Coexpression of Leptin Receptor and Preproneuropeptide Y mRNA in Arcuate Nucleus of Mouse Hypothalamus

Mercer, Julian G.; Hoggard, Nigel; Williams, Lynda M.; Lawrence, Catherine B.; Hannah, L T; Morgan, Peter J.; Trayhurn, Paul

doi:10.1046/j.1365-2826.1996.05161.x

Cited by 438 publications

(246 citation statements)

References 4 publications

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“…CART mRNA expression in the ARC is stimulated by leptin [3,4,53,54] and SL rats are hyperleptinaemic. In this case, our result could suggest that OB-Rb is regulated in a neuronal specific form in the ARC of obese animals, and that the described down-regulation shown in this work occurs specifically in the medial part of the caudal ARC where AgRP/NPY neurons are located [55], but it does not occur in the lateral ARC, where CART neurons are located. This nuclei-specific pattern of regulation of CART expression has been previously described in other feeding disorders, such as those caused by alterations in thyroid status [32] and indicates different roles for these neuronal populations.…”

Section: Discussionmentioning

confidence: 50%

A possible role of neuropeptide Y, agouti-related protein and leptin receptor isoforms in hypothalamic programming by perinatal feeding in the rat

et al. 2004

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Aim/hypothesis: Perinatal overfeeding predisposes humans and rats to obesity and diabetes in later life. One classical model for studying the effect of early feeding is manipulation of the size of rat litters. Rats growing up in small litters gain more weight than rats growing up in normal-sized litters. Interestingly, these obese rats maintain this phenotype in adulthood. Conversely, rats raised in large litters show a delay in growth and a decrease in body weight. The aim of this work was to assess the hypothalamic control mechanisms of food intake regulated by perinatal feeding. Methods: Leptin levels were analysed using RIA. Leptin receptor mRNA levels were analysed using RT-PCR. Neuropeptide mRNA levels were analysed using in situ hybridisation. Results: Perinatally overfed neonatal male rats exhibited hyperleptinaemia and a decrease in hypothalamic mRNA levels of the long isoform of the leptin receptor (OB-Rb), explaining their leptin resistance. Moreover, this obese model showed an increase in the mRNA expression of cocaine-and amphetamine-regulated transcript, neuropeptide Y and agouti-related protein in the hypothalamic arcuate nucleus (ARC). In contrast, perinatally underfed neonatal male rats with hypoleptinaemia showed an increase in hypothalamic mRNA of the short isoforms of the leptin receptor. Furthermore, they exhibited an increase in expression of neuropeptide Y and agoutirelated protein in the ARC. Conclusions/interpretation: Rats overfed during early postnatal life show a leptinresistant state mediated by down-regulation of the hypothalamic OB-Rb. These data, together with the increased expression of neuropeptide Y and agouti-related protein in specific neurons in the ARC, might indicate the existence of regulated programming in this nucleus and may provide a new aetiopathogenic concept in susceptibility to obesity.

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Section: Discussionmentioning

confidence: 50%

A possible role of neuropeptide Y, agouti-related protein and leptin receptor isoforms in hypothalamic programming by perinatal feeding in the rat

et al. 2004

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“…The short-form Ob-Rs, Ob-Ra and Ob-Rc, contribute to transport of leptin into the brain [3]. The long-form Ob-R, Ob-Rb, is abundantly expressed in the ARC, PVN, VMH, and lateral hypothalamic area [16,17,41]. Leptin activates STAT3 with Jak2.…”

Section: Discussionmentioning

confidence: 99%

“…The mRNA coding for the long form of the leptin receptor (Ob-Rb) has been found in various brain structures, including nuclei involved in the regulation of energy balance such as the VMH, the PVN, and the ARC [26,41].…”

Section: Introductionmentioning

confidence: 99%

Regulation of corticotropin-releasing factor and urocortin 2/3 mRNA by leptin in hypothalamic N39 cells

et al. 2013

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Corticotropin-releasing factor (CRF) activates the pituitary-adrenal axis during stress, and shows anorectic effects via CRF type 1 receptors in the hypothalamus.Both urocortin (Ucn) 2 and Ucn3 also act as anorectic neuropeptides via CRF type 2 receptors. Leptin, a product of the obesity gene secreted mainly from adipose tissue, reduces food intake and increases energy expenditure. A possible interaction between leptin and CRF/Ucns has been suggested, as leptin can regulate expression and activation of CRF and Ucns in the hypothalamus. This study aimed to explore the possible function of leptin in the hypothalamus, and its effects in regulating CRF and Ucns. The study identified mRNA expression of the leptin receptor (Ob-R) and its subtypes, CRF, and Ucn2/3 in mouse hypothalamic N39 cells. Leptin stimulated signal transducer and activators of transcription type 3 (STAT3) phosphorylation, directly increased the mRNA levels of both CRF and Ucn2/3 in hypothalamic cells, and increased Ob-Rb mRNA levels. A Janus kinase inhibitor inhibited the leptin-mediated increase in STAT3 phosphorylation, and then the increases in CRF and Ucn2/3 mRNA levels. Leptin may contribute to a stress response or anorectic effect via the regulation 2 of CRF and Ucn2/3 in the hypothalamus.

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“…The discovery of the molecular circuitry that links leptin signaling to alterations in BMD initiated an active area of investigation [1]. It has been established that leptin receptors are expressed in high density on neuropeptide Y (NPY)-secreting neurons in the arcuate nucleus [6] and that suppression of NPY release by leptin mediates anorexigenic effects [7][8][9]. However, a decline in NPY does not appear to be the mechanism for leptin's negative effect on BMD, as intracerebroventricular infusion of NPY also has a deleterious impact on BMD [1].…”

Section: Introductionmentioning

confidence: 99%

Peptide YY (PYY) levels and bone mineral density (BMD) in women with anorexia nervosa

Utz¹,

Lawson²,

Misra³

et al. 2008

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Introduction-Anorexia nervosa is a psychiatric illness that results in significant bone loss. Studies examining the neuroendocrine dysregulation that occurs in AN may increase understanding of endocrine systems that regulate bone mass. PYY is an anorexigenic peptide derived primarily from the intestine, with actions mediated via activation of Y-receptors. We have previously shown that PYY levels are elevated in adolescents with AN. Y2 receptor knockout mice have increased bone mineral density (BMD) and thus PYY may play a role in regulating bone mass. We hypothesized that PYY levels would be inversely associated with BMD in women with AN.

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Coexpression of Leptin Receptor and Preproneuropeptide Y mRNA in Arcuate Nucleus of Mouse Hypothalamus

Cited by 438 publications

References 4 publications

A possible role of neuropeptide Y, agouti-related protein and leptin receptor isoforms in hypothalamic programming by perinatal feeding in the rat

A possible role of neuropeptide Y, agouti-related protein and leptin receptor isoforms in hypothalamic programming by perinatal feeding in the rat

Regulation of corticotropin-releasing factor and urocortin 2/3 mRNA by leptin in hypothalamic N39 cells

Peptide YY (PYY) levels and bone mineral density (BMD) in women with anorexia nervosa

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