Neuropeptide Y and neuropeptide Y receptor subtypes in brain and peripheral tissues

Dumont, Yvan; Martel, Jean-Claude; Fournier, Alain; St‐Pierre, Serge; Quirion, Rémi

doi:10.1016/0301-0082(92)90038-g

Cited by 356 publications

(199 citation statements)

References 490 publications

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“…This results from Y2R-mediated inhibition of parasympathetic neurotransmission. [36][37][38] The functional polymorphism reflected by the Y2R association is likely in LD with 585T4C. 585T4C is silent and not within any putative exonic splicing enhancer site.…”

Section: Discussionmentioning

confidence: 99%

Common neuropeptide Y2 receptor gene variant is protective against obesity among Swedish men

et al. 2005

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Background: Gut hormones and their receptors are considered important in the control of feeding behavior. The gut hormone peptide-YY (PYY) has anorexic effects via the inhibitory neuropeptide Y2 receptor (Y2R) highly expressed in orexigenic NPY/ AGRP neurons within the arcuate nucleus, a major integrator of appetite control in the hypothalamus. Design: Genetic case-control association study of single nucleotide polymorphisms (SNPs) in Y2R and PYY. Subjects: Swedish Caucasians comprising 148 lean, 129 overweight/obese and 226 morbidly obese men. Measurements: Genotypes of the common, silent and conserved SNP Y2R 585T4C and the common SNP PYY Arg72Thr, as well as various obesity-related clinical parameters. Results: Obese men had a lower allele and homozygosity frequency of the common allele 585T4C:T which was particularly evident comparing morbidly obese with lean men (P ¼ 0.002), and analyzing dependence between continuous body mass index (BMI) and genotype (P ¼ 0.002). In agreement, systolic blood pressure tended to be lower in those homozygous for allele T, which was not explained by the BMI -genotype dependence. We found no association to obesity for the PYY Arg72Thr polymorphism, which is located nearby the essential carboxy terminal. Conclusion: A common and conserved variant of the PYY and NPY receptor Y2R is less prevalent among obese compared to among lean Swedish men. This suggests that the common Y2R variant is protective against obesity. Our findings further implicate Y2R in food intake regulation.

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Section: Discussionmentioning

confidence: 99%

Common neuropeptide Y2 receptor gene variant is protective against obesity among Swedish men

et al. 2005

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“…1,2 Within the hypothalamus, neuronal cell bodies in the arcuate nucleus produce NPY and send projections to various other hypothalamic nuclei, including the paraventricular nucleus (PVN) and ventromedial hypothalamus (VMH). 3 These regions of the brain are thought to regulate adiposity by affecting appetite and metabolism.…”

Section: Introductionmentioning

confidence: 99%

Role of neuropeptide Y in diet-, chemical- and genetic-induced obesity of mice

1998

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OBJECTIVE: The goal of this study was to ascertain whether neuropeptide Y (NPY) is required in mice for the development of obesity induced by a high-fat diet (HFD), chemical lesions of the hypothalamus caused by monosodium glutamate (MSG) or gold thioglucose (GTG), impaired brown adipose tissue (BAT) due to a diphtheria toxin transgene driven by the uncoupling protein 1 promoter (UCP-DTA) or the lethal yellow agouti mutation (A y ). BACKGROUND: The obesity syndrome of the leptin-de®cient (ob/ob) mouse can be partially reversed by the genetic removal of NPY. In the murine models of obesity examined in this study, the animals become obese despite increased serum leptin levels, indicating that they are resistant to the weight-limiting actions of leptin. The role of NPY in these obesity models with elevated leptin levels is unknown. EXPERIMENTAL DESIGN: Mice lacking NPY due to genetic disruption of the gene and wildtype littermates were made obese by allowing them access to a highly palatable HFD, by treatment with MSG, or GTG, or by inheriting the dominant UCP-DTA or A y alleles. Food consumption, body weight and dissectable fat pad weights were measured and compared to values obtained from non-obese littermates. RESULTS: In each model of obesity tested, NPY-de®cient mice achieved the same food intake, body weight and fat content as wildtype littermates. CONCLUSION: NPY is not necessary for the progressive development of obesity exhibited by multiple murine models with leptin resistance.

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“…The neuropeptide Y system consists of three peptide precursor genes encoding neuropeptide Y (NPY), peptide YY (PYY) and pancreatic polypeptide (PP) and at least 5 receptor genes encoding the Y 1 , Y 2 , Y 4 , Y 5 and Y 6 receptor (Tatemoto et al, 1982;Katayama-Kumoi et al, 1985;Dumont et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

Compensatory changes in [125I]-PYY binding in Y receptor knockout mice suggest the potential existence of further Y receptor(s)

et al. 2005

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Neuropeptide Y and neuropeptide Y receptor subtypes in brain and peripheral tissues

Cited by 356 publications

References 490 publications

Common neuropeptide Y2 receptor gene variant is protective against obesity among Swedish men

Common neuropeptide Y2 receptor gene variant is protective against obesity among Swedish men

Role of neuropeptide Y in diet-, chemical- and genetic-induced obesity of mice

Compensatory changes in [125I]-PYY binding in Y receptor knockout mice suggest the potential existence of further Y receptor(s)

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