Ignet

Gene Information

Gene symbol: APLN

Gene name: apelin

HGNC ID: 16665

Synonyms: apelin, XNPEP2

Related Genes

#	Gene Symbol	Number of hits
1	ACE2	1 hits
2	ADAMTS3	1 hits
3	ADAMTS5	1 hits
4	ADIPOQ	1 hits
5	AGT	1 hits
6	AGTRL1	1 hits
7	AKT1	1 hits
8	ALB	1 hits
9	C3	1 hits
10	CASP3	1 hits
11	CASP8	1 hits
12	CCK	1 hits
13	COL1A1	1 hits
14	COL2A1	1 hits
15	COX8B	1 hits
16	CRH	1 hits
17	CRP	1 hits
18	CS	1 hits
19	GHRL	1 hits
20	IL1B	1 hits
21	IL6	1 hits
22	INS	1 hits
23	ITLN1	1 hits
24	KDR	1 hits
25	LEP	1 hits
26	MMP3	1 hits
27	NAMPT	1 hits
28	NOS3	1 hits
29	NPY	1 hits
30	PCNA	1 hits
31	PPARGC1A	1 hits
32	PRKAA1	1 hits
33	RARRES2	1 hits
34	RBP4	1 hits
35	RETN	1 hits
36	SERPINA12	1 hits
37	SERPINE1	1 hits
38	SST	1 hits
39	STN	1 hits
40	TEK	1 hits
41	TNF	1 hits
42	UCP3	1 hits
43	VEGFA	1 hits
44	VWF	1 hits

Related Sentences

#	PMID	Sentence
1	15549171	Angiotensin-converting enzyme-2 (ACE2) is the first human homologue of ACE to be described.
2	15549171	ACE2 efficiently hydrolyses the potent vasoconstrictor angiotensin II to angiotensin (1-7).
3	15549171	It is a consequence of this action that ACE2 participates in the renin-angiotensin system.
4	15549171	However, ACE2 also hydrolyses dynorphin A (1-13), apelin-13 and des-Arg(9) bradykinin.
5	15549171	This paper reviews the biochemistry of ACE2 and discusses key findings such as the elucidation of crystal structures for ACE2 and testicular ACE and the development of ACE2 inhibitors that have now provided a basis for future research on this enzyme.
6	16733497	Apelin and visfatin: unique "beneficial" adipokines upregulated in obesity?
7	16733497	Apelin and visfatin are two recently described adipokines, although they are also synthesized outside adipose tissue.
8	16733497	Apelin synthesis in adipocytes is stimulated by insulin, and plasma apelin level markedly increases in obesity associated with insulin resistance and hyperinsulinemia.
9	16733497	Visfatin binds to the insulin receptor at a site distinct from insulin and exerts hypoglycemic effect by reducing glucose release from hepatocytes and stimulating glucose utilization in peripheral tissues.
10	16733497	Thus, apelin and visfatin are unique among adipose tissue hormones in that they are upregulated in the obese state and both exert primarily beneficial effects.
11	16733497	Apelin and visfatin: unique "beneficial" adipokines upregulated in obesity?
12	16733497	Apelin and visfatin are two recently described adipokines, although they are also synthesized outside adipose tissue.
13	16733497	Apelin synthesis in adipocytes is stimulated by insulin, and plasma apelin level markedly increases in obesity associated with insulin resistance and hyperinsulinemia.
14	16733497	Visfatin binds to the insulin receptor at a site distinct from insulin and exerts hypoglycemic effect by reducing glucose release from hepatocytes and stimulating glucose utilization in peripheral tissues.
15	16733497	Thus, apelin and visfatin are unique among adipose tissue hormones in that they are upregulated in the obese state and both exert primarily beneficial effects.
16	16733497	Apelin and visfatin: unique "beneficial" adipokines upregulated in obesity?
17	16733497	Apelin and visfatin are two recently described adipokines, although they are also synthesized outside adipose tissue.
18	16733497	Apelin synthesis in adipocytes is stimulated by insulin, and plasma apelin level markedly increases in obesity associated with insulin resistance and hyperinsulinemia.
19	16733497	Visfatin binds to the insulin receptor at a site distinct from insulin and exerts hypoglycemic effect by reducing glucose release from hepatocytes and stimulating glucose utilization in peripheral tissues.
20	16733497	Thus, apelin and visfatin are unique among adipose tissue hormones in that they are upregulated in the obese state and both exert primarily beneficial effects.
21	16733497	Apelin and visfatin: unique "beneficial" adipokines upregulated in obesity?
22	16733497	Apelin and visfatin are two recently described adipokines, although they are also synthesized outside adipose tissue.
23	16733497	Apelin synthesis in adipocytes is stimulated by insulin, and plasma apelin level markedly increases in obesity associated with insulin resistance and hyperinsulinemia.
24	16733497	Visfatin binds to the insulin receptor at a site distinct from insulin and exerts hypoglycemic effect by reducing glucose release from hepatocytes and stimulating glucose utilization in peripheral tissues.
25	16733497	Thus, apelin and visfatin are unique among adipose tissue hormones in that they are upregulated in the obese state and both exert primarily beneficial effects.
26	16954332	Leptin and apelin mRNA levels in white and brown AT were higher in +/+ offspring from db/+ vs. +/+ dams; however, leptin, apelin, and tumor necrosis factor-alpha expression were boosted more robustly in db/+ offspring.
27	17177135	Changes and relations of circulating visfatin, apelin, and resistin levels in normal, impaired glucose tolerance, and type 2 diabetic subjects.
28	17177135	Visfatin and apelin are two novel adipocyte- secreted hormone proposed to link obesity with insulin resistance.
29	17177135	In this study we investigated whether plasma visfatin and apelin levels were altered in normal, impaired glucose tolerance, and type 2 diabetic subjects.
30	17177135	We also assessed the association between plasma visfatin, or apelin and body composition, metabolic parameters, and resistin concentrations in these subjects.
31	17177135	Fasting plasma visfatin was found to correlate positively and significantly with BMI, WHR, and fasting plasma resistin, but negatively with HbA1c and 2 h OGTT glucose.
32	17177135	The present work indicates the potential link of visfatin and apelin with the pathogenesis of insulin resistance and T2DM.
33	17177135	Changes and relations of circulating visfatin, apelin, and resistin levels in normal, impaired glucose tolerance, and type 2 diabetic subjects.
34	17177135	Visfatin and apelin are two novel adipocyte- secreted hormone proposed to link obesity with insulin resistance.
35	17177135	In this study we investigated whether plasma visfatin and apelin levels were altered in normal, impaired glucose tolerance, and type 2 diabetic subjects.
36	17177135	We also assessed the association between plasma visfatin, or apelin and body composition, metabolic parameters, and resistin concentrations in these subjects.
37	17177135	Fasting plasma visfatin was found to correlate positively and significantly with BMI, WHR, and fasting plasma resistin, but negatively with HbA1c and 2 h OGTT glucose.
38	17177135	The present work indicates the potential link of visfatin and apelin with the pathogenesis of insulin resistance and T2DM.
39	17177135	Changes and relations of circulating visfatin, apelin, and resistin levels in normal, impaired glucose tolerance, and type 2 diabetic subjects.
40	17177135	Visfatin and apelin are two novel adipocyte- secreted hormone proposed to link obesity with insulin resistance.
41	17177135	In this study we investigated whether plasma visfatin and apelin levels were altered in normal, impaired glucose tolerance, and type 2 diabetic subjects.
42	17177135	We also assessed the association between plasma visfatin, or apelin and body composition, metabolic parameters, and resistin concentrations in these subjects.
43	17177135	Fasting plasma visfatin was found to correlate positively and significantly with BMI, WHR, and fasting plasma resistin, but negatively with HbA1c and 2 h OGTT glucose.
44	17177135	The present work indicates the potential link of visfatin and apelin with the pathogenesis of insulin resistance and T2DM.
45	17177135	Changes and relations of circulating visfatin, apelin, and resistin levels in normal, impaired glucose tolerance, and type 2 diabetic subjects.
46	17177135	Visfatin and apelin are two novel adipocyte- secreted hormone proposed to link obesity with insulin resistance.
47	17177135	In this study we investigated whether plasma visfatin and apelin levels were altered in normal, impaired glucose tolerance, and type 2 diabetic subjects.
48	17177135	We also assessed the association between plasma visfatin, or apelin and body composition, metabolic parameters, and resistin concentrations in these subjects.
49	17177135	Fasting plasma visfatin was found to correlate positively and significantly with BMI, WHR, and fasting plasma resistin, but negatively with HbA1c and 2 h OGTT glucose.
50	17177135	The present work indicates the potential link of visfatin and apelin with the pathogenesis of insulin resistance and T2DM.
51	17177135	Changes and relations of circulating visfatin, apelin, and resistin levels in normal, impaired glucose tolerance, and type 2 diabetic subjects.
52	17177135	Visfatin and apelin are two novel adipocyte- secreted hormone proposed to link obesity with insulin resistance.
53	17177135	In this study we investigated whether plasma visfatin and apelin levels were altered in normal, impaired glucose tolerance, and type 2 diabetic subjects.
54	17177135	We also assessed the association between plasma visfatin, or apelin and body composition, metabolic parameters, and resistin concentrations in these subjects.
55	17177135	Fasting plasma visfatin was found to correlate positively and significantly with BMI, WHR, and fasting plasma resistin, but negatively with HbA1c and 2 h OGTT glucose.
56	17177135	The present work indicates the potential link of visfatin and apelin with the pathogenesis of insulin resistance and T2DM.
57	17359956	Apelin modulates aortic vascular tone via endothelial nitric oxide synthase phosphorylation pathway in diabetic mice.
58	17647139	Thirty-three patients with hypercholesterolemia and 50 age-, sex-, and body mass index-matched healthy controls were evaluated for their apelin, adiponectin and high sensitivity C-reactive protein (hsCRP) levels, and homeostasis model assessment (HOMA) indexes.
59	17647139	Plasma apelin-12 and adiponectin were determined by ELISA and RIA, respectively.
60	17647139	Low apelin levels in hypercholesterolemia seem associated with insulin resistance, which needs to be investigated in larger populations as well as in other atherosclerotic conditions.
61	17647139	Thirty-three patients with hypercholesterolemia and 50 age-, sex-, and body mass index-matched healthy controls were evaluated for their apelin, adiponectin and high sensitivity C-reactive protein (hsCRP) levels, and homeostasis model assessment (HOMA) indexes.
62	17647139	Plasma apelin-12 and adiponectin were determined by ELISA and RIA, respectively.
63	17647139	Low apelin levels in hypercholesterolemia seem associated with insulin resistance, which needs to be investigated in larger populations as well as in other atherosclerotic conditions.
64	17647139	Thirty-three patients with hypercholesterolemia and 50 age-, sex-, and body mass index-matched healthy controls were evaluated for their apelin, adiponectin and high sensitivity C-reactive protein (hsCRP) levels, and homeostasis model assessment (HOMA) indexes.
65	17647139	Plasma apelin-12 and adiponectin were determined by ELISA and RIA, respectively.
66	17647139	Low apelin levels in hypercholesterolemia seem associated with insulin resistance, which needs to be investigated in larger populations as well as in other atherosclerotic conditions.
67	17692936	Apelin, a newly identified angiotensin (Ang) II homologue, has been implicated in diabetes.
68	17692936	We previously reported that apelin exerts an opposing influence on the Ang II signaling.
69	17692936	Our aim was to further implore whether apelin could regulate intrarenal artery tone in response to Ang II and Ang IV in diabetes.
70	17692936	The phosphorylation, and protein levels of endothelial nitric oxide (NO) synthase (eNOS), and apelin receptor APJ were analyzed by Western blotting.
71	17692936	Diminished expression of APJ protein and enhanced contractile responses to Ang II and Ang IV were exhibited in renal arteries from db/db mice.
72	17692936	Apelin supplement reversed the abnormal renal vascular responsiveness to Ang II and acetylcholine, but not to Ang IV in db/db mice.
73	17692936	Apelin treatment may regulate the balance between Ang II and NO and thereby exert beneficial effects on the diabetic vascular pathophysiology.
74	17692936	Apelin, a newly identified angiotensin (Ang) II homologue, has been implicated in diabetes.
75	17692936	We previously reported that apelin exerts an opposing influence on the Ang II signaling.
