The effects of high fat diet and estradiol on hypothalamic prepro-QRFP mRNA expression in female rats

Schreiber, Allyson L.; Arceneaux, Kenneth P.; Malbrue, Raphael A.; Mouton, Alan J.; Chen, Christina S.; Bench, Elias M.; Braymer, Hugh D.; Primeaux, Stefany D.

doi:10.1016/j.npep.2016.01.004

Cited by 13 publications

(17 citation statements)

References 77 publications

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“…We found that QRFP neurons are distributed in the basolateral hypothalamic regions, including the tuber cinereum and lateral hypothalamic area, constituting distinct neuronal population from neurons that produce orexin or MCH. It was reported that the expression of QRFP is detected in the arcuate nucleus and ventrolmedial hypothalamus (VMH) in rats [18,22]. However, we did not detect QRFP mRNA or peptide in these regions in this study.…”

Section: Discussioncontrasting

confidence: 82%

“…QRFP mRNA was upregulated by fasting, and downregulated when mice were fed a high-fat diet (HFD) [15,21]. HFD feeding increased expression of QRFP mRNA in the hypothalamus of female rats, and estradiol, which is a potent regulator of feeding behavior was shown to increase QRFP [22]. From these observations, we hypothesized that this neuropeptide is involved in the physiological mechanisms of feeding behavior and energy homeostasis.…”

Section: Introductionmentioning

confidence: 99%

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QRFP-Deficient Mice Are Hypophagic, Lean, Hypoactive and Exhibit Increased Anxiety-Like Behavior

et al. 2016

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How the hypothalamus transmits hunger information to other brain regions to govern whole brain function to orchestrate feeding behavior has remained largely unknown. Our present study suggests the importance of a recently found lateral hypothalamic neuropeptide, QRFP, in this signaling. Qrfp-/- mice were hypophagic and lean, and exhibited increased anxiety-like behavior, and were hypoactive in novel circumstances as compared with wild type littermates. They also showed decreased wakefulness time in the early hours of the dark period. Histological studies suggested that QRFP neurons receive rich innervations from neurons in the arcuate nucleus which is a primary region for sensing the body’s metabolic state by detecting levels of leptin, ghrelin and glucose. These observations suggest that QRFP is an important mediator that acts as a downstream mediator of the arcuate nucleus and regulates feeding behavior, mood, wakefulness and activity.

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Section: Discussioncontrasting

confidence: 82%

Section: Introductionmentioning

confidence: 99%

QRFP-Deficient Mice Are Hypophagic, Lean, Hypoactive and Exhibit Increased Anxiety-Like Behavior

et al. 2016

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“…Consistent with this observation, it has been recently shown that direct administration of 26RFa into the medial hypothalamus increases food consumption (Zagorácz et al, 2015), and that the concentrations of 26RFa/43RFa in the VMH are significantly increased in rats fed a standard chow (Beck and Richy, 2009). It has also been found that 26RFa still stimulates appetite when rats are fed a high fat diet (Primeaux et al, 2008), and this phenomenon is accompanied by an up-regulation of prepro26RFa and GPR103 in the VMH and the Arc (Schreiber et al, 2016). By contrast, these authors (Primeaux et al, 2008; Schreiber et al, 2016) as well as Patel et al (2008) failed to find any effect of 26RFa or 43RFa on food consumption when rats are fed a standard chow.…”

Section: Rfa and Control Of Feeding Behaviormentioning

confidence: 99%

“…It has also been found that 26RFa still stimulates appetite when rats are fed a high fat diet (Primeaux et al, 2008), and this phenomenon is accompanied by an up-regulation of prepro26RFa and GPR103 in the VMH and the Arc (Schreiber et al, 2016). By contrast, these authors (Primeaux et al, 2008; Schreiber et al, 2016) as well as Patel et al (2008) failed to find any effect of 26RFa or 43RFa on food consumption when rats are fed a standard chow. Interestingly, in both mice and rats, 26RFa potently stimulates food intake when the animals are deprived of food for 18 h prior to the injection of the neuropeptide (Chartrel et al, 2003; Do Rego et al, 2006; Lectez et al, 2009) strongly suggesting that starvation potentiates the orexigenic activity of 26RFa.…”

