28. The anorexigenic effect of dietary lysine could be mediated by increased jejunal cholecystokinin secretion in piglets

Gut microbiota can influence the feeding behavior of the host, but the underlying mechanisms are unknown. Recently, caseinolytic protease B (ClpB), a disaggregation chaperon protein of Escherichia coli, was identified as a conformational mimetic of α-melanocyte-stimulating hormone (α-MSH), an anorexigenic neuropeptide. Importantly, ClpB was necessary for E. coli to have an anorexigenic effect in mice, suggesting that it may participate in satiety signaling. To explore this further, we determined the short-term (2 h) effects of three macronutrients: protein (bovine serum albumin), carbohydrate (D-fructose) and fat (oleic acid), on the production of ClpB by E. coli and analyzed whether ClpB can stimulate the secretion of the intestinal satiety hormone, peptide YY (PYY). Isocaloric amounts of all three macronutrients added to a continuous culture of E. coli increased ClpB immunoreactivity. However, to increase the levels of ClpB mRNA and ClpB protein in bacteria and supernatants, supplementation with protein was required. A nanomolar concentration of recombinant E. coli ClpB dose-dependently stimulated PYY secretion from the primary cell cultures of rat intestinal mucosa. Total proteins extracted from E. coli but not from ClpB-deficient E. coli strains also tended to increase PYY secretion. These data support a possible link between E. coli ClpB and protein-induced satiety signaling in the gut.

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The anorexigenic effect of beta-melanocyte-stimulating hormone involves corticotrophin-releasing factor and mesotocin in birds

Neuroscience Letters ◽

10.1016/j.neulet.2020.135282 ◽

2020 ◽

Vol 736 ◽

pp. 135282

Author(s):

Chang Cao ◽

Elizabeth R. Gilbert ◽

Mark A. Cline

Keyword(s):

Melanocyte Stimulating Hormone ◽

Corticotrophin Releasing Factor ◽

Anorexigenic Effect ◽

Stimulating Hormone

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The anorexigenic effect of sustained-release dexedrine preparations

The American Journal of Digestive Diseases ◽

10.1007/bf02895539 ◽

1953 ◽

Vol 20 (10) ◽

pp. 307-312 ◽

Cited By ~ 6

Author(s):

E. Philip Gelvin ◽

Thomas H. McGavack ◽

Samuel Kenigsberg

Keyword(s):

Sustained Release ◽

Anorexigenic Effect

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Peripheral oxytocin activates vagal afferent neurons to suppress feeding in normal and leptin-resistant mice: a route for ameliorating hyperphagia and obesity

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00344.2014 ◽

2015 ◽

Vol 308 (5) ◽

pp. R360-R369 ◽

Cited By ~ 66

Author(s):

Yusaku Iwasaki ◽

Yuko Maejima ◽

Shigetomo Suyama ◽

Masashi Yoshida ◽

Takeshi Arai ◽

...

Keyword(s):

Food Intake ◽

Nucleus Tractus Solitarius ◽

Body Weight Gain ◽

Vagal Afferents ◽

Afferent Neuron ◽

Afferent Neurons ◽

Vagal Afferent ◽

Fos Expression ◽

Novel Target ◽

Anorexigenic Effect

Oxytocin (Oxt), a neuropeptide produced in the hypothalamus, is implicated in regulation of feeding. Recent studies have shown that peripheral administration of Oxt suppresses feeding and, when infused subchronically, ameliorates hyperphagic obesity. However, the route through which peripheral Oxt informs the brain is obscure. This study aimed to explore whether vagal afferents mediate the sensing and anorexigenic effect of peripherally injected Oxt in mice. Intraperitoneal Oxt injection suppressed food intake and increased c-Fos expression in nucleus tractus solitarius to which vagal afferents project. The Oxt-induced feeding suppression and c-Fos expression in nucleus tractus solitarius were blunted in mice whose vagal afferent nerves were blocked by subdiaphragmatic vagotomy or capsaicin treatment. Oxt induced membrane depolarization and increases in cytosolic Ca2+ concentration ([Ca2+]i) in single vagal afferent neurons. The Oxt-induced [Ca2+]i increases were markedly suppressed by Oxt receptor antagonist. These Oxt-responsive neurons also responded to cholecystokinin-8 and contained cocaine- and amphetamine-regulated transcript. In obese diabetic db/db mice, leptin failed to increase, but Oxt increased [Ca2+]i in vagal afferent neurons, and single or subchronic infusion of Oxt decreased food intake and body weight gain. These results demonstrate that peripheral Oxt injection suppresses food intake by activating vagal afferent neurons and thereby ameliorates obesity in leptin-resistant db/db mice. The peripheral Oxt-regulated vagal afferent neuron provides a novel target for treating hyperphagia and obesity.

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Paraventricular NUCB2/nesfatin-1 is directly targeted by leptin and mediates its anorexigenic effect

Biochemical and Biophysical Research Communications ◽

10.1016/j.bbrc.2014.12.065 ◽

2015 ◽

Vol 456 (4) ◽

pp. 913-918 ◽

Cited By ~ 20

Author(s):

Gantulga Darambazar ◽

Masanori Nakata ◽

Takashi Okada ◽

Lei Wang ◽

EnXu Li ◽

...