76	17692936	Our aim was to further implore whether apelin could regulate intrarenal artery tone in response to Ang II and Ang IV in diabetes.
77	17692936	The phosphorylation, and protein levels of endothelial nitric oxide (NO) synthase (eNOS), and apelin receptor APJ were analyzed by Western blotting.
78	17692936	Diminished expression of APJ protein and enhanced contractile responses to Ang II and Ang IV were exhibited in renal arteries from db/db mice.
79	17692936	Apelin supplement reversed the abnormal renal vascular responsiveness to Ang II and acetylcholine, but not to Ang IV in db/db mice.
80	17692936	Apelin treatment may regulate the balance between Ang II and NO and thereby exert beneficial effects on the diabetic vascular pathophysiology.
81	17692936	Apelin, a newly identified angiotensin (Ang) II homologue, has been implicated in diabetes.
82	17692936	We previously reported that apelin exerts an opposing influence on the Ang II signaling.
83	17692936	Our aim was to further implore whether apelin could regulate intrarenal artery tone in response to Ang II and Ang IV in diabetes.
84	17692936	The phosphorylation, and protein levels of endothelial nitric oxide (NO) synthase (eNOS), and apelin receptor APJ were analyzed by Western blotting.
85	17692936	Diminished expression of APJ protein and enhanced contractile responses to Ang II and Ang IV were exhibited in renal arteries from db/db mice.
86	17692936	Apelin supplement reversed the abnormal renal vascular responsiveness to Ang II and acetylcholine, but not to Ang IV in db/db mice.
87	17692936	Apelin treatment may regulate the balance between Ang II and NO and thereby exert beneficial effects on the diabetic vascular pathophysiology.
88	17692936	Apelin, a newly identified angiotensin (Ang) II homologue, has been implicated in diabetes.
89	17692936	We previously reported that apelin exerts an opposing influence on the Ang II signaling.
90	17692936	Our aim was to further implore whether apelin could regulate intrarenal artery tone in response to Ang II and Ang IV in diabetes.
91	17692936	The phosphorylation, and protein levels of endothelial nitric oxide (NO) synthase (eNOS), and apelin receptor APJ were analyzed by Western blotting.
92	17692936	Diminished expression of APJ protein and enhanced contractile responses to Ang II and Ang IV were exhibited in renal arteries from db/db mice.
93	17692936	Apelin supplement reversed the abnormal renal vascular responsiveness to Ang II and acetylcholine, but not to Ang IV in db/db mice.
94	17692936	Apelin treatment may regulate the balance between Ang II and NO and thereby exert beneficial effects on the diabetic vascular pathophysiology.
95	17692936	Apelin, a newly identified angiotensin (Ang) II homologue, has been implicated in diabetes.
96	17692936	We previously reported that apelin exerts an opposing influence on the Ang II signaling.
97	17692936	Our aim was to further implore whether apelin could regulate intrarenal artery tone in response to Ang II and Ang IV in diabetes.
98	17692936	The phosphorylation, and protein levels of endothelial nitric oxide (NO) synthase (eNOS), and apelin receptor APJ were analyzed by Western blotting.
99	17692936	Diminished expression of APJ protein and enhanced contractile responses to Ang II and Ang IV were exhibited in renal arteries from db/db mice.
100	17692936	Apelin supplement reversed the abnormal renal vascular responsiveness to Ang II and acetylcholine, but not to Ang IV in db/db mice.
101	17692936	Apelin treatment may regulate the balance between Ang II and NO and thereby exert beneficial effects on the diabetic vascular pathophysiology.
102	17692936	Apelin, a newly identified angiotensin (Ang) II homologue, has been implicated in diabetes.
103	17692936	We previously reported that apelin exerts an opposing influence on the Ang II signaling.
104	17692936	Our aim was to further implore whether apelin could regulate intrarenal artery tone in response to Ang II and Ang IV in diabetes.
105	17692936	The phosphorylation, and protein levels of endothelial nitric oxide (NO) synthase (eNOS), and apelin receptor APJ were analyzed by Western blotting.
106	17692936	Diminished expression of APJ protein and enhanced contractile responses to Ang II and Ang IV were exhibited in renal arteries from db/db mice.
107	17692936	Apelin supplement reversed the abnormal renal vascular responsiveness to Ang II and acetylcholine, but not to Ang IV in db/db mice.
108	17692936	Apelin treatment may regulate the balance between Ang II and NO and thereby exert beneficial effects on the diabetic vascular pathophysiology.
109	18390031	Therefore, in this context, the roles of leptin, insulin, adiponectin, and lesser known acylation-stimulating protein, visfatin, and apelin are outlined.
110	18390031	Further, adipocyte inflammatory secretagogues are outlined that affect diabetes mellitus 2 with insulin resistance,fatty acid lipotoxicity, dyslipidemia, and hypertension that contribute to the metabolic syndrome.
111	18390031	These effects are opposed by adipocyte hormones adiponectin, acylation-stimulating protein, visfatin, and apelin that help maintain normal energy utilization.
112	18390031	Therefore, in this context, the roles of leptin, insulin, adiponectin, and lesser known acylation-stimulating protein, visfatin, and apelin are outlined.
113	18390031	Further, adipocyte inflammatory secretagogues are outlined that affect diabetes mellitus 2 with insulin resistance,fatty acid lipotoxicity, dyslipidemia, and hypertension that contribute to the metabolic syndrome.
114	18390031	These effects are opposed by adipocyte hormones adiponectin, acylation-stimulating protein, visfatin, and apelin that help maintain normal energy utilization.
115	18457011	In this regard, expression of apelin gene in adipose tissue is increased by insulin and TNFalpha.
116	19100414	We also assessed markers of endothelial cell injury-von Villebrand factor (vWF), thrombomodulin, intracellular adhesion molecule (ICAM), and CD146; markers of inflammation-high-sensitivity-reactive protein (hsCRP); other hemostatic parameters-tissue plasminogen activator (tPA) and its inhibitor (PAI-1); as well as other adipocytokines-adiponectin and resistin-using commercially available kits.
117	19100414	We observed significant correlations between apelin and ICAM, resistin, adiponectin, calcium, phosphate, alanine and aspartate aminotransferase levels, with CAD or diabetes.
118	19100414	Upon multiple regression analysis as well as CAD, adiponectin, and ICAM were predictors of apelin.
119	19100414	We also assessed markers of endothelial cell injury-von Villebrand factor (vWF), thrombomodulin, intracellular adhesion molecule (ICAM), and CD146; markers of inflammation-high-sensitivity-reactive protein (hsCRP); other hemostatic parameters-tissue plasminogen activator (tPA) and its inhibitor (PAI-1); as well as other adipocytokines-adiponectin and resistin-using commercially available kits.
120	19100414	We observed significant correlations between apelin and ICAM, resistin, adiponectin, calcium, phosphate, alanine and aspartate aminotransferase levels, with CAD or diabetes.
121	19100414	Upon multiple regression analysis as well as CAD, adiponectin, and ICAM were predictors of apelin.
122	19362933	Several cytokines, tumor necrosis factor-alpha and its soluble receptor forms, sTNFR1 and sTNFR2, resistin, retinol-binding protein 4, plasminogen activator inhibitor, lipocain 1 inhibit the signalization of insulin receptor causing insulin resistance in target tissues, mainly in adipose, liver and muscle, brain, endothelial as well as in pancreatic beta-cells.
123	19362933	However, many other proteins produced by the fat tissue, such as adiponectin, visfatin, vaspin, apelin, omentin and chemerin enhance the signal transmission of the receptor.
124	19362933	Recently discovered common mechanisms leading to insulin and cytokine resistance in obesity and type 2 diabetes mellitus, e.g. protein family of suppressor of cytokine signaling (SOCS) are also discussed.
125	19474287	Adipocytokines, including leptin, adiponectin, tumor necrosis factor alpha, interleukin 6, as well as the newly discovered resistin, visfatin, and apelin, are also known to be produced within the intrauterine environment.
126	19474287	Focus will be placed on the functions and other potential roles of the novel adipocytokines resistin, visfatin, and apelin.
127	19474287	Adipocytokines, including leptin, adiponectin, tumor necrosis factor alpha, interleukin 6, as well as the newly discovered resistin, visfatin, and apelin, are also known to be produced within the intrauterine environment.
128	19474287	Focus will be placed on the functions and other potential roles of the novel adipocytokines resistin, visfatin, and apelin.
129	19793954	Apelin, is a recently identified adipokine that when given to mice results in increases in skeletal muscle uncoupling protein 3 (UCP3) content.
130	19793954	Similarly, acute apelin treatment has been shown to increase the activity of 5'-AMP-activated protein kinase (AMPK), a reputed mediator of skeletal muscle mitochondrial biogenesis.
131	19793954	We made the novel observation that the activities of citrate synthase, cytochrome c oxidase, and beta-hydroxyacyl coA dehydrogenase (betaHAD) were increased in triceps but not heart and soleus muscles from apelin-treated rats.
132	19793954	The increases in mitochondrial marker proteins were associated with increases in proliferator-activated receptor-gamma coactivator-1 (PGC-1beta) but not PGC-1alpha or Pgc-1-related co-activator (PRC) mRNA expression.
133	19793954	Chronic and acute apelin treatment did not increase the protein content and/or phosphorylation status of AMPK and its downstream substrate acetyl-CoA carboxylase.
134	19793954	Given the lack of an effect of apelin on AMPK signaling and PGC-1alpha mRNA expression, these results suggest that apelin increases skeletal muscle mitochondrial content through a mechanism that is distinct from that of more robust physiological stressors.
135	19793954	Apelin, is a recently identified adipokine that when given to mice results in increases in skeletal muscle uncoupling protein 3 (UCP3) content.
136	19793954	Similarly, acute apelin treatment has been shown to increase the activity of 5'-AMP-activated protein kinase (AMPK), a reputed mediator of skeletal muscle mitochondrial biogenesis.
137	19793954	We made the novel observation that the activities of citrate synthase, cytochrome c oxidase, and beta-hydroxyacyl coA dehydrogenase (betaHAD) were increased in triceps but not heart and soleus muscles from apelin-treated rats.
138	19793954	The increases in mitochondrial marker proteins were associated with increases in proliferator-activated receptor-gamma coactivator-1 (PGC-1beta) but not PGC-1alpha or Pgc-1-related co-activator (PRC) mRNA expression.
139	19793954	Chronic and acute apelin treatment did not increase the protein content and/or phosphorylation status of AMPK and its downstream substrate acetyl-CoA carboxylase.
140	19793954	Given the lack of an effect of apelin on AMPK signaling and PGC-1alpha mRNA expression, these results suggest that apelin increases skeletal muscle mitochondrial content through a mechanism that is distinct from that of more robust physiological stressors.
141	19793954	Apelin, is a recently identified adipokine that when given to mice results in increases in skeletal muscle uncoupling protein 3 (UCP3) content.
142	19793954	Similarly, acute apelin treatment has been shown to increase the activity of 5'-AMP-activated protein kinase (AMPK), a reputed mediator of skeletal muscle mitochondrial biogenesis.
143	19793954	We made the novel observation that the activities of citrate synthase, cytochrome c oxidase, and beta-hydroxyacyl coA dehydrogenase (betaHAD) were increased in triceps but not heart and soleus muscles from apelin-treated rats.
144	19793954	The increases in mitochondrial marker proteins were associated with increases in proliferator-activated receptor-gamma coactivator-1 (PGC-1beta) but not PGC-1alpha or Pgc-1-related co-activator (PRC) mRNA expression.
145	19793954	Chronic and acute apelin treatment did not increase the protein content and/or phosphorylation status of AMPK and its downstream substrate acetyl-CoA carboxylase.
146	19793954	Given the lack of an effect of apelin on AMPK signaling and PGC-1alpha mRNA expression, these results suggest that apelin increases skeletal muscle mitochondrial content through a mechanism that is distinct from that of more robust physiological stressors.
147	19793954	Apelin, is a recently identified adipokine that when given to mice results in increases in skeletal muscle uncoupling protein 3 (UCP3) content.
148	19793954	Similarly, acute apelin treatment has been shown to increase the activity of 5'-AMP-activated protein kinase (AMPK), a reputed mediator of skeletal muscle mitochondrial biogenesis.
