Presence of neuropeptide Y and its messenger ribonucleic acid in human islets: evidence for a possible paracrine role.

Bennet, W. M.; Wang, Z L; Jones, Philip; Wang, R M; James, R F; London, N. J. M.; Ghatei, Mohammed A.; Bloom, Stephen R.

doi:10.1210/jcem.81.6.8964837

Cited by 12 publications

(9 citation statements)

References 21 publications

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“…For static incubation experiments on human islets, pancreata were removed from brain-dead heart-beating donors after informed consent was obtained from their next of kin, and islets were prepared as described previously (Leicester Royal Infirmary, Leicester, UK) (18). Islets were cultured in RPMI 1640 medium (5.5 mmol и liter Ϫ 1 glucose, 10% FCS, 100 U/ml penicillin, and 100 g/ml streptomycin).…”

Section: Methodsmentioning

confidence: 99%

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Leptin rapidly suppresses insulin release from insulinoma cells, rat and human islets and, in vivo, in mice.

Kulkarni¹,

Wang²,

Wang³

et al. 1997

J. Clin. Invest.

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284

216

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Obesity is associated with diabetes, and leptin is known to be elevated in obesity. To investigate whether leptin has a direct effect on insulin secretion, isolated rat and human islets and cultured insulinoma cells were studied. In all cases, mouse leptin inhibited insulin secretion at concentrations within the plasma range reported in humans. Insulin mRNA expression was also suppressed in the cultured cells and rat islets. The long form of the leptin receptor (OB-Rb) mRNA was present in the islets and insulinoma cell lines. To determine the significance of these findings in vivo, normal fed mice were injected with two doses of leptin. A significant decrease in plasma insulin and associated rise in glucose concentration were observed. Fasted normal and leptin receptor-deficient db/db mice showed no response to leptin. A dose of leptin, which mimicked that found in normal mice, was administered to leptin-deficient, hyperinsulinemic ob/ob mice. This caused a marked lowering of plasma insulin concentration and a doubling of plasma glucose. Thus, leptin has a powerful acute inhibitory effect on insulin secretion. These results suggest that the action of leptin may be one mechanism by which excess adipose tissue could acutely impair carbohydrate metabolism. ( J. Clin. Invest. 1997. 100:2729-2736.)

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Section: Methodsmentioning

confidence: 99%

“…RIN 5AH (a gift from Dr. A.E. Karlsson, Hagedorn Research Laboratory, Gentofte, Denmark; passages [14][15][16][17][18][19][20][21][22][23][24] and RIN m5F cells (a gift from Dr. S.J. Ashcroft, Physiology Department, Oxford University, UK; passages 84-100) were cultured in RPMI 1640 medium with 10% FCS (21).…”

Section: Methodsmentioning

confidence: 99%

Leptin rapidly suppresses insulin release from insulinoma cells, rat and human islets and, in vivo, in mice.

Kulkarni¹,

Wang²,

Wang³

et al. 1997

J. Clin. Invest.

Self Cite

284

216

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“…Neuropeptide Y (NPY, OMIM 162640) is a 36-amino acid polypeptide that is present in the central and peripheral nervous systems, several peripheral organs, and plasma (2)(3)(4)(5). Both in vivo and in vitro studies have demonstrated that NPY inhibits glucose-stimulated insulin secretion (6,7).…”

Section: Introductionmentioning

confidence: 99%

Distribution of neuropeptide Y Leu7Pro polymorphism in patients with type 1 diabetes and diabetic nephropathy among Swedish and American populations

