Feeding behavior and gene expression of appetite-related neuropeptides in mice lacking for neuropeptide Y Y5 receptor subclass

Handa, Hiroshi; Niki, Takeshi; Shiiya, Tomohiro

doi:10.3748/wjg.14.6312

Cited by 33 publications

(24 citation statements)

References 23 publications

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“…In contrast, hypothalamus-specific knockout mice demonstrated increased body weight and/or adiposity only under conditions of high fat feeding, not on a normal chow diet. This early-onset obesity in germline knockouts may be due to compensatory responses to gene deletion, as has been observed in germline Y5 receptor knockout mice which exhibit exacerbated fasting-induced increases in hypothalamic expression of NPY and AgRP and exacerbated decreases in that of POMC and CART [18]. In keeping with the possibility of compensatory and obesogenic responses to gene deletion, male but not female Y1Y5 −/− mice exhibited significant reductions in energy expenditure, albeit hypothalamic arcuate nucleus (ARC) NPY mRNA levels were decreased and ARC POMC mRNA levels were unchanged in this model.…”

Section: Discussionmentioning

confidence: 85%

Y1 and Y5 Receptors Are Both Required for the Regulation of Food Intake and Energy Homeostasis in Mice

et al. 2012

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Neuropeptide Y (NPY) acting in the hypothalamus is one of the most powerful orexigenic agents known. Of the five known Y receptors, hypothalamic Y1 and Y5 have been most strongly implicated in mediating hyperphagic effects. However, knockout of individual Y1 or Y5 receptors induces late-onset obesity – and Y5 receptor knockout also induces hyperphagia, possibly due to redundancy in functions of these genes. Here we show that food intake in mice requires the combined actions of both Y1 and Y5 receptors. Germline Y1Y5 ablation in Y1Y5−/− mice results in hypophagia, an effect that is at least partially mediated by the hypothalamus, since mice with adult-onset Y1Y5 receptor dual ablation targeted to the paraventricular nucleus (PVN) of the hypothalamus (Y1Y5Hyp/Hyp) also exhibit reduced spontaneous or fasting-induced food intake when fed a high fat diet. Interestingly, despite hypophagia, mice with germline or hypothalamus-specific Y1Y5 deficiency exhibited increased body weight and/or increased adiposity, possibly due to compensatory responses to gene deletion, such as the decreased energy expenditure observed in male Y1Y5−/− animals relative to wildtype values. While Y1 and Y5 receptors expressed in other hypothalamic areas besides the PVN – such as the dorsomedial nucleus and the ventromedial hypothalamus – cannot be excluded from having a role in the regulation of food intake, these studies demonstrate the pivotal, combined role of both Y1 and Y5 receptors in the mediation of food intake.

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Section: Discussionmentioning

confidence: 85%

Y1 and Y5 Receptors Are Both Required for the Regulation of Food Intake and Energy Homeostasis in Mice

et al. 2012

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“…Furthermore, the slightly, but not significantly higher CART expression in these area can be due to compensatory mechanism as an answer to the larger food consumption. Fast and dynamic change of CART expression and decreased CART-signaling was shown when food-intake was reduced in rodents indicating that CART-producing cells are involved in energy homeostasis (Dandekar et al, 2012; Higuchi et al, 2008; Robson et al, 2002). However, such compensatory mechanism as a response to hyperphagia has never been shown.…”

Section: Discussionmentioning

confidence: 99%

Cocaine- and amphetamine-regulated transcript (CART) peptide immunoreactivity in feeding- and reward-related brain areas of young OLETF rats

Armbruszt

Ábrahám

Figler

et al. 2013

Journal of Chemical Neuroanatomy

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Cocaine- and amphetamine regulated transcript (CART) peptide is expressed in brain areas involved in the control of appetite, drug reward and homeostatic regulation and it has an overall anorexigenic effect. Recently, we have shown that CART peptide immunoreactivity was significantly reduced in the rostral part of the nucleus accumbens and in the rostro-medial part of the nucleus of the solitary tract in adult CCK-1 receptor deficient obese diabetic Otsuka Long Evans Tokushima Fatty (OLETF) rats compared to Long Evans Tokushima Otsuka (LETO) lean controls. It is not clear, however, whether altered CART expression is caused primarily by the deficiency in CCK-1 signaling or whether is related to the obese and diabetic phenotype of the OLETF strain which develops at a later age. Therefore, in the present study, CART-immunoreaction in feeding-related areas of the brain was compared in young, age-matched (6-7 weeks old) non-obese, non-diabetic OLETF rats and in LETO controls. We found that, young, non-diabetic OLETF rats revealed unaltered distribution of CART-peptide expressing neurons and axons throughout the brain when compared to age-matched LETO rats. In contrast to previous results observed in the obese diabetic adult rats, intensity of CART immunoreaction did not differ in the areas related to control of food-intake and reward in the young OLETFs compared to young LETO rats. Our findings suggest that factors secondary to obesity and/or diabetes rather than impaired CCK-1 receptor signaling may contribute to altered CART expression in the OLETF strain.

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“…These results suggest that neural signaling via Y1R mediates central effects of AMPH. However, evidence also reveals that Y5R knockout mice can increase food intake because Y5R is involved in the central feeding regulation of POMC (Higuchi et al, 2008). Thus, we predicted that Y1R and/or Y5R would be involved in the reciprocal regulation of NPY and MC3R in AMPH-treated rats.…”

Section: Introductionmentioning

confidence: 90%

Involvement of neuropeptide Y Y1 receptor in the regulation of amphetamine-mediated appetite suppression

Kuo

Chen

et al. 2012

Neuropharmacology

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Feeding behavior and gene expression of appetite-related neuropeptides in mice lacking for neuropeptide Y Y5 receptor subclass

Abstract: Higuchi H, Niki T, Shiiya T. Feeding behavior and gene expression of appetite-related neuropeptides in mice lacking for neuropeptide Y Y5 receptor subclass.

Cited by 33 publications

References 23 publications

Y1 and Y5 Receptors Are Both Required for the Regulation of Food Intake and Energy Homeostasis in Mice

Y1 and Y5 Receptors Are Both Required for the Regulation of Food Intake and Energy Homeostasis in Mice

Cocaine- and amphetamine-regulated transcript (CART) peptide immunoreactivity in feeding- and reward-related brain areas of young OLETF rats

Involvement of neuropeptide Y Y1 receptor in the regulation of amphetamine-mediated appetite suppression

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