149	19793954	We made the novel observation that the activities of citrate synthase, cytochrome c oxidase, and beta-hydroxyacyl coA dehydrogenase (betaHAD) were increased in triceps but not heart and soleus muscles from apelin-treated rats.
150	19793954	The increases in mitochondrial marker proteins were associated with increases in proliferator-activated receptor-gamma coactivator-1 (PGC-1beta) but not PGC-1alpha or Pgc-1-related co-activator (PRC) mRNA expression.
151	19793954	Chronic and acute apelin treatment did not increase the protein content and/or phosphorylation status of AMPK and its downstream substrate acetyl-CoA carboxylase.
152	19793954	Given the lack of an effect of apelin on AMPK signaling and PGC-1alpha mRNA expression, these results suggest that apelin increases skeletal muscle mitochondrial content through a mechanism that is distinct from that of more robust physiological stressors.
153	19793954	Apelin, is a recently identified adipokine that when given to mice results in increases in skeletal muscle uncoupling protein 3 (UCP3) content.
154	19793954	Similarly, acute apelin treatment has been shown to increase the activity of 5'-AMP-activated protein kinase (AMPK), a reputed mediator of skeletal muscle mitochondrial biogenesis.
155	19793954	We made the novel observation that the activities of citrate synthase, cytochrome c oxidase, and beta-hydroxyacyl coA dehydrogenase (betaHAD) were increased in triceps but not heart and soleus muscles from apelin-treated rats.
156	19793954	The increases in mitochondrial marker proteins were associated with increases in proliferator-activated receptor-gamma coactivator-1 (PGC-1beta) but not PGC-1alpha or Pgc-1-related co-activator (PRC) mRNA expression.
157	19793954	Chronic and acute apelin treatment did not increase the protein content and/or phosphorylation status of AMPK and its downstream substrate acetyl-CoA carboxylase.
158	19793954	Given the lack of an effect of apelin on AMPK signaling and PGC-1alpha mRNA expression, these results suggest that apelin increases skeletal muscle mitochondrial content through a mechanism that is distinct from that of more robust physiological stressors.
159	19815243	Effects of rosiglitazone and metformin treatment on apelin, visfatin, and ghrelin levels in patients with type 2 diabetes mellitus.
160	19815243	Visfatin, ghrelin, and apelin are the most recently identified adipocytokines; but their response to insulin-sensitizing agents is poorly clarified.
161	19815243	Anthropometric parameters, glycemic and lipid profile, high-sensitivity CRP (hs-CRP), insulin resistance (homeostasis model assessment of insulin resistance index [HOMA-IR]), visfatin, ghrelin, and apelin were assessed at baseline and after 14 weeks of therapy.
162	19815243	Both rosiglitazone and metformin led to similar, significant improvement in glycemic profile and apelin levels, whereas lipid parameters, fat mass, and visfatin remained almost unaffected (P > .05).
163	19815243	The aforementioned changes in apelin and ghrelin were independently associated with HOMA-IR changes.
164	19815243	Effects of rosiglitazone and metformin treatment on apelin, visfatin, and ghrelin levels in patients with type 2 diabetes mellitus.
165	19815243	Visfatin, ghrelin, and apelin are the most recently identified adipocytokines; but their response to insulin-sensitizing agents is poorly clarified.
166	19815243	Anthropometric parameters, glycemic and lipid profile, high-sensitivity CRP (hs-CRP), insulin resistance (homeostasis model assessment of insulin resistance index [HOMA-IR]), visfatin, ghrelin, and apelin were assessed at baseline and after 14 weeks of therapy.
167	19815243	Both rosiglitazone and metformin led to similar, significant improvement in glycemic profile and apelin levels, whereas lipid parameters, fat mass, and visfatin remained almost unaffected (P > .05).
168	19815243	The aforementioned changes in apelin and ghrelin were independently associated with HOMA-IR changes.
169	19815243	Effects of rosiglitazone and metformin treatment on apelin, visfatin, and ghrelin levels in patients with type 2 diabetes mellitus.
170	19815243	Visfatin, ghrelin, and apelin are the most recently identified adipocytokines; but their response to insulin-sensitizing agents is poorly clarified.
171	19815243	Anthropometric parameters, glycemic and lipid profile, high-sensitivity CRP (hs-CRP), insulin resistance (homeostasis model assessment of insulin resistance index [HOMA-IR]), visfatin, ghrelin, and apelin were assessed at baseline and after 14 weeks of therapy.
172	19815243	Both rosiglitazone and metformin led to similar, significant improvement in glycemic profile and apelin levels, whereas lipid parameters, fat mass, and visfatin remained almost unaffected (P > .05).
173	19815243	The aforementioned changes in apelin and ghrelin were independently associated with HOMA-IR changes.
174	19815243	Effects of rosiglitazone and metformin treatment on apelin, visfatin, and ghrelin levels in patients with type 2 diabetes mellitus.
175	19815243	Visfatin, ghrelin, and apelin are the most recently identified adipocytokines; but their response to insulin-sensitizing agents is poorly clarified.
176	19815243	Anthropometric parameters, glycemic and lipid profile, high-sensitivity CRP (hs-CRP), insulin resistance (homeostasis model assessment of insulin resistance index [HOMA-IR]), visfatin, ghrelin, and apelin were assessed at baseline and after 14 weeks of therapy.
177	19815243	Both rosiglitazone and metformin led to similar, significant improvement in glycemic profile and apelin levels, whereas lipid parameters, fat mass, and visfatin remained almost unaffected (P > .05).
178	19815243	The aforementioned changes in apelin and ghrelin were independently associated with HOMA-IR changes.
179	19815243	Effects of rosiglitazone and metformin treatment on apelin, visfatin, and ghrelin levels in patients with type 2 diabetes mellitus.
180	19815243	Visfatin, ghrelin, and apelin are the most recently identified adipocytokines; but their response to insulin-sensitizing agents is poorly clarified.
181	19815243	Anthropometric parameters, glycemic and lipid profile, high-sensitivity CRP (hs-CRP), insulin resistance (homeostasis model assessment of insulin resistance index [HOMA-IR]), visfatin, ghrelin, and apelin were assessed at baseline and after 14 weeks of therapy.
182	19815243	Both rosiglitazone and metformin led to similar, significant improvement in glycemic profile and apelin levels, whereas lipid parameters, fat mass, and visfatin remained almost unaffected (P > .05).
183	19815243	The aforementioned changes in apelin and ghrelin were independently associated with HOMA-IR changes.
184	19861585	Apelin is necessary for the maintenance of insulin sensitivity.
185	19861585	The recently discovered peptide apelin is known to be involved in the maintenance of insulin sensitivity.
186	19861585	Fasting glucose, insulin, and adiponectin levels were determined on mice with generalized deficiency of apelin (APKO).
187	19861585	To assess the impact of exogenously delivered apelin on insulin sensitivity, osmotic pumps containing pyroglutamated apelin-13 or saline were implanted in APKO mice for 4 wk.
188	19861585	Soleus muscles were harvested and homogenized in lysis buffer, and insulin-induced Akt phosphorylation was determined by Western blotting.
189	19861585	To probe the underlying mechanism for apelin's effects, apelin-13 was also delivered to cultured C2C12 myotubes. 2-[3H]deoxyglucose uptake and Akt phosphorylation were assessed in the presence of various inhibitors.
190	19861585	APKO mice had diminished insulin sensitivity, were hyperinsulinemic, and had decreased adiponectin levels.
191	19861585	Soleus lysates had decreased insulin-induced Akt phosphorylation.
192	19861585	Administration of apelin to APKO and db/db mice resulted in improved insulin sensitivity.
193	19861585	In C2C12 myotubes, apelin increased glucose uptake and Akt phosphorylation.
194	19861585	We conclude that apelin is necessary for the maintenance of insulin sensitivity in vivo.
195	19861585	Apelin's effects on glucose uptake and Akt phosphorylation are in part mediated by a G(i) and AMPK-dependent pathway.
196	19861585	Apelin is necessary for the maintenance of insulin sensitivity.
197	19861585	The recently discovered peptide apelin is known to be involved in the maintenance of insulin sensitivity.
198	19861585	Fasting glucose, insulin, and adiponectin levels were determined on mice with generalized deficiency of apelin (APKO).
199	19861585	To assess the impact of exogenously delivered apelin on insulin sensitivity, osmotic pumps containing pyroglutamated apelin-13 or saline were implanted in APKO mice for 4 wk.
200	19861585	Soleus muscles were harvested and homogenized in lysis buffer, and insulin-induced Akt phosphorylation was determined by Western blotting.
201	19861585	To probe the underlying mechanism for apelin's effects, apelin-13 was also delivered to cultured C2C12 myotubes. 2-[3H]deoxyglucose uptake and Akt phosphorylation were assessed in the presence of various inhibitors.
202	19861585	APKO mice had diminished insulin sensitivity, were hyperinsulinemic, and had decreased adiponectin levels.
203	19861585	Soleus lysates had decreased insulin-induced Akt phosphorylation.
204	19861585	Administration of apelin to APKO and db/db mice resulted in improved insulin sensitivity.
205	19861585	In C2C12 myotubes, apelin increased glucose uptake and Akt phosphorylation.
206	19861585	We conclude that apelin is necessary for the maintenance of insulin sensitivity in vivo.
207	19861585	Apelin's effects on glucose uptake and Akt phosphorylation are in part mediated by a G(i) and AMPK-dependent pathway.
208	19861585	Apelin is necessary for the maintenance of insulin sensitivity.
209	19861585	The recently discovered peptide apelin is known to be involved in the maintenance of insulin sensitivity.
210	19861585	Fasting glucose, insulin, and adiponectin levels were determined on mice with generalized deficiency of apelin (APKO).
211	19861585	To assess the impact of exogenously delivered apelin on insulin sensitivity, osmotic pumps containing pyroglutamated apelin-13 or saline were implanted in APKO mice for 4 wk.
212	19861585	Soleus muscles were harvested and homogenized in lysis buffer, and insulin-induced Akt phosphorylation was determined by Western blotting.
213	19861585	To probe the underlying mechanism for apelin's effects, apelin-13 was also delivered to cultured C2C12 myotubes. 2-[3H]deoxyglucose uptake and Akt phosphorylation were assessed in the presence of various inhibitors.
214	19861585	APKO mice had diminished insulin sensitivity, were hyperinsulinemic, and had decreased adiponectin levels.
215	19861585	Soleus lysates had decreased insulin-induced Akt phosphorylation.
216	19861585	Administration of apelin to APKO and db/db mice resulted in improved insulin sensitivity.
217	19861585	In C2C12 myotubes, apelin increased glucose uptake and Akt phosphorylation.
218	19861585	We conclude that apelin is necessary for the maintenance of insulin sensitivity in vivo.
219	19861585	Apelin's effects on glucose uptake and Akt phosphorylation are in part mediated by a G(i) and AMPK-dependent pathway.
220	19861585	Apelin is necessary for the maintenance of insulin sensitivity.
221	19861585	The recently discovered peptide apelin is known to be involved in the maintenance of insulin sensitivity.
222	19861585	Fasting glucose, insulin, and adiponectin levels were determined on mice with generalized deficiency of apelin (APKO).
223	19861585	To assess the impact of exogenously delivered apelin on insulin sensitivity, osmotic pumps containing pyroglutamated apelin-13 or saline were implanted in APKO mice for 4 wk.
224	19861585	Soleus muscles were harvested and homogenized in lysis buffer, and insulin-induced Akt phosphorylation was determined by Western blotting.
225	19861585	To probe the underlying mechanism for apelin's effects, apelin-13 was also delivered to cultured C2C12 myotubes. 2-[3H]deoxyglucose uptake and Akt phosphorylation were assessed in the presence of various inhibitors.
226	19861585	APKO mice had diminished insulin sensitivity, were hyperinsulinemic, and had decreased adiponectin levels.
227	19861585	Soleus lysates had decreased insulin-induced Akt phosphorylation.
228	19861585	Administration of apelin to APKO and db/db mice resulted in improved insulin sensitivity.
229	19861585	In C2C12 myotubes, apelin increased glucose uptake and Akt phosphorylation.
230	19861585	We conclude that apelin is necessary for the maintenance of insulin sensitivity in vivo.
231	19861585	Apelin's effects on glucose uptake and Akt phosphorylation are in part mediated by a G(i) and AMPK-dependent pathway.
