY, galanin, and leptin concentrations were measured in peripheral blood samples with radioimmunoassay methods.
409	9439531	Plasma NPY and galanin concentrations in women with anorexia nervosa did not differ from the levels in the control group.
410	9439531	Our results indicate that inappropriate plasma concentrations of NPY, galanin, and leptin in obese women may be a consequence of their weight status, or could be one of many factors involved in the pathogenesis of obesity.
411	9439531	Neuropeptide Y, galanin, and leptin release in obese women and in women with anorexia nervosa.
412	9439531	The study objective was to determine circulating levels of the appetite-controlling neuropeptides, neuropeptide Y (NPY), galanin, and leptin, in subjects with eating disorders.
413	9439531	Plasma NPY, galanin, and leptin concentrations were measured in peripheral blood samples with radioimmunoassay methods.
414	9439531	Plasma NPY and galanin concentrations in women with anorexia nervosa did not differ from the levels in the control group.
415	9439531	Our results indicate that inappropriate plasma concentrations of NPY, galanin, and leptin in obese women may be a consequence of their weight status, or could be one of many factors involved in the pathogenesis of obesity.
416	9524732	Regulation of pulsatile secretion of growth hormone (GH) relies on hypothalamic neuronal loops, major transmitters involved in their operation are growth hormone releasing hormone (GHRH) synthetized mostly in arcuate nucleus (ARC) neurons, and somatostatin (SRIH), synthetized both in hypothalamus periventricular (PVe) and ARC neurons. 2.
417	9524732	Other neuropeptides synthetized in ARC neurons, such as galanin, or in ARC interneurons, such as neuropeptide Y (NPY), are able to modulate synthesis and release of GHRH and SRIH into the hypothalamohypophyseal portal system. 3.
418	9524732	At the pituitary level, major neurotransmitters regulating GH cells act on receptors of the VIP/PACAP/GHRH family and of the somatostatin family, in particular, sst2 and sst3.
419	9524732	Regulation and differentiation of somatotropes also depend upon paracrine processes within the pituitary itself and involve growth factors and several neuropeptides, for instance, vasoactive intestinal peptide, angiotensin 2, endothelin, and activin. 10.
420	9625283	The duodenal content of several neuropeptides, namely vasoactive intestinal polypeptide (VIP), neurotensin, neuropeptide Y (NPY), galanin, gastrin-releasing peptide (GRP) and enkephalin was determined by radioimmunoassay of tissue extracts.
421	9625283	There was no statistically significant difference between controls and NOD mice regarding the duodenal content of neurotensin, NPY, galanin or GRP.
422	9625283	The duodenal content of several neuropeptides, namely vasoactive intestinal polypeptide (VIP), neurotensin, neuropeptide Y (NPY), galanin, gastrin-releasing peptide (GRP) and enkephalin was determined by radioimmunoassay of tissue extracts.
423	9625283	There was no statistically significant difference between controls and NOD mice regarding the duodenal content of neurotensin, NPY, galanin or GRP.
424	9715376	The fact that both insulin resistance and impaired insulin release have been found to precede and predict NIDDM in prospective studies may be in part a reflection of just such relatedness. 4) Direct genetic analysis is effective in rarer forms of glucose intolerance (MODY, mitochondrial mutations, etc.) but encounters serious difficulties with typical late-onset NIDDM.
425	9715376	Incidentally, any defect in insulin secretion, whether in normoglycemic or hyperglycemic persons, could be due to other factors than primary beta-cell dysfunction: amyloid deposits in the pancreas (126), changes in insulin secretagogues (amylin, GLP-1, GIP, galanin) (127-130), early intrauterine malnutrition (131).
426	9934817	The neuroendocrine peptides that we investigated were: secretin, gastric inhibitory polypeptide (GIP), gastrin, motilin, peptide YY (PYY), somatostatin, vasoactive intestinal polypeptide (VIP), substance P, neurotensin, neuropeptide Y (NPY) and galanin.
427	9934817	In the antrum, gastrin, somatostatin, VIP, substance P and NPY concentrations were significantly lower in obese diabetic mice than in the lean controls.
428	9934817	There was no statistical difference between the obese mice and lean controls for neurotensin and galanin content.
429	9934817	There was no statistical difference between obese diabetic mice and lean controls regarding the concentration of secretin, GIP, motilin, gastrin, somatostatin, VIP, neurotensin, NPY or galanin.
430	9934817	In the colon, the levels of PYY, somatostatin, VIP, substance P, NPY and galanin were significantly lower in the obese diabetic mice than the lean controls.
431	9934817	The neuroendocrine peptides that we investigated were: secretin, gastric inhibitory polypeptide (GIP), gastrin, motilin, peptide YY (PYY), somatostatin, vasoactive intestinal polypeptide (VIP), substance P, neurotensin, neuropeptide Y (NPY) and galanin.
432	9934817	In the antrum, gastrin, somatostatin, VIP, substance P and NPY concentrations were significantly lower in obese diabetic mice than in the lean controls.
433	9934817	There was no statistical difference between the obese mice and lean controls for neurotensin and galanin content.
434	9934817	There was no statistical difference between obese diabetic mice and lean controls regarding the concentration of secretin, GIP, motilin, gastrin, somatostatin, VIP, neurotensin, NPY or galanin.
435	9934817	In the colon, the levels of PYY, somatostatin, VIP, substance P, NPY and galanin were significantly lower in the obese diabetic mice than the lean controls.
436	10509878	The neuroendocrine peptides investigated were peptide YY (PYY), somatostatin, vasoactive intestinal polypeptide (VIP), neuropeptide Y (NPY), neurotensin, and galanin.
437	10509878	In the antrum, VIP, NPY, and galanin concentrations were all significantly lower in prediabetic and diabetic NOD mice than in controls.
438	10509878	In the colon, the concentrations of PYY, somatostatin, VIP, NPY, and galanin were lower in prediabetic and diabetic NOD mice than in controls.
439	10509878	The neuroendocrine peptides investigated were peptide YY (PYY), somatostatin, vasoactive intestinal polypeptide (VIP), neuropeptide Y (NPY), neurotensin, and galanin.
440	10509878	In the antrum, VIP, NPY, and galanin concentrations were all significantly lower in prediabetic and diabetic NOD mice than in controls.
441	10509878	In the colon, the concentrations of PYY, somatostatin, VIP, NPY, and galanin were lower in prediabetic and diabetic NOD mice than in controls.
442	10574562	This was accompanied by an elevated number of NPY neurons (p < 0.001) and galanin neurons (p < 0.001) in the ARC in adult GD offspring under basal conditions.
443	10657511	Neuropeptide Y (NPY), melanin concentrating hormone (MCH), orexins A and B, galanin, and agouti -related peptide (AgRP) all act to stimulate feeding while alpha-melanocyte stimulating hormone (alphaMSH), corticotropin releasing hormone (CRH), cholecystokinin (CCK), cocaine and amphetamine regulated transcript (CART), neurotensin, glucagon-like peptide 1 (GLP 1), and bombesin have anorectic actions.(1) Leptin, expressed in the periphery in white adipose tissue, acts in the CNS to modulate the expression of several of these hypothalamic peptides.(1) This creates a functional link between the adipose tissue and the brain that translates the information on body fat provided by leptin to input into energy balance regulating processes.
444	10657511	In the current review we examine the significant role of the melanocortin system (alphaMSH, agouti and AgRP peptides, and their receptors and mahogany protein) and melanin concentrating hormone in the regulation of energy balance.
445	10819232	The neuropeptides, vasoactive intestinal polypeptide, pituitary adenlyate cyclase activating polypeptide and gastrin releasing peptide are constituents of the parasympathetic nerves, whereas the neuropeptides galanin and neuropeptide Y are localised to sympathetic nerve terminals.
446	10963118	There was a decreased number of neurons containing nitric oxide synthase (NOS) in myenteric ganglia of antrum and duodenum.
