Metabolic regulation of feed intake in monogastric mammals

摘要: Nutrients and their metabolites control short long term feed intake through direct or indirect endocrine secretions that interact with local central neural processes. Carbohydrates, fats, proteins products from both mammalian microbial enzymic digestion directly affect the release of hormones gastrointestinal tract pancreas. The quantitative temporal these depends on nutrient composition, site digestion, released within tract. act collectively to meal size many suppressing jejunal, ileal and/or colonic brakes, which reduce gastric emptying, propulsive contractions along intestine, secretions. However, nutrient-stimulated also vagal nervous system specific regions brain have longer-term effects intake. main metabolic long-term intake, energy metabolism, body composition weight is via two opposing monitoring systems, adenosine monophosphateactivated protein kinase (AMPK) target rapamycin (mTOR), peripherally centrally hypothalamus. AMPK activated when cells are depleted triphosphate (ATP) by monophosphate (AMP)/ATP ratio. inhibits ATP-consuming pathways stimulates ATP-producing regulation enzymes involved in lipid, carbohydrate metabolism. regulates concentration a key intake-controlling metabolite, malonyl-CoA, Low status high activation leads inactivation mTOR, contrary AMPK, reflects an animal. Activation mTOR hypothalamus controlled insulin leptin. Basal leptin concentrations increase animal adiposity status. results low malonyl-CoA stimulating expression melanocortin orexigenic peptides, neuropeptide tyrosine agouti-related peptide, reducing anorexigenic pro-opiomelanocortin, α-melanocyte-stimulating hormone cocaineand amphetamine-related transcript, thereby increasing expenditure. By converse mechanisms, perceived reduces while concepts described can help explain how dietary non-dietary situations animals.