RESUMO
The regulatory mechanisms underlying food intake in chickens have been a focus of research in recent decades to improve production efficiency when raising chickens. Lines of evidence have revealed that a number of brain-gut peptides function as a neurotransmitter or peripheral satiety hormone in the regulation of food intake both in mammals and chickens. Glucagon, a 29 amino acid peptide hormone, has long been known to play important roles in maintaining glucose homeostasis in mammals and birds. However, the glucagon gene encodes various peptides that are produced by tissue-specific proglucagon processing: glucagon is produced in the pancreas, whereas oxyntomodulin (OXM), glucagon-like peptide (GLP)-1 and GLP-2 are produced in the intestine and brain. Better understanding of the roles of these peptides in the regulation of energy homeostasis has led to various physiological roles being proposed in mammals. For example, GLP-1 functions as an anorexigenic neurotransmitter in the brain and as a postprandial satiety hormone in the peripheral circulation. There is evidence that OXM and GLP-2 also induce anorexia in mammals. Therefore, it is possible that the brain-gut peptides OXM, GLP-1 and GLP-2 play physiological roles in the regulation of food intake in chickens. More recently, a novel GLP and its specific receptor were identified in the chicken brain. This review summarizes current knowledge about the role of glucagon-related peptides in the regulation of food intake in chickens.
Assuntos
Galinhas/genética , Galinhas/fisiologia , Ingestão de Alimentos/genética , Ingestão de Alimentos/fisiologia , Glucagon/genética , Glucagon/fisiologia , Neurotransmissores , Animais , Encéfalo/metabolismo , Metabolismo Energético/genética , Metabolismo Energético/fisiologia , Glucagon/biossíntese , Peptídeo 1 Semelhante ao Glucagon/biossíntese , Peptídeo 1 Semelhante ao Glucagon/genética , Peptídeo 1 Semelhante ao Glucagon/fisiologia , Peptídeo 2 Semelhante ao Glucagon/biossíntese , Peptídeo 2 Semelhante ao Glucagon/genética , Peptídeo 2 Semelhante ao Glucagon/fisiologia , Glucose/metabolismo , Homeostase/genética , Homeostase/fisiologia , Mucosa Intestinal/metabolismo , Especificidade de Órgãos , Oxintomodulina/biossíntese , Oxintomodulina/genética , Oxintomodulina/fisiologia , Pâncreas/metabolismoRESUMO
Circadian clocks coordinate 24-hr rhythms of behavior and physiology. In mammals, a master clock residing in the suprachiasmatic nucleus (SCN) is reset by the light-dark cycle, while timed food intake is a potent synchronizer of peripheral clocks such as the liver. Alterations in food intake rhythms can uncouple peripheral clocks from the SCN, resulting in internal desynchrony, which promotes obesity and metabolic disorders. Pancreas-derived hormones such as insulin and glucagon have been implicated in signaling mealtime to peripheral clocks. In this study, we identify a novel, more direct pathway of food-driven liver clock resetting involving oxyntomodulin (OXM). In mice, food intake stimulates OXM secretion from the gut, which resets liver transcription rhythms via induction of the core clock genes Per1 and 2. Inhibition of OXM signaling blocks food-mediated resetting of hepatocyte clocks. These data reveal a direct link between gastric filling with food and circadian rhythm phasing in metabolic tissues.
Assuntos
Relógios Circadianos/efeitos dos fármacos , Ritmo Circadiano/efeitos dos fármacos , Fígado/efeitos dos fármacos , Oxintomodulina/farmacologia , Proteínas Circadianas Period/genética , Animais , Relógios Circadianos/genética , Ritmo Circadiano/genética , Ingestão de Alimentos/efeitos dos fármacos , Ingestão de Alimentos/fisiologia , Jejum , Regulação da Expressão Gênica , Insulina/biossíntese , Insulina/metabolismo , Secreção de Insulina , Mucosa Intestinal/metabolismo , Intestinos/efeitos dos fármacos , Fígado/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Microtomia , Oxintomodulina/biossíntese , Oxintomodulina/genética , Oxintomodulina/metabolismo , Proteínas Circadianas Period/metabolismo , Fotoperíodo , Transdução de Sinais , Núcleo Supraquiasmático/efeitos dos fármacos , Núcleo Supraquiasmático/fisiologia , Técnicas de Cultura de TecidosRESUMO
OBJECTIVE: To observe the effect of pBBADs-OXM-transformed bifidobacteria on the body weight of obese mice. METHODS: B. longum was transformed with pBBADs-OXM by electroporation, and arabopyranose-induced oxyntomodulin expression by the bacterium was detected by ELISA. pBBADs-OXM-transformed bifidobacteria was administered orally obese mice on a daily basis with pBBADs-GFP-transformed bifidobacteria as the negative control, and the body weight changes of the mice were observed. RESULTS: OXM was detected by ELISA not only in the supernatant but also the precipitant of the transformed bacterial culture. The body weight of the obese mice fed with pBBADs-OXM-transformed bifidobacteria decreased significantly compared with that of the mice in the obese model group (P<0.05). CONCLUSION: Administration of pBBADs-OXM-transformed B.longum can reduce the body weight of obese mice.
Assuntos
Bifidobacterium , Obesidade/tratamento farmacológico , Oxintomodulina/administração & dosagem , Oxintomodulina/biossíntese , Administração Oral , Animais , Depressores do Apetite/administração & dosagem , Depressores do Apetite/metabolismo , Bifidobacterium/genética , Bifidobacterium/metabolismo , Peso Corporal/efeitos dos fármacos , Eletroporação , Escherichia coli/genética , Escherichia coli/metabolismo , Camundongos , Oxintomodulina/genética , Distribuição Aleatória , Proteínas Recombinantes/administração & dosagem , Proteínas Recombinantes/biossíntese , Proteínas Recombinantes/genéticaRESUMO
An artificial gene encoding oxyntomodulin was obtained using chemical and enzymatic methods and cloned into Escherichia coli. A recombinant plasmid was constructed containing a hybrid oxyntomodulin gene and Ssp dnaB intein from Synechocystis sp. The expression of the resulting hybrid gene in E. coli, its properties, and the conditions of its autocatalytic cleavage to oxyntomodulin were studied.