447	10963118	There was no difference regarding neuropeptide Y (NPY) and galanin between diabetic and control mice; nor was there any difference between pre-diabetic NOD mice and controls regarding all bioactive substances investigated.
448	10982176	Fine-mapping of the type 1 diabetes locus (IDDM4) on chromosome 11q and evaluation of two candidate genes (FADD and GALN) by affected sibpair and linkage-disequilibrium analyses.
449	10982176	Previous studies have identified a susceptibility region for insulin-dependent (type 1) diabetes mellitus on chromosome 11q13 (IDDM4).
450	10982176	We also identified polymorphisms in two candidate genes, Fas-associated death domain protein (FADD) and galanin (GALN).
451	10982176	However, ETDT did reveal significant association/linkage with the marker D11S987 (P=0.0004) within the IDDM4 interval defined by ASP analyses, suggesting that IDDM4 may be in the close proximity of D11S987.
452	10982176	Fine-mapping of the type 1 diabetes locus (IDDM4) on chromosome 11q and evaluation of two candidate genes (FADD and GALN) by affected sibpair and linkage-disequilibrium analyses.
453	10982176	Previous studies have identified a susceptibility region for insulin-dependent (type 1) diabetes mellitus on chromosome 11q13 (IDDM4).
454	10982176	We also identified polymorphisms in two candidate genes, Fas-associated death domain protein (FADD) and galanin (GALN).
455	10982176	However, ETDT did reveal significant association/linkage with the marker D11S987 (P=0.0004) within the IDDM4 interval defined by ASP analyses, suggesting that IDDM4 may be in the close proximity of D11S987.
456	10997641	Plasma insulin, cholecystokinin, galanin, neuropeptide Y and leptin levels in obese women with and without type 2 diabetes mellitus.
457	10997641	Experimental studies provided evidences that leptin, cholecystokinin (CCK), galanin (GAL), neuropeptide Y (NPY) and insulin are involved in feeding behaviour.
458	10997641	Plasma concentrations of FSH, leptin, CCK, GAL, NPY and insulin were determined using commercial RIA kits.
459	10997641	In diabetic subjects positive correlations were found between: CCK and leptin (r= 0.8295; P= 0.011), CCK and insulin (r=0.7832; P=0.022), leptin and insulin (r=0.9302; P=0.001).
460	10997641	In obese subjects a positive correlation between WHR and GAL (r= 0.6624; P= 0.037) and a negative between GAL and insulin (r= -0.6795; P= 0.031) were found.
461	10997641	In controls positive correlations were found between WHR and CCK (r=0.6412; P=0.025), GAL and insulin (r=0.630; P=0.028) and negative between CCK and NPY (r = -0.6505; P= 0.022).
462	10997641	Our results, ie higher mean plasma NPY levels in postmenopausal diabetic women and positive correlation of CCK with leptin and insulin, may suggest the role of these neuropeptides in metabolic disorders leading to type 2 diabetes mellitus.
463	10997641	Plasma insulin, cholecystokinin, galanin, neuropeptide Y and leptin levels in obese women with and without type 2 diabetes mellitus.
464	10997641	Experimental studies provided evidences that leptin, cholecystokinin (CCK), galanin (GAL), neuropeptide Y (NPY) and insulin are involved in feeding behaviour.
465	10997641	Plasma concentrations of FSH, leptin, CCK, GAL, NPY and insulin were determined using commercial RIA kits.
466	10997641	In diabetic subjects positive correlations were found between: CCK and leptin (r= 0.8295; P= 0.011), CCK and insulin (r=0.7832; P=0.022), leptin and insulin (r=0.9302; P=0.001).
467	10997641	In obese subjects a positive correlation between WHR and GAL (r= 0.6624; P= 0.037) and a negative between GAL and insulin (r= -0.6795; P= 0.031) were found.
468	10997641	In controls positive correlations were found between WHR and CCK (r=0.6412; P=0.025), GAL and insulin (r=0.630; P=0.028) and negative between CCK and NPY (r = -0.6505; P= 0.022).
469	10997641	Our results, ie higher mean plasma NPY levels in postmenopausal diabetic women and positive correlation of CCK with leptin and insulin, may suggest the role of these neuropeptides in metabolic disorders leading to type 2 diabetes mellitus.
470	10997641	Plasma insulin, cholecystokinin, galanin, neuropeptide Y and leptin levels in obese women with and without type 2 diabetes mellitus.
471	10997641	Experimental studies provided evidences that leptin, cholecystokinin (CCK), galanin (GAL), neuropeptide Y (NPY) and insulin are involved in feeding behaviour.
472	10997641	Plasma concentrations of FSH, leptin, CCK, GAL, NPY and insulin were determined using commercial RIA kits.
473	10997641	In diabetic subjects positive correlations were found between: CCK and leptin (r= 0.8295; P= 0.011), CCK and insulin (r=0.7832; P=0.022), leptin and insulin (r=0.9302; P=0.001).
474	10997641	In obese subjects a positive correlation between WHR and GAL (r= 0.6624; P= 0.037) and a negative between GAL and insulin (r= -0.6795; P= 0.031) were found.
475	10997641	In controls positive correlations were found between WHR and CCK (r=0.6412; P=0.025), GAL and insulin (r=0.630; P=0.028) and negative between CCK and NPY (r = -0.6505; P= 0.022).
476	10997641	Our results, ie higher mean plasma NPY levels in postmenopausal diabetic women and positive correlation of CCK with leptin and insulin, may suggest the role of these neuropeptides in metabolic disorders leading to type 2 diabetes mellitus.
477	10997641	Plasma insulin, cholecystokinin, galanin, neuropeptide Y and leptin levels in obese women with and without type 2 diabetes mellitus.
478	10997641	Experimental studies provided evidences that leptin, cholecystokinin (CCK), galanin (GAL), neuropeptide Y (NPY) and insulin are involved in feeding behaviour.
479	10997641	Plasma concentrations of FSH, leptin, CCK, GAL, NPY and insulin were determined using commercial RIA kits.
480	10997641	In diabetic subjects positive correlations were found between: CCK and leptin (r= 0.8295; P= 0.011), CCK and insulin (r=0.7832; P=0.022), leptin and insulin (r=0.9302; P=0.001).
481	10997641	In obese subjects a positive correlation between WHR and GAL (r= 0.6624; P= 0.037) and a negative between GAL and insulin (r= -0.6795; P= 0.031) were found.
482	10997641	In controls positive correlations were found between WHR and CCK (r=0.6412; P=0.025), GAL and insulin (r=0.630; P=0.028) and negative between CCK and NPY (r = -0.6505; P= 0.022).
483	10997641	Our results, ie higher mean plasma NPY levels in postmenopausal diabetic women and positive correlation of CCK with leptin and insulin, may suggest the role of these neuropeptides in metabolic disorders leading to type 2 diabetes mellitus.
484	10997641	Plasma insulin, cholecystokinin, galanin, neuropeptide Y and leptin levels in obese women with and without type 2 diabetes mellitus.
485	10997641	Experimental studies provided evidences that leptin, cholecystokinin (CCK), galanin (GAL), neuropeptide Y (NPY) and insulin are involved in feeding behaviour.
486	10997641	Plasma concentrations of FSH, leptin, CCK, GAL, NPY and insulin were determined using commercial RIA kits.
487	10997641	In diabetic subjects positive correlations were found between: CCK and leptin (r= 0.8295; P= 0.011), CCK and insulin (r=0.7832; P=0.022), leptin and insulin (r=0.9302; P=0.001).
488	10997641	In obese subjects a positive correlation between WHR and GAL (r= 0.6624; P= 0.037) and a negative between GAL and insulin (r= -0.6795; P= 0.031) were found.
489	10997641	In controls positive correlations were found between WHR and CCK (r=0.6412; P=0.025), GAL and insulin (r=0.630; P=0.028) and negative between CCK and NPY (r = -0.6505; P= 0.022).