Section: Rfa and Control Of Feeding Behaviormentioning

confidence: 99%

The Neuropeptide 26RFa (QRFP) and Its Role in the Regulation of Energy Homeostasis: A Mini-Review

et al. 2016

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This mini-review deals with the neuropeptide 26RFa (or QRFP) which is a member of the RFamide peptide family discovered simultaneously by three groups in 2003. 26RFa (or its N-extended form 43RFa) was subsequently shown to be the endogenous ligand of the human orphan receptor GPR103. In the brain, 26RFa and GPR103mRNA are primarily expressed in hypothalamic nuclei involved in the control of feeding behavior, and at the periphery, the neuropeptide and its receptor are present in abundance in the gut and the pancreatic islets, suggesting that 26RFa is involved in the regulation of energy metabolism. Indeed, 26RFa stimulates food intake when injected centrally, and its orexigenic effect is even more pronounced in obese animals. The expression of 26RFa is up-regulated in the hypothalamus of obese animals, supporting that the 26RFa/GPR103 system may play a role in the development and/or maintenance of the obese status. Recent data indicate that 26RFa is also involved in the regulation of glucose homeostasis. 26RFa reduces glucose-induced hyperglycemia, increases insulin sensitivity and insulinemia. Furthermore, an oral ingestion of glucose strongly stimulates 26RFa release by the gut, indicating that 26RFa is a novel incretin. Finally, 26RFa is able to prevent pancreatic β cell death and apoptosis. This brief overview reveals that 26RFa is a key neuropeptide in the regulation of energy metabolism. Further fields of research are suggested including the pathophysiological implication of the 26RFa/GPR103 system.

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“…QRFP has orexigenic effects in rodents [1][2][3][4][5]. QRFP also regulates behavioral arousal, blood pressure, locomotor activity, and aldosterone and insulin secretion [2,6,7].…”

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confidence: 99%

Regulation of the expression of corticotropin-releasing factor gene by pyroglutamylated RFamide peptide in rat hypothalamic 4B cells

et al. 2016

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PYROGLUTAMYLATED RFAMIDE PEPTIDES (QRFP), including a 26-aa (QRFP26) and a 43-aa (QRFP43) peptides, are important regulators of metabolism or energy homeostasis. QRFP has orexigenic effects in rodents [1][2][3][4][5]. QRFP also regulates behavioral arousal, blood pressure, locomotor activity, and aldosterone and insulin secretion [2,6,7]. QRFP acts via a specific receptor, Gpr103, which belongs to the G proteincoupled receptor superfamily [2,8]. QRFP43 exhibits more potent agonistic activity than QRFP26 [9].Gpr103 mRNA is expressed in the hypothalamus and pituitary of humans and mice [2,8] Abstract. Pyroglutamylated RFamide peptide (QRFP), an important regulator of metabolism and energy homeostasis, has orexigenic effects. QRFP acts via a specific receptor, Gpr103. Gpr103 mRNA is expressed in the rat hypothalamic paraventricular nucleus (PVN). In the PVN, corticotropin-releasing factor (CRF), which plays a central role in regulating the stress response and is produced in response to stress, stimulates the release of adrenocorticotropic hormone from the anterior pituitary. We hypothesized that QRFP regulates CRF gene expression directly in the hypothalamus, and thus examined the direct effect of QRFP on the promoter activity and mRNA levels of CRF in hypothalamic cells. To examine these pathways, we used hypothalamic 4B cells, a homologous PVN neuronal cell line. Gpr103a and Gpr103b mRNA, and Gpr103 (a and b) proteins were expressed in the hypothalamic cells. The Gpr103 mRNA and protein levels were increased by QRFP. QRFP also stimulated CRF mRNA levels and CRF promoter activity directly in 4B cells following their transfection with the CRF promoter. The protein kinase A (PKA) and protein kinase C (PKC) pathways were involved in the QRFP-induced increases in CRF promoter activity. QRFP stimulated cAMP response element-binding protein (CREB) phosphorylation. CREB phosphorylation was inhibited by a PKC inhibitor. PKC-dependent signaling would be upstream of the CREB phosphorylation. Thus, QRFP-dependent pathways are involved in the regulation of CRF gene expression in the hypothalamus.

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The effects of high fat diet and estradiol on hypothalamic prepro-QRFP mRNA expression in female rats

Cited by 13 publications

References 77 publications

QRFP-Deficient Mice Are Hypophagic, Lean, Hypoactive and Exhibit Increased Anxiety-Like Behavior

QRFP-Deficient Mice Are Hypophagic, Lean, Hypoactive and Exhibit Increased Anxiety-Like Behavior

The Neuropeptide 26RFa (QRFP) and Its Role in the Regulation of Energy Homeostasis: A Mini-Review

Regulation of the expression of corticotropin-releasing factor gene by pyroglutamylated RFamide peptide in rat hypothalamic 4B cells

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