232	19861585	Apelin is necessary for the maintenance of insulin sensitivity.
233	19861585	The recently discovered peptide apelin is known to be involved in the maintenance of insulin sensitivity.
234	19861585	Fasting glucose, insulin, and adiponectin levels were determined on mice with generalized deficiency of apelin (APKO).
235	19861585	To assess the impact of exogenously delivered apelin on insulin sensitivity, osmotic pumps containing pyroglutamated apelin-13 or saline were implanted in APKO mice for 4 wk.
236	19861585	Soleus muscles were harvested and homogenized in lysis buffer, and insulin-induced Akt phosphorylation was determined by Western blotting.
237	19861585	To probe the underlying mechanism for apelin's effects, apelin-13 was also delivered to cultured C2C12 myotubes. 2-[3H]deoxyglucose uptake and Akt phosphorylation were assessed in the presence of various inhibitors.
238	19861585	APKO mice had diminished insulin sensitivity, were hyperinsulinemic, and had decreased adiponectin levels.
239	19861585	Soleus lysates had decreased insulin-induced Akt phosphorylation.
240	19861585	Administration of apelin to APKO and db/db mice resulted in improved insulin sensitivity.
241	19861585	In C2C12 myotubes, apelin increased glucose uptake and Akt phosphorylation.
242	19861585	We conclude that apelin is necessary for the maintenance of insulin sensitivity in vivo.
243	19861585	Apelin's effects on glucose uptake and Akt phosphorylation are in part mediated by a G(i) and AMPK-dependent pathway.
244	19861585	Apelin is necessary for the maintenance of insulin sensitivity.
245	19861585	The recently discovered peptide apelin is known to be involved in the maintenance of insulin sensitivity.
246	19861585	Fasting glucose, insulin, and adiponectin levels were determined on mice with generalized deficiency of apelin (APKO).
247	19861585	To assess the impact of exogenously delivered apelin on insulin sensitivity, osmotic pumps containing pyroglutamated apelin-13 or saline were implanted in APKO mice for 4 wk.
248	19861585	Soleus muscles were harvested and homogenized in lysis buffer, and insulin-induced Akt phosphorylation was determined by Western blotting.
249	19861585	To probe the underlying mechanism for apelin's effects, apelin-13 was also delivered to cultured C2C12 myotubes. 2-[3H]deoxyglucose uptake and Akt phosphorylation were assessed in the presence of various inhibitors.
250	19861585	APKO mice had diminished insulin sensitivity, were hyperinsulinemic, and had decreased adiponectin levels.
251	19861585	Soleus lysates had decreased insulin-induced Akt phosphorylation.
252	19861585	Administration of apelin to APKO and db/db mice resulted in improved insulin sensitivity.
253	19861585	In C2C12 myotubes, apelin increased glucose uptake and Akt phosphorylation.
254	19861585	We conclude that apelin is necessary for the maintenance of insulin sensitivity in vivo.
255	19861585	Apelin's effects on glucose uptake and Akt phosphorylation are in part mediated by a G(i) and AMPK-dependent pathway.
256	19861585	Apelin is necessary for the maintenance of insulin sensitivity.
257	19861585	The recently discovered peptide apelin is known to be involved in the maintenance of insulin sensitivity.
258	19861585	Fasting glucose, insulin, and adiponectin levels were determined on mice with generalized deficiency of apelin (APKO).
259	19861585	To assess the impact of exogenously delivered apelin on insulin sensitivity, osmotic pumps containing pyroglutamated apelin-13 or saline were implanted in APKO mice for 4 wk.
260	19861585	Soleus muscles were harvested and homogenized in lysis buffer, and insulin-induced Akt phosphorylation was determined by Western blotting.
261	19861585	To probe the underlying mechanism for apelin's effects, apelin-13 was also delivered to cultured C2C12 myotubes. 2-[3H]deoxyglucose uptake and Akt phosphorylation were assessed in the presence of various inhibitors.
262	19861585	APKO mice had diminished insulin sensitivity, were hyperinsulinemic, and had decreased adiponectin levels.
263	19861585	Soleus lysates had decreased insulin-induced Akt phosphorylation.
264	19861585	Administration of apelin to APKO and db/db mice resulted in improved insulin sensitivity.
265	19861585	In C2C12 myotubes, apelin increased glucose uptake and Akt phosphorylation.
266	19861585	We conclude that apelin is necessary for the maintenance of insulin sensitivity in vivo.
267	19861585	Apelin's effects on glucose uptake and Akt phosphorylation are in part mediated by a G(i) and AMPK-dependent pathway.
268	19861585	Apelin is necessary for the maintenance of insulin sensitivity.
269	19861585	The recently discovered peptide apelin is known to be involved in the maintenance of insulin sensitivity.
270	19861585	Fasting glucose, insulin, and adiponectin levels were determined on mice with generalized deficiency of apelin (APKO).
271	19861585	To assess the impact of exogenously delivered apelin on insulin sensitivity, osmotic pumps containing pyroglutamated apelin-13 or saline were implanted in APKO mice for 4 wk.
272	19861585	Soleus muscles were harvested and homogenized in lysis buffer, and insulin-induced Akt phosphorylation was determined by Western blotting.
273	19861585	To probe the underlying mechanism for apelin's effects, apelin-13 was also delivered to cultured C2C12 myotubes. 2-[3H]deoxyglucose uptake and Akt phosphorylation were assessed in the presence of various inhibitors.
274	19861585	APKO mice had diminished insulin sensitivity, were hyperinsulinemic, and had decreased adiponectin levels.
275	19861585	Soleus lysates had decreased insulin-induced Akt phosphorylation.
276	19861585	Administration of apelin to APKO and db/db mice resulted in improved insulin sensitivity.
277	19861585	In C2C12 myotubes, apelin increased glucose uptake and Akt phosphorylation.
278	19861585	We conclude that apelin is necessary for the maintenance of insulin sensitivity in vivo.
279	19861585	Apelin's effects on glucose uptake and Akt phosphorylation are in part mediated by a G(i) and AMPK-dependent pathway.
280	19861585	Apelin is necessary for the maintenance of insulin sensitivity.
281	19861585	The recently discovered peptide apelin is known to be involved in the maintenance of insulin sensitivity.
282	19861585	Fasting glucose, insulin, and adiponectin levels were determined on mice with generalized deficiency of apelin (APKO).
283	19861585	To assess the impact of exogenously delivered apelin on insulin sensitivity, osmotic pumps containing pyroglutamated apelin-13 or saline were implanted in APKO mice for 4 wk.
284	19861585	Soleus muscles were harvested and homogenized in lysis buffer, and insulin-induced Akt phosphorylation was determined by Western blotting.
285	19861585	To probe the underlying mechanism for apelin's effects, apelin-13 was also delivered to cultured C2C12 myotubes. 2-[3H]deoxyglucose uptake and Akt phosphorylation were assessed in the presence of various inhibitors.
286	19861585	APKO mice had diminished insulin sensitivity, were hyperinsulinemic, and had decreased adiponectin levels.
287	19861585	Soleus lysates had decreased insulin-induced Akt phosphorylation.
288	19861585	Administration of apelin to APKO and db/db mice resulted in improved insulin sensitivity.
289	19861585	In C2C12 myotubes, apelin increased glucose uptake and Akt phosphorylation.
290	19861585	We conclude that apelin is necessary for the maintenance of insulin sensitivity in vivo.
291	19861585	Apelin's effects on glucose uptake and Akt phosphorylation are in part mediated by a G(i) and AMPK-dependent pathway.
292	19908160	We investigated plasma apelin as well other adipocytokines: resistin, visfatin and von Willebrand factor (vWF)-a marker of endothelial cell injury.
293	19908160	Patients with forearm a-v fistula had lower left ventricular internal end-diastolic dimension (LVIDd) (P < 0.05), left ventricular internal end-systolic dimension (LVISd) (P < 0.05), NYHA class (P < 0.05), hsCRP (P < 0.01), plasma vWF (P < 0.01), and plasma resistin (P < 0.05), whereas the ejection fraction was higher than in patients with arm a-v fistula (P < 0.05), as well as hemoglobin (P < 0.05), hematocrit (P < 0.01), prevalence of diabetes (n < 0.05), prevalence of coronary heart disease (P < 0.05), serum pH (P < 0.05), serum bicarbonate (P < 0.05).
294	19908160	Apelin was related to echocardiographic parameters, presence of diabetes, coronary artery disease, chronic heart failure, NYHA class and serum lipids (total cholesterol, LDL, triglycerides), hsCRP, vWF, residual renal function, and Kt/V.
295	19908160	We investigated plasma apelin as well other adipocytokines: resistin, visfatin and von Willebrand factor (vWF)-a marker of endothelial cell injury.
296	19908160	Patients with forearm a-v fistula had lower left ventricular internal end-diastolic dimension (LVIDd) (P < 0.05), left ventricular internal end-systolic dimension (LVISd) (P < 0.05), NYHA class (P < 0.05), hsCRP (P < 0.01), plasma vWF (P < 0.01), and plasma resistin (P < 0.05), whereas the ejection fraction was higher than in patients with arm a-v fistula (P < 0.05), as well as hemoglobin (P < 0.05), hematocrit (P < 0.01), prevalence of diabetes (n < 0.05), prevalence of coronary heart disease (P < 0.05), serum pH (P < 0.05), serum bicarbonate (P < 0.05).
297	19908160	Apelin was related to echocardiographic parameters, presence of diabetes, coronary artery disease, chronic heart failure, NYHA class and serum lipids (total cholesterol, LDL, triglycerides), hsCRP, vWF, residual renal function, and Kt/V.
298	19940327	Adipose tissue produces multiple cytokines(TNF-alpha, IL-6, PAI-1, CRP, angiotensinogen, leptin, adiponectin, visfatin, apelin, resistin)which decrease insulin sensitivity and induce inflammatory processes, endothelial dysfunction,and atherosclerosis.
299	19940327	In human studies, the influence of resistin on the development of insulin resistance is controversial.
300	20416860	The discovery of apelin, an endogenous ligand of the orphan APJ receptor, constitutes an important advance in both fundamental research and clinical medicine.
301	20416860	Besides its diuretic action, when injected into the blood stream, apelin decreases blood pressure and increases the contractile force of the myocardium while decreasing pre- and post-load, actions opposing those of vasopressin and angiotensin II.
302	20416860	Finally, a systemic injection of apelin in insulin-resistant mice decreases glycemia and enhances glucose uptake in skeletal muscle and adipose tissue, contributing to homeostatic control of blood glucose.
303	20416860	The discovery of apelin, an endogenous ligand of the orphan APJ receptor, constitutes an important advance in both fundamental research and clinical medicine.
304	20416860	Besides its diuretic action, when injected into the blood stream, apelin decreases blood pressure and increases the contractile force of the myocardium while decreasing pre- and post-load, actions opposing those of vasopressin and angiotensin II.
305	20416860	Finally, a systemic injection of apelin in insulin-resistant mice decreases glycemia and enhances glucose uptake in skeletal muscle and adipose tissue, contributing to homeostatic control of blood glucose.
306	20416860	The discovery of apelin, an endogenous ligand of the orphan APJ receptor, constitutes an important advance in both fundamental research and clinical medicine.
307	20416860	Besides its diuretic action, when injected into the blood stream, apelin decreases blood pressure and increases the contractile force of the myocardium while decreasing pre- and post-load, actions opposing those of vasopressin and angiotensin II.
308	20416860	Finally, a systemic injection of apelin in insulin-resistant mice decreases glycemia and enhances glucose uptake in skeletal muscle and adipose tissue, contributing to homeostatic control of blood glucose.
309	20664951	In vitro, we examined the effects of apelin on normal chondrocyte proliferation and gene expression of metalloproteinases (MMPs) and interleukin-1beta (IL-1beta).
310	20664951	In vivo, by intra-articular injection with apelin, we examined MMP-3, -9, collagen II and IL-1beta at both gene and protein levels.
311	20664951	Furthermore, we measured the messenger RNA (mRNA) expression of ADAMTS-4 and -5 (a disintegrin and metalloproteinase with thrombospondin motifs 4 and 5) and the proteoglycan content in articular cartilage.
312	20664951	Apelin stimulated the proliferation of chondrocytes and significantly increased mRNA levels of MMP-1, -3, -9 and IL-1beta in vitro.