490	10997641	Our results, ie higher mean plasma NPY levels in postmenopausal diabetic women and positive correlation of CCK with leptin and insulin, may suggest the role of these neuropeptides in metabolic disorders leading to type 2 diabetes mellitus.
491	11460563	Specifically, attention is paid to incretins such as glucagon-like peptide 1 (GLP-1), galanin, and other peptides produced in the gastrointestinal tract and by neuronal cells with the potential of governing beta-cell function in physiological and diabetic states.
492	11489087	The effect of galanin on insulin secretion from intact rat pancreatic tissue fragments was also investigated using a radioimmunoassay technique.
493	11489087	Galanin was colocalized with insulin in the islets of normal and diabetic rats.
494	11489087	Galanin had an inhibitory effect on insulin secretion from the isolated pancreatic tissue fragments of normal and diabetic rats at all concentrations (10(-12) to 10(-6) M) employed.
495	11489087	Galanin at 10(-9) M caused a significant (P < 0.02) decrease in insulin secretion from normal rat pancreatic tissue fragments compared to basal.
496	11489087	These observations indicate that galanin may play a significant role in the regulation of insulin secretion.
497	11489087	The effect of galanin on insulin secretion from intact rat pancreatic tissue fragments was also investigated using a radioimmunoassay technique.
498	11489087	Galanin was colocalized with insulin in the islets of normal and diabetic rats.
499	11489087	Galanin had an inhibitory effect on insulin secretion from the isolated pancreatic tissue fragments of normal and diabetic rats at all concentrations (10(-12) to 10(-6) M) employed.
500	11489087	Galanin at 10(-9) M caused a significant (P < 0.02) decrease in insulin secretion from normal rat pancreatic tissue fragments compared to basal.
501	11489087	These observations indicate that galanin may play a significant role in the regulation of insulin secretion.
502	11489087	The effect of galanin on insulin secretion from intact rat pancreatic tissue fragments was also investigated using a radioimmunoassay technique.
503	11489087	Galanin was colocalized with insulin in the islets of normal and diabetic rats.
504	11489087	Galanin had an inhibitory effect on insulin secretion from the isolated pancreatic tissue fragments of normal and diabetic rats at all concentrations (10(-12) to 10(-6) M) employed.
505	11489087	Galanin at 10(-9) M caused a significant (P < 0.02) decrease in insulin secretion from normal rat pancreatic tissue fragments compared to basal.
506	11489087	These observations indicate that galanin may play a significant role in the regulation of insulin secretion.
507	11489087	The effect of galanin on insulin secretion from intact rat pancreatic tissue fragments was also investigated using a radioimmunoassay technique.
508	11489087	Galanin was colocalized with insulin in the islets of normal and diabetic rats.
509	11489087	Galanin had an inhibitory effect on insulin secretion from the isolated pancreatic tissue fragments of normal and diabetic rats at all concentrations (10(-12) to 10(-6) M) employed.
510	11489087	Galanin at 10(-9) M caused a significant (P < 0.02) decrease in insulin secretion from normal rat pancreatic tissue fragments compared to basal.
511	11489087	These observations indicate that galanin may play a significant role in the regulation of insulin secretion.
512	11489087	The effect of galanin on insulin secretion from intact rat pancreatic tissue fragments was also investigated using a radioimmunoassay technique.
513	11489087	Galanin was colocalized with insulin in the islets of normal and diabetic rats.
514	11489087	Galanin had an inhibitory effect on insulin secretion from the isolated pancreatic tissue fragments of normal and diabetic rats at all concentrations (10(-12) to 10(-6) M) employed.
515	11489087	Galanin at 10(-9) M caused a significant (P < 0.02) decrease in insulin secretion from normal rat pancreatic tissue fragments compared to basal.
516	11489087	These observations indicate that galanin may play a significant role in the regulation of insulin secretion.
517	11561557	Changes in the antral content of VIP, duodenal somatostatin, and colonic galanin in NOD mice with LTD may cause low intestinal secretion and, together with rapid GI, give rise to diarrhoea, which is a common symptom in diabetes.
518	11673332	At 2 months, sensory neurones had no detectable alterations in their calibre or gene expression, assessed using quantitative in situ hybridization studies for mRNA markers that included alpha CGRP, beta CGRP, NFM, t alpha 1-tubulin, SP, VIP, B50 (GAP43), galanin, somatostatin, PACAP, HSP27, c-jun, SNAP 25, p75, TrkA, TrkB and TrkC.
519	11673332	By 12 months, however, diabetics had developed neurone perikaryal and distal axon atrophy, accompanied by generalized downregulation of mRNA expression, particularly of CGRP transcripts, PACAP, SP, NFM, p75, trkA and trkC.
520	11673332	With the exception of HSP-27, no elevation in mRNAs that increase after injury, such as VIP, galanin, CCK, PACAP, B50 and t alpha 1-tubulin, was observed and constitutive levels, when detectable, trended towards lower rather than increased levels.
521	11673332	At 2 months, sensory neurones had no detectable alterations in their calibre or gene expression, assessed using quantitative in situ hybridization studies for mRNA markers that included alpha CGRP, beta CGRP, NFM, t alpha 1-tubulin, SP, VIP, B50 (GAP43), galanin, somatostatin, PACAP, HSP27, c-jun, SNAP 25, p75, TrkA, TrkB and TrkC.
522	11673332	By 12 months, however, diabetics had developed neurone perikaryal and distal axon atrophy, accompanied by generalized downregulation of mRNA expression, particularly of CGRP transcripts, PACAP, SP, NFM, p75, trkA and trkC.
523	11673332	With the exception of HSP-27, no elevation in mRNAs that increase after injury, such as VIP, galanin, CCK, PACAP, B50 and t alpha 1-tubulin, was observed and constitutive levels, when detectable, trended towards lower rather than increased levels.
524	11718847	Triple label immunofluorescence staining of brain sections for galanin, GnRH and the presynaptic vesicle marker synaptophysin coupled with confocal microscopy was employed to identify galanin synapses to GnRH perikarya.
525	11723048	Interplay between galanin and leptin in the hypothalamic control of feeding via corticotropin-releasing hormone and neuropeptide Y.
526	11723048	We have developed a system of perifused hypothalamic neurons to characterize the relationships existing between the orexigenic peptide galanin and two other physiological modulators of feeding: neuropeptide Y (NPY) and corticotropin-releasing hormone (CRH).
527	11723048	We demonstrated that galanin stimulates CRH and NPY secretion from hypothalamic neurons in a dose-dependent manner.
528	11723048	Exposure to leptin for 24 h before galanin stimulation decreased NPY secretion by 30%, leaving the responsiveness of CRH neurons intact.
529	11723048	These results suggest that CRH and NPY neurons participate to the intrahypothalamic signaling pathway of galanin, an observation that can explain the lower potency of galanin to stimulate food intake in vivo compared with NPY.
530	11723048	The differential effects exerted by leptin on CRH and NPY suggest that there exists a subset of NPY neurons that are exquisitely sensitive to marked variations in leptin levels, and that the CRH neurons are less responsive to increases in leptin concentrations.
531	11723048	Interplay between galanin and leptin in the hypothalamic control of feeding via corticotropin-releasing hormone and neuropeptide Y.
532	11723048	We have developed a system of perifused hypothalamic neurons to characterize the relationships existing between the orexigenic peptide galanin and two other physiological modulators of feeding: neuropeptide Y (NPY) and corticotropin-releasing hormone (CRH).
533	11723048	We demonstrated that galanin stimulates CRH and NPY secretion from hypothalamic neurons in a dose-dependent manner.
534	11723048	Exposure to leptin for 24 h before galanin stimulation decreased NPY secretion by 30%, leaving the responsiveness of CRH neurons intact.
535	11723048	These results suggest that CRH and NPY neurons participate to the intrahypothalamic signaling pathway of galanin, an observation that can explain the lower potency of galanin to stimulate food intake in vivo compared with NPY.