Ma¹,

Nordman²,

Möllsten

et al. 2007

European Journal of Endocrinology

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Objective: The distribution of Leu7Pro polymorphism in the neuropeptide Y gene shows a geographical north to south gradient of decreasing frequency, suggesting that it may be a population-specific causal variant. This polymorphism is found to be associated with diabetic nephropathy (DN) and coronary heart disease in Finnish women with type 1 diabetes (T1D). The present study aims to evaluate the susceptibility of this polymorphism to the development of DN in two different populations. Design: One sample set consists of 174 (females 98 and males 76) Swedish T1D patients with DN and 249 (females 132 and males 117) patients without DN. Another sample set includes 597 (females 356 and males 241) American T1D patients without DN and 577 (females 264 and males 313) patients with DN, who were descents of European Caucasians and were from the Genetics of Kidneys in Diabetes (GoKinD) Study. Methods: Genotyping of Leu7Pro polymorphism was performed by dynamic allele-specific hybridization. Results: The C allele frequencies of Leu7Pro polymorphism in T1D patients between Swedish and American GoKinD populations were significantly different (6.3 vs 4.0%; PZ0.006). Particularly, the C allele frequency in Swedish female T1D patients with DN was significantly higher in comparison with T1D patients without DN (10.2 vs 4.2%; PZ0.011, ORZ2.614, 95% confidence intervals: 1.249-5.467). No significant association of this polymorphism with DN was observed in Swedish male T1D patients and the patients from GoKinD. Conclusions:The present study provides further evidence that Leu7Pro polymorphism confers the susceptibility to the development of DN in Swedish female T1D patients.European Journal of Endocrinology 157 641-645

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“…We and others have shown that NPY mRNA is present in rat and human islets and clonal -cell lines (Jamal et al 1991, Wang et al 1994, Bennet et al 1996, Myrsen-Axcrona et al 1997. Both in vivo and in vitro studies have demonstrated that NPY inhibits glucose-stimulated insulin secretion (Petterson et al 1987, Skoglund et al 1991, probably acting via the Y1 receptor (Morgan et al 1998).…”

Section: Introductionmentioning

confidence: 96%

Glibenclamide but not other sulphonylureas stimulates release of neuropeptide Y from perifused rat islets and hamster insulinoma cells

Kulkarni¹,

Zl²,

Wang³

et al. 2000

Journal of Endocrinology

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We have studied the effects of first and second generation sulphonylureas on the release of insulin and neuropeptide tyrosine (NPY) from hamster insulinoma tumour (HIT-T15) cells and isolated rat islets. In the presence of 5·5 mmol/l glucose all sulphonylureas stimulated insulin release from the HIT cells (P<0·01 ANOVA, nd4) but only glibenclamide (GLIB, 10 µmol/l) stimulated the release of NPY (mean ... control 11·1 1·3 vs GLIB 28·4 4·1 fmol/h per 10 6 cells, P<0001, n=16). In isolated perifused rat islets both glibenclamide (10 µmol/l) (control 3·5 0·3 vs GLIB 6·3 0·2 fmol/min per islet, P<0·01, n=6) and tolbutamide (50 µmol/l) (control 4·7 0·1 vs TOLB 6·7 0·3 fmol/min per islet, P<0·01, n=6) enhanced glucose (8 mmol/l)-stimulated insulin release. However, only glibenclamide stimulated the release of NPY from the islets (control 3·4 0·8 vs GLIB 24·5 5 attomol/min per islet, P<0·01, n=6). Similar results were obtained in islets isolated from dexamethasonetreated rats. Glibenclamide treatment of HIT cells showed a prompt insulin release (10 min) while NPY secretion was slower (60 min), suggesting that internalization of the sulphonylurea is required to stimulate NPY release. Glibenclamide, the most common oral therapeutic agent in type 2 diabetes mellitus, is associated with release of the autocrine insulin secretion inhibitor, NPY.

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Presence of neuropeptide Y and its messenger ribonucleic acid in human islets: evidence for a possible paracrine role.

Cited by 12 publications

References 21 publications

Leptin rapidly suppresses insulin release from insulinoma cells, rat and human islets and, in vivo, in mice.

Leptin rapidly suppresses insulin release from insulinoma cells, rat and human islets and, in vivo, in mice.

Distribution of neuropeptide Y Leu7Pro polymorphism in patients with type 1 diabetes and diabetic nephropathy among Swedish and American populations

Glibenclamide but not other sulphonylureas stimulates release of neuropeptide Y from perifused rat islets and hamster insulinoma cells

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