313	20664951	Intra-articular injection with apelin in vivo up-regulated the expression of MMP-3, -9, and IL-1beta as well as decreased the level of collagen II.
314	20664951	Additionally, after treatment with apelin, mRNA levels of ADAMTS-4 and -5 markedly increased and depletion of proteoglycan in articular cartilage was found by histological assessment.
315	20664951	In vitro, we examined the effects of apelin on normal chondrocyte proliferation and gene expression of metalloproteinases (MMPs) and interleukin-1beta (IL-1beta).
316	20664951	In vivo, by intra-articular injection with apelin, we examined MMP-3, -9, collagen II and IL-1beta at both gene and protein levels.
317	20664951	Furthermore, we measured the messenger RNA (mRNA) expression of ADAMTS-4 and -5 (a disintegrin and metalloproteinase with thrombospondin motifs 4 and 5) and the proteoglycan content in articular cartilage.
318	20664951	Apelin stimulated the proliferation of chondrocytes and significantly increased mRNA levels of MMP-1, -3, -9 and IL-1beta in vitro.
319	20664951	Intra-articular injection with apelin in vivo up-regulated the expression of MMP-3, -9, and IL-1beta as well as decreased the level of collagen II.
320	20664951	Additionally, after treatment with apelin, mRNA levels of ADAMTS-4 and -5 markedly increased and depletion of proteoglycan in articular cartilage was found by histological assessment.
321	20664951	In vitro, we examined the effects of apelin on normal chondrocyte proliferation and gene expression of metalloproteinases (MMPs) and interleukin-1beta (IL-1beta).
322	20664951	In vivo, by intra-articular injection with apelin, we examined MMP-3, -9, collagen II and IL-1beta at both gene and protein levels.
323	20664951	Furthermore, we measured the messenger RNA (mRNA) expression of ADAMTS-4 and -5 (a disintegrin and metalloproteinase with thrombospondin motifs 4 and 5) and the proteoglycan content in articular cartilage.
324	20664951	Apelin stimulated the proliferation of chondrocytes and significantly increased mRNA levels of MMP-1, -3, -9 and IL-1beta in vitro.
325	20664951	Intra-articular injection with apelin in vivo up-regulated the expression of MMP-3, -9, and IL-1beta as well as decreased the level of collagen II.
326	20664951	Additionally, after treatment with apelin, mRNA levels of ADAMTS-4 and -5 markedly increased and depletion of proteoglycan in articular cartilage was found by histological assessment.
327	20664951	In vitro, we examined the effects of apelin on normal chondrocyte proliferation and gene expression of metalloproteinases (MMPs) and interleukin-1beta (IL-1beta).
328	20664951	In vivo, by intra-articular injection with apelin, we examined MMP-3, -9, collagen II and IL-1beta at both gene and protein levels.
329	20664951	Furthermore, we measured the messenger RNA (mRNA) expression of ADAMTS-4 and -5 (a disintegrin and metalloproteinase with thrombospondin motifs 4 and 5) and the proteoglycan content in articular cartilage.
330	20664951	Apelin stimulated the proliferation of chondrocytes and significantly increased mRNA levels of MMP-1, -3, -9 and IL-1beta in vitro.
331	20664951	Intra-articular injection with apelin in vivo up-regulated the expression of MMP-3, -9, and IL-1beta as well as decreased the level of collagen II.
332	20664951	Additionally, after treatment with apelin, mRNA levels of ADAMTS-4 and -5 markedly increased and depletion of proteoglycan in articular cartilage was found by histological assessment.
333	20664951	In vitro, we examined the effects of apelin on normal chondrocyte proliferation and gene expression of metalloproteinases (MMPs) and interleukin-1beta (IL-1beta).
334	20664951	In vivo, by intra-articular injection with apelin, we examined MMP-3, -9, collagen II and IL-1beta at both gene and protein levels.
335	20664951	Furthermore, we measured the messenger RNA (mRNA) expression of ADAMTS-4 and -5 (a disintegrin and metalloproteinase with thrombospondin motifs 4 and 5) and the proteoglycan content in articular cartilage.
336	20664951	Apelin stimulated the proliferation of chondrocytes and significantly increased mRNA levels of MMP-1, -3, -9 and IL-1beta in vitro.
337	20664951	Intra-articular injection with apelin in vivo up-regulated the expression of MMP-3, -9, and IL-1beta as well as decreased the level of collagen II.
338	20664951	Additionally, after treatment with apelin, mRNA levels of ADAMTS-4 and -5 markedly increased and depletion of proteoglycan in articular cartilage was found by histological assessment.
339	20865382	These adipocytokines include not only, e.g., adiponectin, apelin, resistin, and visfatin, but also inflammatory cytokines and steroid hormones such as estrogens and glucocorticoids.
340	20890241	Vitreous and plasma concentrations of apelin and vascular endothelial growth factor after intravitreal bevacizumab in eyes with proliferative diabetic retinopathy.
341	21081794	Among them are classical neurotransmitters (epinephrine and norepinephrine, serotonin, GABA), classical (CRH, vasopressin, neuropeptide Y) and newly discovered (orexins, apelin, leptin IL-1beta, TNF-alpha, ghrelin) neuropeptides, gasotransmitters, eicozanoids, endocannabinoids, and some other compounds involved in regulation of neuroendocrine, sympatho-adrenal and parasympathetic nervous systems.
342	21081794	With regard to the pathogenic background of the cardiovascular diseases especially valuable are the studies showing inappropriate function of angiotensin peptides, vasopressin, CRH, apelin, cytokines and orexins in chronic stress, cardiovascular and metabolic diseases.
343	21081794	Among them are classical neurotransmitters (epinephrine and norepinephrine, serotonin, GABA), classical (CRH, vasopressin, neuropeptide Y) and newly discovered (orexins, apelin, leptin IL-1beta, TNF-alpha, ghrelin) neuropeptides, gasotransmitters, eicozanoids, endocannabinoids, and some other compounds involved in regulation of neuroendocrine, sympatho-adrenal and parasympathetic nervous systems.
344	21081794	With regard to the pathogenic background of the cardiovascular diseases especially valuable are the studies showing inappropriate function of angiotensin peptides, vasopressin, CRH, apelin, cytokines and orexins in chronic stress, cardiovascular and metabolic diseases.
345	21264801	Furthermore we examined the association of apelin serum levels with insulin sensitivity/resistance and body fat distribution as probably dependent cardiovascular risk factors.
346	21264801	Furthermore, neither parameters of insulin sensitivity like insulin sensitivity index (ISI), nor fat distribution like BMI, grade of adiposity, total adipose tissue or VAT were associated with apelin serum levels.
347	21264801	Furthermore we examined the association of apelin serum levels with insulin sensitivity/resistance and body fat distribution as probably dependent cardiovascular risk factors.
348	21264801	Furthermore, neither parameters of insulin sensitivity like insulin sensitivity index (ISI), nor fat distribution like BMI, grade of adiposity, total adipose tissue or VAT were associated with apelin serum levels.
349	21461750	Apelin is a novel adipokine with potential beneficial actions on glucose metabolism and insulin resistance.
350	21461750	However the insulin-sensitizing effect of LA in vivo is not related to changes in apelin gene expression in our model of diet-induced obesity.
351	21461750	Apelin is a novel adipokine with potential beneficial actions on glucose metabolism and insulin resistance.
352	21461750	However the insulin-sensitizing effect of LA in vivo is not related to changes in apelin gene expression in our model of diet-induced obesity.
353	21537431	We now know that it is an endocrine organ, producing adipokines like leptin, adiponectin, visfatin, resistin, apelin, etc, which modulate metabolic processes in the body.
354	21748474	Effects of atorvastatin on apelin, visfatin (nampt), ghrelin and early carotid atherosclerosis in patients with type 2 diabetes.
355	21748474	To investigate the influence of atrovastatin treatment on carotid intima-media thickness (CIMT) and serum levels of novel adipokines, like apelin, visfatin (nampt), and ghrelin, in patients with type 2 diabetes mellitus (T2DM). 87 statin-free patients (50 males) with T2DM, aged 55-70, but without carotid atherosclerotic plaques were initially enrolled.
356	21748474	Anthropometric parameters, blood pressure, glycemic and lipid profile, high-sensitivity CRP (hsCRP), insulin resistance (HOMA-IR), apelin, visfatin and ghrelin were measured at baseline and after 12 months.
357	21748474	Atorvastatin treatment significantly improved lipid profile across with increased apelin (from 0.307 ± 0.130 pg/ml to 1.537 ± 0.427 pg/ml; P < 0.001) and suppressed visfatin (from 21.54 ± 10.14 ng/ml to 15.13 ± 7.61 ng/ml; P = 0.002) serum levels in our diabetic patients.
358	21748474	Standard multiple regression analysis showed that the atorvastatin-induced increment in apelin was independently associated with changes in total cholesterol (β = -0.510, P = 0.030) and LDL-cholesterol (β = -0.590, P < 0.001) (R (2) = 0.449, P = 0.014), while the reduction of visfatin concentration was independently associated with the change in hsCRP (β = 0.589, P < 0.001; R (2) = 0.256, P = 0.006), after adjustment for age, sex and BMI.
359	21748474	Among participants, high-dose (80 mg) rather than low-dose (10 mg) of atorvastatin treatment yielded greater (P < 0.05) changes in apelin, visfatin and CIMT levels despite the final equivalent levels of LDL.
360	21748474	Atorvastatin administration increased apelin and decreased visfatin serum levels significantly, without change of CIMT, in patients with T2DM.
361	21748474	Effects of atorvastatin on apelin, visfatin (nampt), ghrelin and early carotid atherosclerosis in patients with type 2 diabetes.
362	21748474	To investigate the influence of atrovastatin treatment on carotid intima-media thickness (CIMT) and serum levels of novel adipokines, like apelin, visfatin (nampt), and ghrelin, in patients with type 2 diabetes mellitus (T2DM). 87 statin-free patients (50 males) with T2DM, aged 55-70, but without carotid atherosclerotic plaques were initially enrolled.
363	21748474	Anthropometric parameters, blood pressure, glycemic and lipid profile, high-sensitivity CRP (hsCRP), insulin resistance (HOMA-IR), apelin, visfatin and ghrelin were measured at baseline and after 12 months.
364	21748474	Atorvastatin treatment significantly improved lipid profile across with increased apelin (from 0.307 ± 0.130 pg/ml to 1.537 ± 0.427 pg/ml; P < 0.001) and suppressed visfatin (from 21.54 ± 10.14 ng/ml to 15.13 ± 7.61 ng/ml; P = 0.002) serum levels in our diabetic patients.
365	21748474	Standard multiple regression analysis showed that the atorvastatin-induced increment in apelin was independently associated with changes in total cholesterol (β = -0.510, P = 0.030) and LDL-cholesterol (β = -0.590, P < 0.001) (R (2) = 0.449, P = 0.014), while the reduction of visfatin concentration was independently associated with the change in hsCRP (β = 0.589, P < 0.001; R (2) = 0.256, P = 0.006), after adjustment for age, sex and BMI.
366	21748474	Among participants, high-dose (80 mg) rather than low-dose (10 mg) of atorvastatin treatment yielded greater (P < 0.05) changes in apelin, visfatin and CIMT levels despite the final equivalent levels of LDL.
367	21748474	Atorvastatin administration increased apelin and decreased visfatin serum levels significantly, without change of CIMT, in patients with T2DM.
368	21748474	Effects of atorvastatin on apelin, visfatin (nampt), ghrelin and early carotid atherosclerosis in patients with type 2 diabetes.
369	21748474	To investigate the influence of atrovastatin treatment on carotid intima-media thickness (CIMT) and serum levels of novel adipokines, like apelin, visfatin (nampt), and ghrelin, in patients with type 2 diabetes mellitus (T2DM). 87 statin-free patients (50 males) with T2DM, aged 55-70, but without carotid atherosclerotic plaques were initially enrolled.
370	21748474	Anthropometric parameters, blood pressure, glycemic and lipid profile, high-sensitivity CRP (hsCRP), insulin resistance (HOMA-IR), apelin, visfatin and ghrelin were measured at baseline and after 12 months.
371	21748474	Atorvastatin treatment significantly improved lipid profile across with increased apelin (from 0.307 ± 0.130 pg/ml to 1.537 ± 0.427 pg/ml; P < 0.001) and suppressed visfatin (from 21.54 ± 10.14 ng/ml to 15.13 ± 7.61 ng/ml; P = 0.002) serum levels in our diabetic patients.