536	11723048	The differential effects exerted by leptin on CRH and NPY suggest that there exists a subset of NPY neurons that are exquisitely sensitive to marked variations in leptin levels, and that the CRH neurons are less responsive to increases in leptin concentrations.
537	11723048	Interplay between galanin and leptin in the hypothalamic control of feeding via corticotropin-releasing hormone and neuropeptide Y.
538	11723048	We have developed a system of perifused hypothalamic neurons to characterize the relationships existing between the orexigenic peptide galanin and two other physiological modulators of feeding: neuropeptide Y (NPY) and corticotropin-releasing hormone (CRH).
539	11723048	We demonstrated that galanin stimulates CRH and NPY secretion from hypothalamic neurons in a dose-dependent manner.
540	11723048	Exposure to leptin for 24 h before galanin stimulation decreased NPY secretion by 30%, leaving the responsiveness of CRH neurons intact.
541	11723048	These results suggest that CRH and NPY neurons participate to the intrahypothalamic signaling pathway of galanin, an observation that can explain the lower potency of galanin to stimulate food intake in vivo compared with NPY.
542	11723048	The differential effects exerted by leptin on CRH and NPY suggest that there exists a subset of NPY neurons that are exquisitely sensitive to marked variations in leptin levels, and that the CRH neurons are less responsive to increases in leptin concentrations.
543	11723048	Interplay between galanin and leptin in the hypothalamic control of feeding via corticotropin-releasing hormone and neuropeptide Y.
544	11723048	We have developed a system of perifused hypothalamic neurons to characterize the relationships existing between the orexigenic peptide galanin and two other physiological modulators of feeding: neuropeptide Y (NPY) and corticotropin-releasing hormone (CRH).
545	11723048	We demonstrated that galanin stimulates CRH and NPY secretion from hypothalamic neurons in a dose-dependent manner.
546	11723048	Exposure to leptin for 24 h before galanin stimulation decreased NPY secretion by 30%, leaving the responsiveness of CRH neurons intact.
547	11723048	These results suggest that CRH and NPY neurons participate to the intrahypothalamic signaling pathway of galanin, an observation that can explain the lower potency of galanin to stimulate food intake in vivo compared with NPY.
548	11723048	The differential effects exerted by leptin on CRH and NPY suggest that there exists a subset of NPY neurons that are exquisitely sensitive to marked variations in leptin levels, and that the CRH neurons are less responsive to increases in leptin concentrations.
549	11723048	Interplay between galanin and leptin in the hypothalamic control of feeding via corticotropin-releasing hormone and neuropeptide Y.
550	11723048	We have developed a system of perifused hypothalamic neurons to characterize the relationships existing between the orexigenic peptide galanin and two other physiological modulators of feeding: neuropeptide Y (NPY) and corticotropin-releasing hormone (CRH).
551	11723048	We demonstrated that galanin stimulates CRH and NPY secretion from hypothalamic neurons in a dose-dependent manner.
552	11723048	Exposure to leptin for 24 h before galanin stimulation decreased NPY secretion by 30%, leaving the responsiveness of CRH neurons intact.
553	11723048	These results suggest that CRH and NPY neurons participate to the intrahypothalamic signaling pathway of galanin, an observation that can explain the lower potency of galanin to stimulate food intake in vivo compared with NPY.
554	11723048	The differential effects exerted by leptin on CRH and NPY suggest that there exists a subset of NPY neurons that are exquisitely sensitive to marked variations in leptin levels, and that the CRH neurons are less responsive to increases in leptin concentrations.
555	12047718	Galanin synaptic input onto gonadotropin-releasing hormone (GnRH) neuronal cell bodies was analysed in female mice using the presynaptic vesicle-specific protein, synaptophysin (Syn) as a marker.
556	12047718	In the first experiment, forebrain sections from normal ovariectomized ovarian steroid-primed mice exhibiting a surge of luteinizing hormone were processed for immunohistochemical labelling for GnRH, synaptophysin, galanin and Fos.
557	12047718	Galanin synaptic input onto gonadotropin-releasing hormone (GnRH) neuronal cell bodies was analysed in female mice using the presynaptic vesicle-specific protein, synaptophysin (Syn) as a marker.
558	12047718	In the first experiment, forebrain sections from normal ovariectomized ovarian steroid-primed mice exhibiting a surge of luteinizing hormone were processed for immunohistochemical labelling for GnRH, synaptophysin, galanin and Fos.
559	12147141	Meal size is controlled by a series of short-term hormonal and neural signals that derive from the gastrointestinal tract, such as cholecystokinin whereas others may initiate meals, such as the recently discovered hormone, ghrelin.
560	12147141	Other hormones such as insulin and leptin, together with circulating nutrients, indicate long-term energy stores.
561	12147141	When energy stores are low, production of leptin from adipose tissue, and thus circulating leptin concentrations fall, leading to increased production of hypothalamic neurotransmitters that strongly increase food intake, such as neuropeptide Y (NPY), galanin and agouti-related protein (AGRP) and decreased levels of alpha-melanocyte-stimulating hormone (alpha-MSH), cocaine and amphetamine-regulated transcript (CART) and neurotensin that reduce food intake and increase energy expenditure.
562	12147141	The finding that mutations in leptin and POMC lead to severe early onset obesity in humans has highlighted the importance of these peptides in humans.
563	12602781	The neuroendocrine peptides known to regulate gastrointestinal motility, namely secretin, gastric inhibitory peptide (GIP), motilin, somatostatin, peptide YY (PYY), substance P, vasoactive intestinal polypeptide (VIP) and galanin, were measured in tissue extracts of different segments of the gut by radioimmunoassay.
564	12602781	The concentrations of antral somatostatin, VIP and galanin, and duodenal secretin as well as jejunal motilin in NOD mice were higher than those of controls.
565	12602781	Duodenal GIP and colonic PYY concentration in NOD mice was lower than controls.
566	12602781	Duodenal GIP and VIP, and colonic somatostatin and VIP levels were lower in obese diabetic mice than controls.
567	12602781	Whereas the high concentrations of antral VIP and galanin and the low level of colonic PYY in diabetic NOD mice may contribute to the development of diarrhea in NOD mice, the decreased levels of duodenal and colonic VIP and colonic somatostatin in obese diabetic mice may account for the constipation encountered in these animals.
568	12602781	The neuroendocrine peptides known to regulate gastrointestinal motility, namely secretin, gastric inhibitory peptide (GIP), motilin, somatostatin, peptide YY (PYY), substance P, vasoactive intestinal polypeptide (VIP) and galanin, were measured in tissue extracts of different segments of the gut by radioimmunoassay.
569	12602781	The concentrations of antral somatostatin, VIP and galanin, and duodenal secretin as well as jejunal motilin in NOD mice were higher than those of controls.
570	12602781	Duodenal GIP and colonic PYY concentration in NOD mice was lower than controls.
571	12602781	Duodenal GIP and VIP, and colonic somatostatin and VIP levels were lower in obese diabetic mice than controls.
572	12602781	Whereas the high concentrations of antral VIP and galanin and the low level of colonic PYY in diabetic NOD mice may contribute to the development of diarrhea in NOD mice, the decreased levels of duodenal and colonic VIP and colonic somatostatin in obese diabetic mice may account for the constipation encountered in these animals.
573	12602781	The neuroendocrine peptides known to regulate gastrointestinal motility, namely secretin, gastric inhibitory peptide (GIP), motilin, somatostatin, peptide YY (PYY), substance P, vasoactive intestinal polypeptide (VIP) and galanin, were measured in tissue extracts of different segments of the gut by radioimmunoassay.
574	12602781	The concentrations of antral somatostatin, VIP and galanin, and duodenal secretin as well as jejunal motilin in NOD mice were higher than those of controls.
575	12602781	Duodenal GIP and colonic PYY concentration in NOD mice was lower than controls.
576	12602781	Duodenal GIP and VIP, and colonic somatostatin and VIP levels were lower in obese diabetic mice than controls.
