Ignet

Gene Pair Information

Gene Pair: NPY, INS

Related Sentences

#	PMID	Sentence
1	21801810	Our data suggest that in 3T3-L1 adipocytes NPY inhibits insulin-stimulated glucose uptake in a GLUT4-dependent manner.
2	21801810	This study provides evidence that NPY impairs the insulin sensitivity of adipocytes and suggests that the Y1 receptor could be a potential therapeutic target for type 2 diabetes.
3	2527701	Alterations of hypothalamic neuropeptide Y, which has potent experimental effects on hypothalamo-pituitary function, may contribute to certain neuroendocrine disturbances in insulin-deficient diabetes.
4	2097094	Therefore, we examined the influence of NPY alone and together with noradrenaline (NA) on insulin release in the rat.
5	2097094	When infused alone for 30 min under basal conditions, NPY increased basal plasma insulin concentrations by 32 +/- 13 microU/ml at the highest dose level tested (68 pmol/min), as compared to +7 +/- 7 microU/ml in the controls (p less than 0.05).
6	2097094	In contrast, NPY at 17 pmol/min reduced the plasma insulin response to both glucose (by 11%; p less than 0.001) and to arginine (by 26%; p less than 0.001).
7	2097094	In isolated rat islets, both NPY (10(-6) M) and NA (10(-6) M) inhibited glucose-stimulated insulin secretion.
8	2097094	We conclude that, in the rat, NPY and NA both elevate basal plasma insulin levels and inhibit stimulated insulin secretion.
9	2097094	In combination, NPY also induces a more rapid onset of the inhibitory action of NA on glucose-induced insulin secretion.
10	1551314	Our results demonstrate that two models of insulin-deficient diabetes in the rat are associated with increased hypothalamic neuropeptide Y mRNA.
11	1437714	Untreated insulin-deficient diabetes causes hyperphagia and neuroendocrine disturbances that may be partly mediated by increased hypothalamic activity of neuropeptide Y (NPY), a potent central appetite stimulant.
12	8335171	When diabetic rats were treated for 20 h with s.c. insulin, there was decreased neuropeptide Y mRNA in the arcuate nucleus.
13	8335171	We conclude that neuropeptide Y mRNA in the arcuate nucleus is responsive to small changes in circulating insulin levels and the response occurs within 20 h.
14	8284270	Insulin-deficient diabetes and food deprivation markedly increase hypothalamic NPY and NPY mRNA levels, suggesting increased activity of NPYergic pathways in the hypothalamus, which could account for hyperphagia and neuroendocrine changes in these conditions.
15	8194661	NPY administration also resulted in a pronounced increase in the in vivo insulin-stimulated glucose uptake by adipose tissue but in a marked decrease in uptake by eight different muscle types.
16	7840315	We hypothesized that corticosteroids and insulin might serve as interacting, reciprocal signals for energy balance, acting on energy acquisition, in part through their effects on hypothalamic NPY, as well as on energy stores.
17	7840315	Glucocorticoids stimulated and insulin inhibited NPY mRNA and food intake.
18	7840315	The effects of corticosterone and insulin on food intake may be mediated, in part, through regulation of hypothalamic NPY synthesis and secretion.
19	7479313	NPY synthesis in the ARC is thought to be regulated by several factors, notably insulin, which may exert an inhibitory action.
20	7479313	The effects of NPY injected into the PVN and other sites include hyperphagia, reduced energy expenditure and enhanced weight gain, insulin secretion, and stimulation of corticotropin and corticosterone release.
21	8719940	The study aimed to assess vascular reactivity to noradrenaline with and without neuropeptide Y in diabetic rats, and to determine whether any abnormality could be attributed to insulin deficiency or to hyperglycaemia per se.
22	16177033	Conversely, insulin (10(-11) to 10(-9) M) significantly inhibited NPY expression stimulated by DEX, and the inhibitory action of insulin was abolished in the presence of TTX.
23	16177033	The GABAB agonist baclofen significantly inhibited NPY expression stimulated by DEX, and the inhibitory action of insulin was completely abolished in the presence of either the GABAA antagonist bicuculline or the GABAB antagonist CGP35348 (p-3-aminopropyl-p-diethoxymethyl phosphoric acid).
24	16177033	Experiments in vivo also demonstrated that increases in GAD65 mRNA expression in the arcuate nucleus preceded decreases in the NPY mRNA expression in a fasting-refeeding paradigm and that intracerebroventricular injection of insulin increased GAD65 mRNA expression in the arcuate nucleus in fasted rats.
25	16177033	These data suggest that insulin inhibits NPY gene expression in the arcuate nucleus through GABAergic systems.
26	16210367	In contrast, whereas insulin increased proopiomelanocortin mRNA and both insulin and glucose reduced NPY mRNA in arcuate nucleus neurons, neither prevented the fasting-induced suppression in hypophysiotropic TRH mRNA or circulating thyroid hormone levels.
27	18638024	Arcuate nucleus neuropeptide Y, but not pro-opiomelanocortin, mRNA expression was elevated by STZ treatment and all vagal manipulations; however, exogenous insulin treatment failed to prevent this, in keeping with their previously documented elevated caloric intake.
28	21574956	The age-related central resistance to leptin and insulin does not reduce their inhibitory effects on the activity of NPY and AgRP neurons.
29	21760856	We evaluated the effects of insulin-induced improved glycaemic control on leptin, adiponectin, ghrelin, neuropeptide Y (NPY) levels and patient characteristics.
30	21760856	In both genders, insulin therapy (Group A) was associated with significant (p = 0.003 to <0.001) increases in weight, body mass index and leptin levels and significant decreases in glucose, HbA(1c) and NPY levels.
31	21760856	Changes in leptin, adiponectin and NPY levels may occur after insulin-induced improved glycaemic control.
32	11179781	Insulin replacement was also associated with a return of hypothalamic AGRP mRNA (111.7+/-8.3% of controls) and NPY mRNA (125.0+/-8.9% of controls) from the elevated levels that were observed in untreated diabetic rats.