372	21748474	Standard multiple regression analysis showed that the atorvastatin-induced increment in apelin was independently associated with changes in total cholesterol (β = -0.510, P = 0.030) and LDL-cholesterol (β = -0.590, P < 0.001) (R (2) = 0.449, P = 0.014), while the reduction of visfatin concentration was independently associated with the change in hsCRP (β = 0.589, P < 0.001; R (2) = 0.256, P = 0.006), after adjustment for age, sex and BMI.
373	21748474	Among participants, high-dose (80 mg) rather than low-dose (10 mg) of atorvastatin treatment yielded greater (P < 0.05) changes in apelin, visfatin and CIMT levels despite the final equivalent levels of LDL.
374	21748474	Atorvastatin administration increased apelin and decreased visfatin serum levels significantly, without change of CIMT, in patients with T2DM.
375	21748474	Effects of atorvastatin on apelin, visfatin (nampt), ghrelin and early carotid atherosclerosis in patients with type 2 diabetes.
376	21748474	To investigate the influence of atrovastatin treatment on carotid intima-media thickness (CIMT) and serum levels of novel adipokines, like apelin, visfatin (nampt), and ghrelin, in patients with type 2 diabetes mellitus (T2DM). 87 statin-free patients (50 males) with T2DM, aged 55-70, but without carotid atherosclerotic plaques were initially enrolled.
377	21748474	Anthropometric parameters, blood pressure, glycemic and lipid profile, high-sensitivity CRP (hsCRP), insulin resistance (HOMA-IR), apelin, visfatin and ghrelin were measured at baseline and after 12 months.
378	21748474	Atorvastatin treatment significantly improved lipid profile across with increased apelin (from 0.307 ± 0.130 pg/ml to 1.537 ± 0.427 pg/ml; P < 0.001) and suppressed visfatin (from 21.54 ± 10.14 ng/ml to 15.13 ± 7.61 ng/ml; P = 0.002) serum levels in our diabetic patients.
379	21748474	Standard multiple regression analysis showed that the atorvastatin-induced increment in apelin was independently associated with changes in total cholesterol (β = -0.510, P = 0.030) and LDL-cholesterol (β = -0.590, P < 0.001) (R (2) = 0.449, P = 0.014), while the reduction of visfatin concentration was independently associated with the change in hsCRP (β = 0.589, P < 0.001; R (2) = 0.256, P = 0.006), after adjustment for age, sex and BMI.
380	21748474	Among participants, high-dose (80 mg) rather than low-dose (10 mg) of atorvastatin treatment yielded greater (P < 0.05) changes in apelin, visfatin and CIMT levels despite the final equivalent levels of LDL.
381	21748474	Atorvastatin administration increased apelin and decreased visfatin serum levels significantly, without change of CIMT, in patients with T2DM.
382	21748474	Effects of atorvastatin on apelin, visfatin (nampt), ghrelin and early carotid atherosclerosis in patients with type 2 diabetes.
383	21748474	To investigate the influence of atrovastatin treatment on carotid intima-media thickness (CIMT) and serum levels of novel adipokines, like apelin, visfatin (nampt), and ghrelin, in patients with type 2 diabetes mellitus (T2DM). 87 statin-free patients (50 males) with T2DM, aged 55-70, but without carotid atherosclerotic plaques were initially enrolled.
384	21748474	Anthropometric parameters, blood pressure, glycemic and lipid profile, high-sensitivity CRP (hsCRP), insulin resistance (HOMA-IR), apelin, visfatin and ghrelin were measured at baseline and after 12 months.
385	21748474	Atorvastatin treatment significantly improved lipid profile across with increased apelin (from 0.307 ± 0.130 pg/ml to 1.537 ± 0.427 pg/ml; P < 0.001) and suppressed visfatin (from 21.54 ± 10.14 ng/ml to 15.13 ± 7.61 ng/ml; P = 0.002) serum levels in our diabetic patients.
386	21748474	Standard multiple regression analysis showed that the atorvastatin-induced increment in apelin was independently associated with changes in total cholesterol (β = -0.510, P = 0.030) and LDL-cholesterol (β = -0.590, P < 0.001) (R (2) = 0.449, P = 0.014), while the reduction of visfatin concentration was independently associated with the change in hsCRP (β = 0.589, P < 0.001; R (2) = 0.256, P = 0.006), after adjustment for age, sex and BMI.
387	21748474	Among participants, high-dose (80 mg) rather than low-dose (10 mg) of atorvastatin treatment yielded greater (P < 0.05) changes in apelin, visfatin and CIMT levels despite the final equivalent levels of LDL.
388	21748474	Atorvastatin administration increased apelin and decreased visfatin serum levels significantly, without change of CIMT, in patients with T2DM.
389	21748474	Effects of atorvastatin on apelin, visfatin (nampt), ghrelin and early carotid atherosclerosis in patients with type 2 diabetes.
390	21748474	To investigate the influence of atrovastatin treatment on carotid intima-media thickness (CIMT) and serum levels of novel adipokines, like apelin, visfatin (nampt), and ghrelin, in patients with type 2 diabetes mellitus (T2DM). 87 statin-free patients (50 males) with T2DM, aged 55-70, but without carotid atherosclerotic plaques were initially enrolled.
391	21748474	Anthropometric parameters, blood pressure, glycemic and lipid profile, high-sensitivity CRP (hsCRP), insulin resistance (HOMA-IR), apelin, visfatin and ghrelin were measured at baseline and after 12 months.
392	21748474	Atorvastatin treatment significantly improved lipid profile across with increased apelin (from 0.307 ± 0.130 pg/ml to 1.537 ± 0.427 pg/ml; P < 0.001) and suppressed visfatin (from 21.54 ± 10.14 ng/ml to 15.13 ± 7.61 ng/ml; P = 0.002) serum levels in our diabetic patients.
393	21748474	Standard multiple regression analysis showed that the atorvastatin-induced increment in apelin was independently associated with changes in total cholesterol (β = -0.510, P = 0.030) and LDL-cholesterol (β = -0.590, P < 0.001) (R (2) = 0.449, P = 0.014), while the reduction of visfatin concentration was independently associated with the change in hsCRP (β = 0.589, P < 0.001; R (2) = 0.256, P = 0.006), after adjustment for age, sex and BMI.
394	21748474	Among participants, high-dose (80 mg) rather than low-dose (10 mg) of atorvastatin treatment yielded greater (P < 0.05) changes in apelin, visfatin and CIMT levels despite the final equivalent levels of LDL.
395	21748474	Atorvastatin administration increased apelin and decreased visfatin serum levels significantly, without change of CIMT, in patients with T2DM.
396	21748474	Effects of atorvastatin on apelin, visfatin (nampt), ghrelin and early carotid atherosclerosis in patients with type 2 diabetes.
397	21748474	To investigate the influence of atrovastatin treatment on carotid intima-media thickness (CIMT) and serum levels of novel adipokines, like apelin, visfatin (nampt), and ghrelin, in patients with type 2 diabetes mellitus (T2DM). 87 statin-free patients (50 males) with T2DM, aged 55-70, but without carotid atherosclerotic plaques were initially enrolled.
398	21748474	Anthropometric parameters, blood pressure, glycemic and lipid profile, high-sensitivity CRP (hsCRP), insulin resistance (HOMA-IR), apelin, visfatin and ghrelin were measured at baseline and after 12 months.
399	21748474	Atorvastatin treatment significantly improved lipid profile across with increased apelin (from 0.307 ± 0.130 pg/ml to 1.537 ± 0.427 pg/ml; P < 0.001) and suppressed visfatin (from 21.54 ± 10.14 ng/ml to 15.13 ± 7.61 ng/ml; P = 0.002) serum levels in our diabetic patients.
400	21748474	Standard multiple regression analysis showed that the atorvastatin-induced increment in apelin was independently associated with changes in total cholesterol (β = -0.510, P = 0.030) and LDL-cholesterol (β = -0.590, P < 0.001) (R (2) = 0.449, P = 0.014), while the reduction of visfatin concentration was independently associated with the change in hsCRP (β = 0.589, P < 0.001; R (2) = 0.256, P = 0.006), after adjustment for age, sex and BMI.
401	21748474	Among participants, high-dose (80 mg) rather than low-dose (10 mg) of atorvastatin treatment yielded greater (P < 0.05) changes in apelin, visfatin and CIMT levels despite the final equivalent levels of LDL.
402	21748474	Atorvastatin administration increased apelin and decreased visfatin serum levels significantly, without change of CIMT, in patients with T2DM.
403	21808634	Altered gut microbiota and endocannabinoid system tone in obese and diabetic leptin-resistant mice: impact on apelin regulation in adipose tissue.
404	21808634	We identified the roles of the eCB and LPS in the regulation of apelinergic system tone (apelin and APJ mRNA expression) in genetic obese and diabetic mice.
405	21808634	By using in vivo and in vitro models, we have demonstrated that both the eCB and low-grade inflammation differentially regulate apelin and APJ mRNA expression in adipose tissue.
406	21808634	Altered gut microbiota and endocannabinoid system tone in obese and diabetic leptin-resistant mice: impact on apelin regulation in adipose tissue.
407	21808634	We identified the roles of the eCB and LPS in the regulation of apelinergic system tone (apelin and APJ mRNA expression) in genetic obese and diabetic mice.
408	21808634	By using in vivo and in vitro models, we have demonstrated that both the eCB and low-grade inflammation differentially regulate apelin and APJ mRNA expression in adipose tissue.
409	21808634	Altered gut microbiota and endocannabinoid system tone in obese and diabetic leptin-resistant mice: impact on apelin regulation in adipose tissue.
410	21808634	We identified the roles of the eCB and LPS in the regulation of apelinergic system tone (apelin and APJ mRNA expression) in genetic obese and diabetic mice.
411	21808634	By using in vivo and in vitro models, we have demonstrated that both the eCB and low-grade inflammation differentially regulate apelin and APJ mRNA expression in adipose tissue.
412	22125210	Apelin is a recently discovered biologically active peptide present in several isoforms that are agonists for orphan receptor APJ.
413	22125210	Apelin and APJ receptor were found in the central nervous system and in different peripheral tissues.
414	22125210	Apelin interacts with other compounds regulating blood pressure; for instance with angiotensin II, vasopressin, and with the sympathetic nervous system.
415	22125210	It appears that apelin may play essential role in pathogenesis of insulin-resistant obesity.
416	22125210	Apelin is a recently discovered biologically active peptide present in several isoforms that are agonists for orphan receptor APJ.
417	22125210	Apelin and APJ receptor were found in the central nervous system and in different peripheral tissues.
418	22125210	Apelin interacts with other compounds regulating blood pressure; for instance with angiotensin II, vasopressin, and with the sympathetic nervous system.
419	22125210	It appears that apelin may play essential role in pathogenesis of insulin-resistant obesity.
420	22125210	Apelin is a recently discovered biologically active peptide present in several isoforms that are agonists for orphan receptor APJ.
421	22125210	Apelin and APJ receptor were found in the central nervous system and in different peripheral tissues.
422	22125210	Apelin interacts with other compounds regulating blood pressure; for instance with angiotensin II, vasopressin, and with the sympathetic nervous system.
423	22125210	It appears that apelin may play essential role in pathogenesis of insulin-resistant obesity.
424	22125210	Apelin is a recently discovered biologically active peptide present in several isoforms that are agonists for orphan receptor APJ.
425	22125210	Apelin and APJ receptor were found in the central nervous system and in different peripheral tissues.
426	22125210	Apelin interacts with other compounds regulating blood pressure; for instance with angiotensin II, vasopressin, and with the sympathetic nervous system.
427	22125210	It appears that apelin may play essential role in pathogenesis of insulin-resistant obesity.
428	22138721	The aim of this study was to investigate (i) the cholecystokinin, somatostatin and apelin mRNA levels, (ii) the changes in levels and localization of these peptides, (iii) relation between these peptides, (iv) antiapoptotic effects and (v) antioxidant effects of ghrelin.
429	22138721	Cholecystokinin mRNA and peptide, somatostatin mRNA, release to duodenal lumen of apelin peptide and apelin mRNA signals decreased in ghrelin-treated diabetic rats compared to the diabetic group.