577	12602781	Whereas the high concentrations of antral VIP and galanin and the low level of colonic PYY in diabetic NOD mice may contribute to the development of diarrhea in NOD mice, the decreased levels of duodenal and colonic VIP and colonic somatostatin in obese diabetic mice may account for the constipation encountered in these animals.
578	12701881	A cross-talk between insulin and leptin receptors has been observed in the brain, and a regulation of central insulin actions, potentially via serotonin modulation, by leptin, galanin, melancortins, and neuropeptide Y (NPY) is suggested. 6.
579	14700749	Tumor galanin and ACTH contents were closely correlated in all tumors.
580	14700749	In some tumors galanin mRNA and POMC levels coexisted, in others they were essentially in different cell populations.
581	14700749	Corticotrophin releasing hormone injections in two patients caused ACTH, but no detectable galanin release into sinus petrosus.
582	14700749	Our results demonstrate that corticotroph, but not GH adenomas, express high levels of galanin, in addition to ACTH, and that in some tumors both polypeptides are synthesised in the same cell population.
583	14700749	Tumor galanin and ACTH contents were closely correlated in all tumors.
584	14700749	In some tumors galanin mRNA and POMC levels coexisted, in others they were essentially in different cell populations.
585	14700749	Corticotrophin releasing hormone injections in two patients caused ACTH, but no detectable galanin release into sinus petrosus.
586	14700749	Our results demonstrate that corticotroph, but not GH adenomas, express high levels of galanin, in addition to ACTH, and that in some tumors both polypeptides are synthesised in the same cell population.
587	14700749	Tumor galanin and ACTH contents were closely correlated in all tumors.
588	14700749	In some tumors galanin mRNA and POMC levels coexisted, in others they were essentially in different cell populations.
589	14700749	Corticotrophin releasing hormone injections in two patients caused ACTH, but no detectable galanin release into sinus petrosus.
590	14700749	Our results demonstrate that corticotroph, but not GH adenomas, express high levels of galanin, in addition to ACTH, and that in some tumors both polypeptides are synthesised in the same cell population.
591	14700749	Tumor galanin and ACTH contents were closely correlated in all tumors.
592	14700749	In some tumors galanin mRNA and POMC levels coexisted, in others they were essentially in different cell populations.
593	14700749	Corticotrophin releasing hormone injections in two patients caused ACTH, but no detectable galanin release into sinus petrosus.
594	14700749	Our results demonstrate that corticotroph, but not GH adenomas, express high levels of galanin, in addition to ACTH, and that in some tumors both polypeptides are synthesised in the same cell population.
595	14988462	In the ARC, orexigenic neuropeptides such as neuropeptide Y (NPY), galanin (GAL), and agouti-related peptide (AGRP) and anorexigenic neuropeptides such as proopiomelanocortin (POMC) and alpha-melanocyte-stimulating hormone (MSH) are expressed.
596	14988462	The ARC of CO-GD rats showed increased immunopositivity of both NPY and AGRP under basal conditions, despite normal levels of glucose, leptin, and insulin.
597	15111492	Effects of diabetes and insulin on the expression of galanin-like peptide in the hypothalamus of the rat.
598	15111492	Galanin-like peptide (GALP) is produced in a small population of neurons in the arcuate nucleus of the hypothalamus, and leptin stimulates the hypothalamic expression of GALP mRNA.
599	15111492	Because insulin and leptin share common signaling pathways in the brain, we reasoned that GALP neurons might also be responsive to changes in circulating concentrations of insulin.
600	15111492	To test this hypothesis, we first studied the effect of insulin deficiency on the expression of GALP by comparing levels of GALP mRNA between normal and diabetic animals.
601	15111492	Streptozotocin-induced diabetes was associated with a significant reduction in the expression of GALP mRNA, which was reversed by treatment with either insulin or leptin.
602	15111492	Second, we examined the effect of insulin administered directly into the brain on the expression of GALP mRNA in fasted rats.
603	15111492	Hypothalamic levels of GALP mRNA were lower in animals after a 48-h fast, and central treatment with insulin reversed this effect.
604	15111492	These results suggest that GALP neurons are direct targets for regulation by insulin and implicate these cells for a role in the metabolic and behavioral sequelae of type 1 diabetes.
605	15111492	Effects of diabetes and insulin on the expression of galanin-like peptide in the hypothalamus of the rat.
606	15111492	Galanin-like peptide (GALP) is produced in a small population of neurons in the arcuate nucleus of the hypothalamus, and leptin stimulates the hypothalamic expression of GALP mRNA.
607	15111492	Because insulin and leptin share common signaling pathways in the brain, we reasoned that GALP neurons might also be responsive to changes in circulating concentrations of insulin.
608	15111492	To test this hypothesis, we first studied the effect of insulin deficiency on the expression of GALP by comparing levels of GALP mRNA between normal and diabetic animals.
609	15111492	Streptozotocin-induced diabetes was associated with a significant reduction in the expression of GALP mRNA, which was reversed by treatment with either insulin or leptin.
610	15111492	Second, we examined the effect of insulin administered directly into the brain on the expression of GALP mRNA in fasted rats.
611	15111492	Hypothalamic levels of GALP mRNA were lower in animals after a 48-h fast, and central treatment with insulin reversed this effect.
612	15111492	These results suggest that GALP neurons are direct targets for regulation by insulin and implicate these cells for a role in the metabolic and behavioral sequelae of type 1 diabetes.
613	15256810	Galanin-like peptide mRNA alterations in arcuate nucleus and neural lobe of streptozotocin-diabetic and obese zucker rats.
614	15256810	Galanin-like peptide (GALP) is a 60-amino-acid peptide with structural similarities to galanin and a high affinity for galanin receptors.
615	15256810	GALP neurons express leptin receptors and GALP mRNA levels are decreased slightly in fasted rats and stimulated significantly by acute leptin treatment in combination with fasting.
616	15256810	In studies to further explore the leptin dependence of GALP expression, we examined GALP mRNA levels in the hypothalamus of obese Zucker and streptozotocin-induced diabetic (STZ-DM) rats.
617	15256810	In leptin receptor-deficient obese Zucker rats, with 75% higher body weight than lean littermates, GALP mRNA levels in the ARC were decreased by 75%, while neuropeptide Y (NPY) mRNA levels were increased 7-fold (n = 5, p < 0.001), consistent with earlier reports.
618	15256810	In hypoleptinemic diabetic rats with 4.5-fold higher blood glucose and 15% lower body weight than controls, GALP mRNA levels in the ARC were decreased by 90%, while NPY mRNA levels were increased 9-fold (n = 5, p < 0.001).
619	15256810	The current findings are consistent with a strong tonic influence of leptin receptor signalling on hypothalamic GALP expression under normal conditions, and possible abnormalities in GALP neuronal signalling and their putative targets, thyrotropin-releasing hormone and gonadotropin hormone-releasing hormone neurons, under pathophysiological conditions such as diabetes and obesity.
620	15256810	Galanin-like peptide mRNA alterations in arcuate nucleus and neural lobe of streptozotocin-diabetic and obese zucker rats.
621	15256810	Galanin-like peptide (GALP) is a 60-amino-acid peptide with structural similarities to galanin and a high affinity for galanin receptors.
622	15256810	GALP neurons express leptin receptors and GALP mRNA levels are decreased slightly in fasted rats and stimulated significantly by acute leptin treatment in combination with fasting.
623	15256810	In studies to further explore the leptin dependence of GALP expression, we examined GALP mRNA levels in the hypothalamus of obese Zucker and streptozotocin-induced diabetic (STZ-DM) rats.
624	15256810	In leptin receptor-deficient obese Zucker rats, with 75% higher body weight than lean littermates, GALP mRNA levels in the ARC were decreased by 75%, while neuropeptide Y (NPY) mRNA levels were increased 7-fold (n = 5, p < 0.001), consistent with earlier reports.