Keyword(s):

Anorexigenic Effect

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Central neuropeptide W has anorexigenic effect in rats

Journal of Animal Physiology and Animal Nutrition ◽

10.1111/jpn.12067 ◽

2013 ◽

Vol 98 (2) ◽

pp. 228-234 ◽

Cited By ~ 3

Author(s):

T. Naso ◽

S. Shousha ◽

A. El-Kirdasy

Keyword(s):

Anorexigenic Effect

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Possible involvement of uncoupling protein 1 in appetite control by leptin

Experimental Biology and Medicine ◽

10.1258/ebm.2011.011143 ◽

2011 ◽

Vol 236 (11) ◽

pp. 1274-1281 ◽

Cited By ~ 22

Author(s):

Yuko Okamatsu-Ogura ◽

Junko Nio-Kobayashi ◽

Toshihiko Iwanaga ◽

Akira Terao ◽

Kazuhiro Kimura ◽

...

Keyword(s):

Adipose Tissue ◽

Food Intake ◽

Energy Expenditure ◽

Single Injection ◽

Uncoupling Protein ◽

Day Treatment ◽

Repeated Injection ◽

Appetite Control ◽

Brown Adipose ◽

Anorexigenic Effect

Leptin reduces body fat by decreasing food intake and increasing energy expenditure. Uncoupling protein (UCP) 1, a key molecule for brown adipose tissue (BAT) thermogenesis, was reported to contribute to the stimulatory effect of leptin on energy expenditure. To clarify whether UCP1 is also involved in the anorexigenic effect of leptin, in this study we examined the effect of leptin on food intake using wild-type (WT) and UCP1-deficient (UCP1-KO) mice. Repeated injection of leptin decreased food intake more markedly in WT mice than in UCP1-KO mice, while a single injection of leptin showed similar effects in the two groups of mice. As chronic leptin stimulation induces UCP1 expression in BAT and ectopically in white adipose tissue (WAT), we mimicked the UCP1 induction by repeated injection of CL316,243 (CL), a highly specific β3-adrenoceptor agonist, and measured food intake in response to a single injection of leptin. Two-week treatment with CL enhanced the anorexigenic effect of leptin in WT mice, but not in UCP1-KO mice. Three-day treatment with CL in WT mice also enhanced the anorexigenic effect of leptin and leptin-induced phosphorylation of signal transducer and activator of transcription 3 (STAT3) in the arcuate nucleus of the hypothalamus, without any notable change in adiposity. These results indicate that UCP1 enhances leptin action at the hypothalamus level, suggesting UCP1 contributes to the control of energy balance not only through the regulation of energy expenditure but also through appetite control by modulating leptin action.

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Synergistic effect of leptin and lipidized PrRP on metabolic pathways in ob/ob mice

Journal of Molecular Endocrinology ◽

10.1530/jme-19-0188 ◽

2020 ◽

Vol 64 (2) ◽

pp. 77-90 ◽

Cited By ~ 1

Author(s):

Lucia Kořínková ◽

Martina Holubová ◽

Barbora Neprašová ◽

Lucie Hrubá ◽

Veronika Pražienková ◽

...

Keyword(s):

Synergistic Effect ◽

Metabolic Pathways ◽

Liver Weight ◽

The Body ◽

Janus Kinase ◽

Anorexigenic Effect ◽

Amp Activated Protein Kinase ◽

Prolactin Releasing Peptide ◽

Transcription 3 ◽

The Brain

Lack of leptin production in ob/ob mice results in obesity and prediabetes that could be partly reversed by leptin supplementation. In the hypothalamus, leptin supports the production of prolactin-releasing peptide (PrRP), an anorexigenic neuropeptide synthesized and active in the brain. In our recent studies, the palmitoylated PrRP analog palm11-PrRP31 showed a central anorexigenic effect after peripheral administration. This study investigates whether PrRP could compensate for the deficient leptin in ob/ob mice. In two separate experiments, palm11-PrRP31 (5 mg/kg) and leptin (5 or 10 μg/kg) were administered subcutaneously twice daily for 2 or 8 weeks to 8- (younger) or 16-(older) week-old ob/ob mice, respectively, either separately or in combination. The body weight decreasing effect of palm11-PrRP31 in both younger and older ob/ob mice was significantly powered by a subthreshold leptin dose, the combined effect could be then considered synergistic. Leptin and palm11-PrRP31 also synergistically lowered liver weight and blood glucose in younger ob/ob mice. Reduced liver weight was linked to decreased mRNA expression of lipogenic enzymes. In the hypothalamus of older ob/ob mice, two main leptin anorexigenic signaling pathways, namely, Janus kinase, signal transducer and activator of transcription-3 activation and AMP-activated protein kinase de-activation, were induced by leptin, palm11-PrRP31, and their combination. Thus, palm11-PrRP31 could partially compensate for leptin deficiency in ob/ob mice. In conclusion, the results demonstrate a synergistic effect of leptin and our lipidized palm11-PrRP31 analog.

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