430	22138721	There was no statistically significant difference among the four groups for somatostatin and apelin peptides.
431	22138721	Caspase-3 signals were not observed only in diabetic group treated with ghrelin.
432	22138721	Caspase-8 signals were increased while PCNA signals were decreased in diabetic group given ghrelin compared to diabetic group.
433	22138721	Small intestine CAT, SOD, GP(x) and GST activities and GSH levels were decreased and LPO, PC levels were increased in diabetic rats.
434	22138721	The aim of this study was to investigate (i) the cholecystokinin, somatostatin and apelin mRNA levels, (ii) the changes in levels and localization of these peptides, (iii) relation between these peptides, (iv) antiapoptotic effects and (v) antioxidant effects of ghrelin.
435	22138721	Cholecystokinin mRNA and peptide, somatostatin mRNA, release to duodenal lumen of apelin peptide and apelin mRNA signals decreased in ghrelin-treated diabetic rats compared to the diabetic group.
436	22138721	There was no statistically significant difference among the four groups for somatostatin and apelin peptides.
437	22138721	Caspase-3 signals were not observed only in diabetic group treated with ghrelin.
438	22138721	Caspase-8 signals were increased while PCNA signals were decreased in diabetic group given ghrelin compared to diabetic group.
439	22138721	Small intestine CAT, SOD, GP(x) and GST activities and GSH levels were decreased and LPO, PC levels were increased in diabetic rats.
440	22138721	The aim of this study was to investigate (i) the cholecystokinin, somatostatin and apelin mRNA levels, (ii) the changes in levels and localization of these peptides, (iii) relation between these peptides, (iv) antiapoptotic effects and (v) antioxidant effects of ghrelin.
441	22138721	Cholecystokinin mRNA and peptide, somatostatin mRNA, release to duodenal lumen of apelin peptide and apelin mRNA signals decreased in ghrelin-treated diabetic rats compared to the diabetic group.
442	22138721	There was no statistically significant difference among the four groups for somatostatin and apelin peptides.
443	22138721	Caspase-3 signals were not observed only in diabetic group treated with ghrelin.
444	22138721	Caspase-8 signals were increased while PCNA signals were decreased in diabetic group given ghrelin compared to diabetic group.
445	22138721	Small intestine CAT, SOD, GP(x) and GST activities and GSH levels were decreased and LPO, PC levels were increased in diabetic rats.
446	22203468	We did not find a correlation between maternal serum apelin-36 and nesfatin-1 levels, maternal age, BMI, fasting glucose, fasting insulin, and HOMA-IR.
447	22203468	Also cord blood apelin-36 and nesfatin-1 levels did not correlate with the maternal age, BMI, HOMA-IR, cord blood glucose, and cord blood insulin levels.
448	22203468	We did not find a correlation between maternal serum apelin-36 and nesfatin-1 levels, maternal age, BMI, fasting glucose, fasting insulin, and HOMA-IR.
449	22203468	Also cord blood apelin-36 and nesfatin-1 levels did not correlate with the maternal age, BMI, HOMA-IR, cord blood glucose, and cord blood insulin levels.
450	22210322	Apelin treatment increases complete Fatty Acid oxidation, mitochondrial oxidative capacity, and biogenesis in muscle of insulin-resistant mice.
451	22210322	Both acute and chronic apelin treatment have been shown to improve insulin sensitivity in mice.
452	22210322	However, the effects of apelin on fatty acid oxidation (FAO) during obesity-related insulin resistance have not yet been addressed.
453	22210322	High-fat diet (HFD)-induced obese and insulin-resistant mice treated by an apelin injection (0.1 μmol/kg/day i.p.) during 4 weeks had decreased fat mass, glycemia, and plasma levels of triglycerides and were protected from hyperinsulinemia compared with HFD PBS-treated mice.
454	22210322	The action of apelin was AMP-activated protein kinase (AMPK) dependent since all the effects studied were abrogated in HFD apelin-treated mice with muscle-specific inactive AMPK.
455	22210322	Finally, the apelin-stimulated improvement of oxidative capacity led to decreased levels of acylcarnitines and enhanced insulin-stimulated glucose uptake in soleus.
456	22210322	Thus, by promoting complete lipid use in muscle of insulin-resistant mice through mitochondrial biogenesis and tighter matching between FAO and the tricarboxylic acid cycle, apelin treatment could contribute to insulin sensitivity improvement.
457	22210322	Apelin treatment increases complete Fatty Acid oxidation, mitochondrial oxidative capacity, and biogenesis in muscle of insulin-resistant mice.
458	22210322	Both acute and chronic apelin treatment have been shown to improve insulin sensitivity in mice.
459	22210322	However, the effects of apelin on fatty acid oxidation (FAO) during obesity-related insulin resistance have not yet been addressed.
460	22210322	High-fat diet (HFD)-induced obese and insulin-resistant mice treated by an apelin injection (0.1 μmol/kg/day i.p.) during 4 weeks had decreased fat mass, glycemia, and plasma levels of triglycerides and were protected from hyperinsulinemia compared with HFD PBS-treated mice.
461	22210322	The action of apelin was AMP-activated protein kinase (AMPK) dependent since all the effects studied were abrogated in HFD apelin-treated mice with muscle-specific inactive AMPK.
462	22210322	Finally, the apelin-stimulated improvement of oxidative capacity led to decreased levels of acylcarnitines and enhanced insulin-stimulated glucose uptake in soleus.
463	22210322	Thus, by promoting complete lipid use in muscle of insulin-resistant mice through mitochondrial biogenesis and tighter matching between FAO and the tricarboxylic acid cycle, apelin treatment could contribute to insulin sensitivity improvement.
464	22210322	Apelin treatment increases complete Fatty Acid oxidation, mitochondrial oxidative capacity, and biogenesis in muscle of insulin-resistant mice.
465	22210322	Both acute and chronic apelin treatment have been shown to improve insulin sensitivity in mice.
466	22210322	However, the effects of apelin on fatty acid oxidation (FAO) during obesity-related insulin resistance have not yet been addressed.
467	22210322	High-fat diet (HFD)-induced obese and insulin-resistant mice treated by an apelin injection (0.1 μmol/kg/day i.p.) during 4 weeks had decreased fat mass, glycemia, and plasma levels of triglycerides and were protected from hyperinsulinemia compared with HFD PBS-treated mice.
468	22210322	The action of apelin was AMP-activated protein kinase (AMPK) dependent since all the effects studied were abrogated in HFD apelin-treated mice with muscle-specific inactive AMPK.
469	22210322	Finally, the apelin-stimulated improvement of oxidative capacity led to decreased levels of acylcarnitines and enhanced insulin-stimulated glucose uptake in soleus.
470	22210322	Thus, by promoting complete lipid use in muscle of insulin-resistant mice through mitochondrial biogenesis and tighter matching between FAO and the tricarboxylic acid cycle, apelin treatment could contribute to insulin sensitivity improvement.
471	22210322	Apelin treatment increases complete Fatty Acid oxidation, mitochondrial oxidative capacity, and biogenesis in muscle of insulin-resistant mice.
472	22210322	Both acute and chronic apelin treatment have been shown to improve insulin sensitivity in mice.
473	22210322	However, the effects of apelin on fatty acid oxidation (FAO) during obesity-related insulin resistance have not yet been addressed.
474	22210322	High-fat diet (HFD)-induced obese and insulin-resistant mice treated by an apelin injection (0.1 μmol/kg/day i.p.) during 4 weeks had decreased fat mass, glycemia, and plasma levels of triglycerides and were protected from hyperinsulinemia compared with HFD PBS-treated mice.
475	22210322	The action of apelin was AMP-activated protein kinase (AMPK) dependent since all the effects studied were abrogated in HFD apelin-treated mice with muscle-specific inactive AMPK.
476	22210322	Finally, the apelin-stimulated improvement of oxidative capacity led to decreased levels of acylcarnitines and enhanced insulin-stimulated glucose uptake in soleus.
477	22210322	Thus, by promoting complete lipid use in muscle of insulin-resistant mice through mitochondrial biogenesis and tighter matching between FAO and the tricarboxylic acid cycle, apelin treatment could contribute to insulin sensitivity improvement.
478	22210322	Apelin treatment increases complete Fatty Acid oxidation, mitochondrial oxidative capacity, and biogenesis in muscle of insulin-resistant mice.
479	22210322	Both acute and chronic apelin treatment have been shown to improve insulin sensitivity in mice.
480	22210322	However, the effects of apelin on fatty acid oxidation (FAO) during obesity-related insulin resistance have not yet been addressed.
481	22210322	High-fat diet (HFD)-induced obese and insulin-resistant mice treated by an apelin injection (0.1 μmol/kg/day i.p.) during 4 weeks had decreased fat mass, glycemia, and plasma levels of triglycerides and were protected from hyperinsulinemia compared with HFD PBS-treated mice.
482	22210322	The action of apelin was AMP-activated protein kinase (AMPK) dependent since all the effects studied were abrogated in HFD apelin-treated mice with muscle-specific inactive AMPK.
483	22210322	Finally, the apelin-stimulated improvement of oxidative capacity led to decreased levels of acylcarnitines and enhanced insulin-stimulated glucose uptake in soleus.
484	22210322	Thus, by promoting complete lipid use in muscle of insulin-resistant mice through mitochondrial biogenesis and tighter matching between FAO and the tricarboxylic acid cycle, apelin treatment could contribute to insulin sensitivity improvement.
485	22210322	Apelin treatment increases complete Fatty Acid oxidation, mitochondrial oxidative capacity, and biogenesis in muscle of insulin-resistant mice.
486	22210322	Both acute and chronic apelin treatment have been shown to improve insulin sensitivity in mice.
487	22210322	However, the effects of apelin on fatty acid oxidation (FAO) during obesity-related insulin resistance have not yet been addressed.
488	22210322	High-fat diet (HFD)-induced obese and insulin-resistant mice treated by an apelin injection (0.1 μmol/kg/day i.p.) during 4 weeks had decreased fat mass, glycemia, and plasma levels of triglycerides and were protected from hyperinsulinemia compared with HFD PBS-treated mice.
489	22210322	The action of apelin was AMP-activated protein kinase (AMPK) dependent since all the effects studied were abrogated in HFD apelin-treated mice with muscle-specific inactive AMPK.
490	22210322	Finally, the apelin-stimulated improvement of oxidative capacity led to decreased levels of acylcarnitines and enhanced insulin-stimulated glucose uptake in soleus.
491	22210322	Thus, by promoting complete lipid use in muscle of insulin-resistant mice through mitochondrial biogenesis and tighter matching between FAO and the tricarboxylic acid cycle, apelin treatment could contribute to insulin sensitivity improvement.
492	22210322	Apelin treatment increases complete Fatty Acid oxidation, mitochondrial oxidative capacity, and biogenesis in muscle of insulin-resistant mice.
493	22210322	Both acute and chronic apelin treatment have been shown to improve insulin sensitivity in mice.
494	22210322	However, the effects of apelin on fatty acid oxidation (FAO) during obesity-related insulin resistance have not yet been addressed.
495	22210322	High-fat diet (HFD)-induced obese and insulin-resistant mice treated by an apelin injection (0.1 μmol/kg/day i.p.) during 4 weeks had decreased fat mass, glycemia, and plasma levels of triglycerides and were protected from hyperinsulinemia compared with HFD PBS-treated mice.
496	22210322	The action of apelin was AMP-activated protein kinase (AMPK) dependent since all the effects studied were abrogated in HFD apelin-treated mice with muscle-specific inactive AMPK.
497	22210322	Finally, the apelin-stimulated improvement of oxidative capacity led to decreased levels of acylcarnitines and enhanced insulin-stimulated glucose uptake in soleus.
498	22210322	Thus, by promoting complete lipid use in muscle of insulin-resistant mice through mitochondrial biogenesis and tighter matching between FAO and the tricarboxylic acid cycle, apelin treatment could contribute to insulin sensitivity improvement.
499	22534708	The impact of aerobic exercise training on novel adipokines, apelin and ghrelin, in patients with type 2 diabetes.
500	22991412	In this review, we consider the published evidence for the role of individual adipokines on the function, proliferation, death and failure of β-cells, focusing on those reported to have the most significant effects (leptin, adiponectin, tumour necrosis factor α, resistin, visfatin, dipeptidyl peptidase IV and apelin).