625	15256810	In hypoleptinemic diabetic rats with 4.5-fold higher blood glucose and 15% lower body weight than controls, GALP mRNA levels in the ARC were decreased by 90%, while NPY mRNA levels were increased 9-fold (n = 5, p < 0.001).
626	15256810	The current findings are consistent with a strong tonic influence of leptin receptor signalling on hypothalamic GALP expression under normal conditions, and possible abnormalities in GALP neuronal signalling and their putative targets, thyrotropin-releasing hormone and gonadotropin hormone-releasing hormone neurons, under pathophysiological conditions such as diabetes and obesity.
627	15582161	Expression of the axotomy-responsive genes coding for growth-associated protein 43 (GAP-43), galanin, neuropeptide Y (NPY), pre-pro-vasoactive intestinal polypeptide (pre-pro-VIP), neuronal nitric oxide synthase (nNOS), protease nexin 1, heat-shock protein 27 (HSP 27) and myosin light chain kinase II (MLCK II) was unaffected in ganglia from diabetic rats compared to controls; thus, no axotomised phenotype was established.
628	15582161	The expression of the majority of proapoptotic genes in the DRG was also unaltered (bax, bad, bid, bok, c-Jun, p38, TNFR1, caspase 3 and NOS2).
629	15582161	Similarly there was no change in expression of the majority of antiapoptotic genes (bcl2, bcl-xL, bcl-w, NfkappaB).
630	15670772	Effects of galnon, a non-peptide galanin-receptor agonist, on insulin release from rat pancreatic islets.
631	15670772	Galanin is a neurotransmitter peptide that suppresses insulin secretion.
632	15670772	The present study aimed at investigating how a non-peptide galanin receptor agonist, galnon, affects insulin secretion from isolated pancreatic islets of healthy Wistar and diabetic Goto-Kakizaki (GK) rats.
633	16046316	Galanin-like peptide rescues reproductive function in the diabetic rat.
634	16046316	Galanin-like peptide (GALP) is expressed in the hypothalamic arcuate nucleus and is regulated by leptin and insulin.
635	16046316	Third, we examined whether intracerebroventricular administration of affinity-purified GALP antibody could block the effect of insulin and leptin in reversing the effects of diabetes on LH and sexual behavior.
636	16046316	We found that treatment of diabetic animals with insulin and leptin nearly normalized LH levels and sexual behaviors; however, this effect was attenuated by intracerebroventricular administration of GALP antibody (P < 0.05).
637	16046316	Galanin-like peptide rescues reproductive function in the diabetic rat.
638	16046316	Galanin-like peptide (GALP) is expressed in the hypothalamic arcuate nucleus and is regulated by leptin and insulin.
639	16046316	Third, we examined whether intracerebroventricular administration of affinity-purified GALP antibody could block the effect of insulin and leptin in reversing the effects of diabetes on LH and sexual behavior.
640	16046316	We found that treatment of diabetic animals with insulin and leptin nearly normalized LH levels and sexual behaviors; however, this effect was attenuated by intracerebroventricular administration of GALP antibody (P < 0.05).
641	16060906	Circulating acylated and total ghrelin and galanin in children with insulin-treated type 1 diabetes: relationship to insulin therapy, metabolic control and pubertal development.
642	16487586	We conclude that the selective damage to islet sympathetic nerve terminals seen in BB diabetic rats, rather than the systemic factors of diabetic hyperglycemia or insulin deficiency, causes the increased galanin expression observed in the CG of this animal model of type 1 diabetes.
643	16522529	Genetic factors play a significant role and include several gene candidates: polymorphisms of genes for ss(2)-adrenoreceptor, resistin, estrogen receptor-a and peroxisome proliferator-activated receptor-gamma.
644	16522529	Moreover, peptides regulating hunger and satiety, e.g. leptin, galanin, cholecystokinin and neuropeptide Y, and altered nutritional patterns have been implicated.
645	16965293	Young adult-specific hyperphagia in diabetic Goto-kakizaki rats is associated with leptin resistance and elevation of neuropeptide Y mRNA in the arcuate nucleus.
646	16965293	In GK rats, leptin-induced phosphorylation of signal transducer and activator of transcription 3 was significantly reduced in the cells of the hypothalamic arcuate nucleus (ARC), but not of the ventromedial hypothalamus, whereas the mRNA level of functional leptin receptor was unaltered.
647	16965293	By real-time polymerase chain reaction and in situ hybridisation, mRNA levels of neuropeptide Y, but not pro-opiomelanocortin and galanin-like peptide, were significantly increased in the ARC of GK rats at 11 weeks, but not 26 weeks.
648	16965293	These results demonstrate that young adult GK rats display hyperphagia in association with leptin resistance and increased NPY mRNA level in the ARC.
649	17226114	Blood samples were collected at 0, 30, 60, 90, 120 and 180 minutes for the measurement of plasma glucose, insulin, C-peptide and human galanin (hGal).
650	17437948	Among the neurotransmitters and neuropeptids of the hypothalamus, serotonin, norepinephrine, GABA, cholecystokinin, neuropeptide-Y, Agouti-related protein, alpha-MSH and ghrelin have essential importance in the eating disorders.
651	17437948	The levels of leptin and galanin determine whether formation of anabolic or catabolic neurotransmitters should take place.
652	17712724	Galanin is colocalized with adrenocorticotrophin (ACTH) in the human pituitary and with corticotrophin releasing hormone, arginine, vasopressin, and oxytocin in the hypothalamus.
653	17712724	Galanin, vasopressin, and oxytocin influence the secretion of pituitary ACTH.
654	17712724	The aim of this study was to investigate if the endogenous stimulation of ACTH release in Addison's disease was reflected in plasma galanin, vasopressin, and oxytocin.
655	17712724	ACTH, galanin, vasopressin, and oxytocin were measured in plasma from 14 patients with Addison's disease, one patient with Nelson's syndrome, and 14 healthy controls.
656	17712724	There was no difference in galanin or vasopressin between patients and controls or between samples with low or high ACTH concentrations.
657	17712724	The highest ACTH and galanin levels were found in the patient with Nelson's syndrome.
658	17712724	In conclusion, increased plasma ACTH was not reflected in elevated plasma galanin or vasopressin.
659	17712724	Galanin is colocalized with adrenocorticotrophin (ACTH) in the human pituitary and with corticotrophin releasing hormone, arginine, vasopressin, and oxytocin in the hypothalamus.
660	17712724	Galanin, vasopressin, and oxytocin influence the secretion of pituitary ACTH.
661	17712724	The aim of this study was to investigate if the endogenous stimulation of ACTH release in Addison's disease was reflected in plasma galanin, vasopressin, and oxytocin.
662	17712724	ACTH, galanin, vasopressin, and oxytocin were measured in plasma from 14 patients with Addison's disease, one patient with Nelson's syndrome, and 14 healthy controls.
663	17712724	There was no difference in galanin or vasopressin between patients and controls or between samples with low or high ACTH concentrations.
664	17712724	The highest ACTH and galanin levels were found in the patient with Nelson's syndrome.
665	17712724	In conclusion, increased plasma ACTH was not reflected in elevated plasma galanin or vasopressin.
666	17712724	Galanin is colocalized with adrenocorticotrophin (ACTH) in the human pituitary and with corticotrophin releasing hormone, arginine, vasopressin, and oxytocin in the hypothalamus.
667	17712724	Galanin, vasopressin, and oxytocin influence the secretion of pituitary ACTH.
668	17712724	The aim of this study was to investigate if the endogenous stimulation of ACTH release in Addison's disease was reflected in plasma galanin, vasopressin, and oxytocin.
669	17712724	ACTH, galanin, vasopressin, and oxytocin were measured in plasma from 14 patients with Addison's disease, one patient with Nelson's syndrome, and 14 healthy controls.
670	17712724	There was no difference in galanin or vasopressin between patients and controls or between samples with low or high ACTH concentrations.
671	17712724	The highest ACTH and galanin levels were found in the patient with Nelson's syndrome.
672	17712724	In conclusion, increased plasma ACTH was not reflected in elevated plasma galanin or vasopressin.
673	17712724	Galanin is colocalized with adrenocorticotrophin (ACTH) in the human pituitary and with corticotrophin releasing hormone, arginine, vasopressin, and oxytocin in the hypothalamus.
674	17712724	Galanin, vasopressin, and oxytocin influence the secretion of pituitary ACTH.
675	17712724	The aim of this study was to investigate if the endogenous stimulation of ACTH release in Addison's disease was reflected in plasma galanin, vasopressin, and oxytocin.
676	17712724	ACTH, galanin, vasopressin, and oxytocin were measured in plasma from 14 patients with Addison's disease, one patient with Nelson's syndrome, and 14 healthy controls.
677	17712724	There was no difference in galanin or vasopressin between patients and controls or between samples with low or high ACTH concentrations.
678	17712724	The highest ACTH and galanin levels were found in the patient with Nelson's syndrome.
679	17712724	In conclusion, increased plasma ACTH was not reflected in elevated plasma galanin or vasopressin.
680	17712724	Galanin is colocalized with adrenocorticotrophin (ACTH) in the human pituitary and with corticotrophin releasing hormone, arginine, vasopressin, and oxytocin in the hypothalamus.
681	17712724	Galanin, vasopressin, and oxytocin influence the secretion of pituitary ACTH.
682	17712724	The aim of this study was to investigate if the endogenous stimulation of ACTH release in Addison's disease was reflected in plasma galanin, vasopressin, and oxytocin.
683	17712724	ACTH, galanin, vasopressin, and oxytocin were measured in plasma from 14 patients with Addison's disease, one patient with Nelson's syndrome, and 14 healthy controls.
684	17712724	There was no difference in galanin or vasopressin between patients and controls or between samples with low or high ACTH concentrations.
685	17712724	The highest ACTH and galanin levels were found in the patient with Nelson's syndrome.
686	17712724	In conclusion, increased plasma ACTH was not reflected in elevated plasma galanin or vasopressin.
687	17712724	Galanin is colocalized with adrenocorticotrophin (ACTH) in the human pituitary and with corticotrophin releasing hormone, arginine, vasopressin, and oxytocin in the hypothalamus.
688	17712724	Galanin, vasopressin, and oxytocin influence the secretion of pituitary ACTH.
689	17712724	The aim of this study was to investigate if the endogenous stimulation of ACTH release in Addison's disease was reflected in plasma galanin, vasopressin, and oxytocin.
690	17712724	ACTH, galanin, vasopressin, and oxytocin were measured in plasma from 14 patients with Addison's disease, one patient with Nelson's syndrome, and 14 healthy controls.
691	17712724	There was no difference in galanin or vasopressin between patients and controls or between samples with low or high ACTH concentrations.
692	17712724	The highest ACTH and galanin levels were found in the patient with Nelson's syndrome.
693	17712724	In conclusion, increased plasma ACTH was not reflected in elevated plasma galanin or vasopressin.
694	17712724	Galanin is colocalized with adrenocorticotrophin (ACTH) in the human pituitary and with corticotrophin releasing hormone, arginine, vasopressin, and oxytocin in the hypothalamus.
695	17712724	Galanin, vasopressin, and oxytocin influence the secretion of pituitary ACTH.
696	17712724	The aim of this study was to investigate if the endogenous stimulation of ACTH release in Addison's disease was reflected in plasma galanin, vasopressin, and oxytocin.
697	17712724	ACTH, galanin, vasopressin, and oxytocin were measured in plasma from 14 patients with Addison's disease, one patient with Nelson's syndrome, and 14 healthy controls.
698	17712724	There was no difference in galanin or vasopressin between patients and controls or between samples with low or high ACTH concentrations.
699	17712724	The highest ACTH and galanin levels were found in the patient with Nelson's syndrome.
700	17712724	In conclusion, increased plasma ACTH was not reflected in elevated plasma galanin or vasopressin.
701	18421906	The various hormones, proteins and other compounds related to developing obesity, insulin resistance and type 2 diabetes are analyzed in the paper. 1) Leptin, ciliary neurutrophic factor, adiponectin, glucagon-like peptide 1, peptide YY, neuromedin S, as well as the protein receptors of these hormones decrease the food consumption, increase the energy turnover, and prevent obesity, insulin resistance, and type 2 diabetes development.
702	18421906	The mediators of these hormone and receptor actions are melanocyte stimulating hormone (MSH), corticotropin-releasing hormone (CRH), and the others. 2) Ghrelin, endogenose cannabinoides, galanin-like peptide and the mediators of their actions: neuropeptide Y (NPY) and Agouti gene related protein (AGRP) increase the appetite and food consumption.
703	21664358	Galanin antagonist increases insulin resistance by reducing glucose transporter 4 effect in adipocytes of rats.
704	21664358	Seeing that galanin increases animal body weight on the conditions of inhibiting insulin secretion and animals with metabolic disorder of galanin easily suffer from diabetes, we postulate that endogenous galanin is necessary to reduce insulin resistance in adipocytes.
705	21664358	To test this hypothesis, we compared four groups of rats to examine whether an increase in galanin secretion stimulated by swimming may reduce insulin resistance.
706	21664358	We found that exercise significantly elevated plasma galanin contents and glucose transporter 4 (GLUT4) mRNA levels in adipocytes.
707	21664358	These observations suggest that endogenous galanin reduces insulin resistance by increasing GLUT4 contents and promoting GLUT4 transportation from intracellular membranes to plasma membranes in adipocytes.
708	21664358	Galanin is an important hormone to reduce insulin resistance in rats.
709	21664358	Galanin antagonist increases insulin resistance by reducing glucose transporter 4 effect in adipocytes of rats.
710	21664358	Seeing that galanin increases animal body weight on the conditions of inhibiting insulin secretion and animals with metabolic disorder of galanin easily suffer from diabetes, we postulate that endogenous galanin is necessary to reduce insulin resistance in adipocytes.
711	21664358	To test this hypothesis, we compared four groups of rats to examine whether an increase in galanin secretion stimulated by swimming may reduce insulin resistance.
712	21664358	We found that exercise significantly elevated plasma galanin contents and glucose transporter 4 (GLUT4) mRNA levels in adipocytes.
713	21664358	These observations suggest that endogenous galanin reduces insulin resistance by increasing GLUT4 contents and promoting GLUT4 transportation from intracellular membranes to plasma membranes in adipocytes.
714	21664358	Galanin is an important hormone to reduce insulin resistance in rats.
715	21664358	Galanin antagonist increases insulin resistance by reducing glucose transporter 4 effect in adipocytes of rats.
716	21664358	Seeing that galanin increases animal body weight on the conditions of inhibiting insulin secretion and animals with metabolic disorder of galanin easily suffer from diabetes, we postulate that endogenous galanin is necessary to reduce insulin resistance in adipocytes.
717	21664358	To test this hypothesis, we compared four groups of rats to examine whether an increase in galanin secretion stimulated by swimming may reduce insulin resistance.
718	21664358	We found that exercise significantly elevated plasma galanin contents and glucose transporter 4 (GLUT4) mRNA levels in adipocytes.
719	21664358	These observations suggest that endogenous galanin reduces insulin resistance by increasing GLUT4 contents and promoting GLUT4 transportation from intracellular membranes to plasma membranes in adipocytes.
720	21664358	Galanin is an important hormone to reduce insulin resistance in rats.
721	21664358	Galanin antagonist increases insulin resistance by reducing glucose transporter 4 effect in adipocytes of rats.
722	21664358	Seeing that galanin increases animal body weight on the conditions of inhibiting insulin secretion and animals with metabolic disorder of galanin easily suffer from diabetes, we postulate that endogenous galanin is necessary to reduce insulin resistance in adipocytes.
723	21664358	To test this hypothesis, we compared four groups of rats to examine whether an increase in galanin secretion stimulated by swimming may reduce insulin resistance.