501	23348852	In addition to the well known function of storage and release on non esterified fatty acids (NEFAs), the adipocytes synthesize and secrete circulating hormones (called adipokines such as leptin, adiponectin and apelin) which are acting as signaling molecules and which are mediators/modulators of the inflammatory processes.
502	23378608	Fatty acids present in the HFD induced hyperpermeability of endothelial cells, causing adipocyte differentiation, whereas apelin promoted vascular stabilization.
503	23422767	Differences in plasma apelin and visfatin levels between patients with type 1 diabetes mellitus and healthy subjects and response after acute hyperglycemia and insulin administration.
504	23430572	ASP and C3 in the media were evaluated in relation to changes in adipocyte lipid metabolism (cellular triglyceride stores).
505	23430572	Leptin, adiponectin, IL-10, LPS and TNF-α increased ASP production (151%, 153%, 190%, 318%, 134%, P<0.05, respectively,).
506	23430572	C5a and RANTES (Regulated and normal T cell expressed and secreted) decreased ASP production ( - 34%, - 47%, P<0.05), which was also associated with a decrease in the precursor protein C3 ( - 39% to - 51%, P<0.01), while keratinocyte chemoattractant (KC; murine IL-8 ortholog) had no effect on ASP and C3 secretion.
507	23430572	By contrast, apelin, omentin and visfatin also decreased ASP ( - 27%, - 49%, - 22%, P<0.05), but without changes in precursor protein C3 secretion.
508	23566555	Regulation of oxidative stress and somatostatin, cholecystokinin, apelin gene expressions by ghrelin in stomach of newborn diabetic rats.
509	23566555	The gene expressions of: somatostatin, cholecystokinin, apelin and the altered active caspase-3, active caspase-8, proliferating cell nuclear antigen, were investigated in the pyloric region of the stomach and antioxidant parameters were measured in all the stomach.
510	23566555	Exogenous ghrelin caused an increased activities of stomach catalase, superoxide dismutase, glutathione reductase and glutathione peroxidase in diabetic rats.
511	23566555	Numbers of somatostatin, cholecystokinin and proliferating cell nuclear antigen immunoreactive cells decreased in the diabetic+ghrelin group compared to the diabetic group.
512	23566555	Apelin mRNA expressions were remarkably less in the diabetic+ghrelin rats than in diabetic rats.
513	23566555	Regulation of oxidative stress and somatostatin, cholecystokinin, apelin gene expressions by ghrelin in stomach of newborn diabetic rats.
514	23566555	The gene expressions of: somatostatin, cholecystokinin, apelin and the altered active caspase-3, active caspase-8, proliferating cell nuclear antigen, were investigated in the pyloric region of the stomach and antioxidant parameters were measured in all the stomach.
515	23566555	Exogenous ghrelin caused an increased activities of stomach catalase, superoxide dismutase, glutathione reductase and glutathione peroxidase in diabetic rats.
516	23566555	Numbers of somatostatin, cholecystokinin and proliferating cell nuclear antigen immunoreactive cells decreased in the diabetic+ghrelin group compared to the diabetic group.
517	23566555	Apelin mRNA expressions were remarkably less in the diabetic+ghrelin rats than in diabetic rats.
518	23566555	Regulation of oxidative stress and somatostatin, cholecystokinin, apelin gene expressions by ghrelin in stomach of newborn diabetic rats.
519	23566555	The gene expressions of: somatostatin, cholecystokinin, apelin and the altered active caspase-3, active caspase-8, proliferating cell nuclear antigen, were investigated in the pyloric region of the stomach and antioxidant parameters were measured in all the stomach.
520	23566555	Exogenous ghrelin caused an increased activities of stomach catalase, superoxide dismutase, glutathione reductase and glutathione peroxidase in diabetic rats.
521	23566555	Numbers of somatostatin, cholecystokinin and proliferating cell nuclear antigen immunoreactive cells decreased in the diabetic+ghrelin group compared to the diabetic group.
522	23566555	Apelin mRNA expressions were remarkably less in the diabetic+ghrelin rats than in diabetic rats.
523	23577111	Apelin receptor (APLNR) and the endogenous ligand of APLNR, apelin, induce the sprouting of endothelial cells in an autocrine or paracrine manner, which may be one of the mechanisms of DN.
524	23577111	Therefore, we observed apelin/APLNR expression in kidneys from patients with type 2 diabetes as well as the correlation between albuminuria and serum apelin in patients with type 2 diabetes.
525	23577111	The results showed that serum apelin was significantly higher in the patients with type 2 diabetes compared to healthy people (p<0.05, Fig. 1B) and that urinary albumin was positively correlated with serum apelin (R = 0.78, p<0.05).
526	23577111	Apelin also promoted the permeability of glomerular endothelial cells (p<0.05) and upregulated the expression of VEGFR2 and Tie2 in glomerular endothelial cells (p<0.05).
527	23577111	These results indicated that upregulated apelin in type 2 diabetes, which may be attributed to increased fat mass, promotes angiogenesis in glomeruli to form abnormal vessels and that enhanced apelin increases permeability via upregulating the expression of VEGFR2 and Tie2 in glomerular endothelial cells.
528	23577111	Apelin receptor (APLNR) and the endogenous ligand of APLNR, apelin, induce the sprouting of endothelial cells in an autocrine or paracrine manner, which may be one of the mechanisms of DN.
529	23577111	Therefore, we observed apelin/APLNR expression in kidneys from patients with type 2 diabetes as well as the correlation between albuminuria and serum apelin in patients with type 2 diabetes.
530	23577111	The results showed that serum apelin was significantly higher in the patients with type 2 diabetes compared to healthy people (p<0.05, Fig. 1B) and that urinary albumin was positively correlated with serum apelin (R = 0.78, p<0.05).
531	23577111	Apelin also promoted the permeability of glomerular endothelial cells (p<0.05) and upregulated the expression of VEGFR2 and Tie2 in glomerular endothelial cells (p<0.05).
532	23577111	These results indicated that upregulated apelin in type 2 diabetes, which may be attributed to increased fat mass, promotes angiogenesis in glomeruli to form abnormal vessels and that enhanced apelin increases permeability via upregulating the expression of VEGFR2 and Tie2 in glomerular endothelial cells.
533	23577111	Apelin receptor (APLNR) and the endogenous ligand of APLNR, apelin, induce the sprouting of endothelial cells in an autocrine or paracrine manner, which may be one of the mechanisms of DN.
534	23577111	Therefore, we observed apelin/APLNR expression in kidneys from patients with type 2 diabetes as well as the correlation between albuminuria and serum apelin in patients with type 2 diabetes.
535	23577111	The results showed that serum apelin was significantly higher in the patients with type 2 diabetes compared to healthy people (p<0.05, Fig. 1B) and that urinary albumin was positively correlated with serum apelin (R = 0.78, p<0.05).
536	23577111	Apelin also promoted the permeability of glomerular endothelial cells (p<0.05) and upregulated the expression of VEGFR2 and Tie2 in glomerular endothelial cells (p<0.05).
537	23577111	These results indicated that upregulated apelin in type 2 diabetes, which may be attributed to increased fat mass, promotes angiogenesis in glomeruli to form abnormal vessels and that enhanced apelin increases permeability via upregulating the expression of VEGFR2 and Tie2 in glomerular endothelial cells.
538	23577111	Apelin receptor (APLNR) and the endogenous ligand of APLNR, apelin, induce the sprouting of endothelial cells in an autocrine or paracrine manner, which may be one of the mechanisms of DN.
539	23577111	Therefore, we observed apelin/APLNR expression in kidneys from patients with type 2 diabetes as well as the correlation between albuminuria and serum apelin in patients with type 2 diabetes.
540	23577111	The results showed that serum apelin was significantly higher in the patients with type 2 diabetes compared to healthy people (p<0.05, Fig. 1B) and that urinary albumin was positively correlated with serum apelin (R = 0.78, p<0.05).
541	23577111	Apelin also promoted the permeability of glomerular endothelial cells (p<0.05) and upregulated the expression of VEGFR2 and Tie2 in glomerular endothelial cells (p<0.05).
542	23577111	These results indicated that upregulated apelin in type 2 diabetes, which may be attributed to increased fat mass, promotes angiogenesis in glomeruli to form abnormal vessels and that enhanced apelin increases permeability via upregulating the expression of VEGFR2 and Tie2 in glomerular endothelial cells.
543	23577111	Apelin receptor (APLNR) and the endogenous ligand of APLNR, apelin, induce the sprouting of endothelial cells in an autocrine or paracrine manner, which may be one of the mechanisms of DN.
544	23577111	Therefore, we observed apelin/APLNR expression in kidneys from patients with type 2 diabetes as well as the correlation between albuminuria and serum apelin in patients with type 2 diabetes.
545	23577111	The results showed that serum apelin was significantly higher in the patients with type 2 diabetes compared to healthy people (p<0.05, Fig. 1B) and that urinary albumin was positively correlated with serum apelin (R = 0.78, p<0.05).
546	23577111	Apelin also promoted the permeability of glomerular endothelial cells (p<0.05) and upregulated the expression of VEGFR2 and Tie2 in glomerular endothelial cells (p<0.05).
547	23577111	These results indicated that upregulated apelin in type 2 diabetes, which may be attributed to increased fat mass, promotes angiogenesis in glomeruli to form abnormal vessels and that enhanced apelin increases permeability via upregulating the expression of VEGFR2 and Tie2 in glomerular endothelial cells.
548	23634778	Leptin, resistin and visfatin: the missing link between endocrine metabolic disorders and immunity.
549	23634778	Additionally, adipose tissue-secreted hormones such as leptin, visfatin, resistin, apelin, omentin, sex steroids, and various growth factors are now regarded as a functional part of the endocrine system.
550	23634778	In obese and diabetic conditions, leptin deficiency inhibited the Jak/Stat3/PI3K and insulin pathways.
551	23747606	It has been proposed that the apelinergic system (apelin and its receptor APJ) may be a promising therapeutic target in obesity-associated insulin resistance syndrome.
552	23747606	To unravel specific tissular dysfunctions of this system under obesity and insulin-resistance conditions, we measured the apelinemia and gene-expression level of both apelin (APL) and APJ in 12-selected tissues of insulin-resistant obese female mice fed with a high fat (HF) diet.
553	23747606	In obese and insulin-resistant HF female mice, plasma apelin concentration after fasting was not modified but, the gene-expression level of the APL/APJ system was augmented in the white adipose tissue (WAT) and reduced in the brown adipose tissue (BAT), the liver and in kidneys.
554	23747606	It has been proposed that the apelinergic system (apelin and its receptor APJ) may be a promising therapeutic target in obesity-associated insulin resistance syndrome.
555	23747606	To unravel specific tissular dysfunctions of this system under obesity and insulin-resistance conditions, we measured the apelinemia and gene-expression level of both apelin (APL) and APJ in 12-selected tissues of insulin-resistant obese female mice fed with a high fat (HF) diet.
556	23747606	In obese and insulin-resistant HF female mice, plasma apelin concentration after fasting was not modified but, the gene-expression level of the APL/APJ system was augmented in the white adipose tissue (WAT) and reduced in the brown adipose tissue (BAT), the liver and in kidneys.
557	23747606	It has been proposed that the apelinergic system (apelin and its receptor APJ) may be a promising therapeutic target in obesity-associated insulin resistance syndrome.
558	23747606	To unravel specific tissular dysfunctions of this system under obesity and insulin-resistance conditions, we measured the apelinemia and gene-expression level of both apelin (APL) and APJ in 12-selected tissues of insulin-resistant obese female mice fed with a high fat (HF) diet.
559	23747606	In obese and insulin-resistant HF female mice, plasma apelin concentration after fasting was not modified but, the gene-expression level of the APL/APJ system was augmented in the white adipose tissue (WAT) and reduced in the brown adipose tissue (BAT), the liver and in kidneys.
560	23772224	These adipokines including leptin, visfatin, resistin, apelin, vaspin, and retinol binding protein-4 can regulate inflammatory responses and contribute to the pathogenesis of diabetes.
561	23772224	These effects are mediated by key inflammatory signaling molecules including activated serine kinases such as c-Jun N-terminal kinase and serine kinases inhibitor κB kinase and insulin signaling molecules including insulin receptor substrates, protein kinase B (PKB, also known as Akt), and nuclear factor kappa B.