724	21664358	We found that exercise significantly elevated plasma galanin contents and glucose transporter 4 (GLUT4) mRNA levels in adipocytes.
725	21664358	These observations suggest that endogenous galanin reduces insulin resistance by increasing GLUT4 contents and promoting GLUT4 transportation from intracellular membranes to plasma membranes in adipocytes.
726	21664358	Galanin is an important hormone to reduce insulin resistance in rats.
727	21664358	Galanin antagonist increases insulin resistance by reducing glucose transporter 4 effect in adipocytes of rats.
728	21664358	Seeing that galanin increases animal body weight on the conditions of inhibiting insulin secretion and animals with metabolic disorder of galanin easily suffer from diabetes, we postulate that endogenous galanin is necessary to reduce insulin resistance in adipocytes.
729	21664358	To test this hypothesis, we compared four groups of rats to examine whether an increase in galanin secretion stimulated by swimming may reduce insulin resistance.
730	21664358	We found that exercise significantly elevated plasma galanin contents and glucose transporter 4 (GLUT4) mRNA levels in adipocytes.
731	21664358	These observations suggest that endogenous galanin reduces insulin resistance by increasing GLUT4 contents and promoting GLUT4 transportation from intracellular membranes to plasma membranes in adipocytes.
732	21664358	Galanin is an important hormone to reduce insulin resistance in rats.
733	21664358	Galanin antagonist increases insulin resistance by reducing glucose transporter 4 effect in adipocytes of rats.
734	21664358	Seeing that galanin increases animal body weight on the conditions of inhibiting insulin secretion and animals with metabolic disorder of galanin easily suffer from diabetes, we postulate that endogenous galanin is necessary to reduce insulin resistance in adipocytes.
735	21664358	To test this hypothesis, we compared four groups of rats to examine whether an increase in galanin secretion stimulated by swimming may reduce insulin resistance.
736	21664358	We found that exercise significantly elevated plasma galanin contents and glucose transporter 4 (GLUT4) mRNA levels in adipocytes.
737	21664358	These observations suggest that endogenous galanin reduces insulin resistance by increasing GLUT4 contents and promoting GLUT4 transportation from intracellular membranes to plasma membranes in adipocytes.
738	21664358	Galanin is an important hormone to reduce insulin resistance in rats.
739	22079346	Exercise-induced galanin release facilitated GLUT4 translocation in adipocytes of type 2 diabetic rats.
740	22079346	Although galanin has been shown to increase insulin sensitivity in skeletal muscle of rats, there is no literature available about the effect of galanin on Glucose Transporter 4 (GLUT4) translocation from intracellular membrane pools to plasma membranes in adipocytes of type 2 diabetic rats.
741	22079346	In the present study M35, a galanin antagonist was used to elucidate whether exercise-induced galanin release increased GLUT4 translocation in adipocytes of streptozotocin-induced diabetic rats.
742	22079346	These data demonstrate a beneficial role of endogenous galanin to transfer GLUT4 from internal stores to plasma membranes in adipocytes of type 2 diabetic rats.
743	22079346	Exercise-induced galanin release facilitated GLUT4 translocation in adipocytes of type 2 diabetic rats.
744	22079346	Although galanin has been shown to increase insulin sensitivity in skeletal muscle of rats, there is no literature available about the effect of galanin on Glucose Transporter 4 (GLUT4) translocation from intracellular membrane pools to plasma membranes in adipocytes of type 2 diabetic rats.
745	22079346	In the present study M35, a galanin antagonist was used to elucidate whether exercise-induced galanin release increased GLUT4 translocation in adipocytes of streptozotocin-induced diabetic rats.
746	22079346	These data demonstrate a beneficial role of endogenous galanin to transfer GLUT4 from internal stores to plasma membranes in adipocytes of type 2 diabetic rats.
747	22079346	Exercise-induced galanin release facilitated GLUT4 translocation in adipocytes of type 2 diabetic rats.
748	22079346	Although galanin has been shown to increase insulin sensitivity in skeletal muscle of rats, there is no literature available about the effect of galanin on Glucose Transporter 4 (GLUT4) translocation from intracellular membrane pools to plasma membranes in adipocytes of type 2 diabetic rats.
749	22079346	In the present study M35, a galanin antagonist was used to elucidate whether exercise-induced galanin release increased GLUT4 translocation in adipocytes of streptozotocin-induced diabetic rats.
750	22079346	These data demonstrate a beneficial role of endogenous galanin to transfer GLUT4 from internal stores to plasma membranes in adipocytes of type 2 diabetic rats.
751	22079346	Exercise-induced galanin release facilitated GLUT4 translocation in adipocytes of type 2 diabetic rats.
752	22079346	Although galanin has been shown to increase insulin sensitivity in skeletal muscle of rats, there is no literature available about the effect of galanin on Glucose Transporter 4 (GLUT4) translocation from intracellular membrane pools to plasma membranes in adipocytes of type 2 diabetic rats.
753	22079346	In the present study M35, a galanin antagonist was used to elucidate whether exercise-induced galanin release increased GLUT4 translocation in adipocytes of streptozotocin-induced diabetic rats.
754	22079346	These data demonstrate a beneficial role of endogenous galanin to transfer GLUT4 from internal stores to plasma membranes in adipocytes of type 2 diabetic rats.
755	22564511	Intracerebroventricular administration of galanin antagonist sustains insulin resistance in adipocytes of type 2 diabetic trained rats.
756	22564511	The aim of this study is to investigate whether galanin (GAL) central receptors are involved in regulation of insulin resistance.
757	22564511	These results suggest a facilitating role for GAL on GLUT4 translocation and insulin sensitivity via its central receptors in rats.
758	22564511	Intracerebroventricular administration of galanin antagonist sustains insulin resistance in adipocytes of type 2 diabetic trained rats.
759	22564511	The aim of this study is to investigate whether galanin (GAL) central receptors are involved in regulation of insulin resistance.
760	22564511	These results suggest a facilitating role for GAL on GLUT4 translocation and insulin sensitivity via its central receptors in rats.
761	23376774	Recent studies provided some compelling clues that neuropeptide galanin is closely associated with insulin sensitivity in the heart.
762	23376774	Galanin may directly affect glucose homeostasis and carbohydrate metabolism in cardiac and skeletal muscles as well as increase glucose transporter 4 (GLUT4) expression and translocation in insulin-sensitive cells to reduce insulin resistance.
763	23376774	This paper highlights the effect of galanin on regulating heart rate, blood pressure, insulin sensitivity and glucose homeostasis to protect the diabetic heart.
764	23376774	Recent studies provided some compelling clues that neuropeptide galanin is closely associated with insulin sensitivity in the heart.
765	23376774	Galanin may directly affect glucose homeostasis and carbohydrate metabolism in cardiac and skeletal muscles as well as increase glucose transporter 4 (GLUT4) expression and translocation in insulin-sensitive cells to reduce insulin resistance.
766	23376774	This paper highlights the effect of galanin on regulating heart rate, blood pressure, insulin sensitivity and glucose homeostasis to protect the diabetic heart.
767	23376774	Recent studies provided some compelling clues that neuropeptide galanin is closely associated with insulin sensitivity in the heart.
768	23376774	Galanin may directly affect glucose homeostasis and carbohydrate metabolism in cardiac and skeletal muscles as well as increase glucose transporter 4 (GLUT4) expression and translocation in insulin-sensitive cells to reduce insulin resistance.
769	23376774	This paper highlights the effect of galanin on regulating heart rate, blood pressure, insulin sensitivity and glucose homeostasis to protect the diabetic heart.
770	23653288	Blocking central galanin receptors attenuates insulin sensitivity in myocytes of diabetic trained rats.
771	23653288	These results imply that endogenous Gal, acting through its central receptor, may facilitate GLUT4 translocation from cytoplasm vesicles to cellular surface of myocytes to accelerate glucose uptake and to enhance insulin sensitivity in healthy and type 2 diabetic rats.