Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the responses in the omnivorous rodent A. azarae submitted to a low quality diet at morphological, physiological and biochemical levels. At short term, a decrease in body mass occurred. A later increase in food consumption constituted a strategy that allowed a temporal recovery of physical condition. However, hyperphagia appeared not to be enough to maintain physical condition after 30 days of low quality diet consumption. At the morphological level, an increase in length (9%) of the anterior portion of the gut occurred, the part of the gut where digestion and absorption take place. A decrease in small intestine weight could be related with the long-term impairment of body condition. Inhibition of sucrase specific activity in small intestine would indicate a down-regulation of sucrase-isomaltase complex. Total maltase specific activity in small intestine was not affected suggesting an up-regulation of sucrase-independent maltase specific activity. A down-regulation of protease specific activity in small intestine occurred in response to low quality diet. The specific activity of disaccharidases in caecum and large intestine was down-regulated. The strategies and constraints at different levels of A. azarae upon low quality diet are discussed.
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PMID:Phenotypic plasticity in response to low quality diet in the South American omnivorous rodent Akodon azarae (Rodentia: Sigmodontinae). 1695 12

In small mammals, marked phenotypic plasticity of digestive physiology has been shown to make it easier for them to cope with energetically stressful periods, such as lactation. It has been proposed that the capacity of the gut to digest and absorb food is not the limiting factor to sustained energy intake (SusEI) during peak lactation. In this study, plasticity in energy intake and gastrointestinal morphology was examined in striped hamsters at different stages of reproduction and when raising litters of different sizes. Mechanisms associated with digestive enzymes and neuroendocrine hormones underpinning the plasticity were also examined. Females significantly increased energy intake, digestibility, digestive tract mass and the activity of stomach pepsin and small intestine maltase, sucrase and aminopeptidase in peak lactation compared with the non-productive and post-lactating periods. Further, females raising large litters significantly increased energy intake, digestibility, gastrointestinal mass and activity of digestive enzymes, and weaned heavier offspring compared with those nursing small and medium litters, indicating that the significant plasticity of digestive physiology increased reproductive performance. Agouti-related protein (AgRP) mRNA expression in the hypothalamus was up-regulated significantly in females raising large litters relative to those raising small litters. Serum leptin levels, and mRNA expression of hypothalamus neuropeptide Y (NPY) and the anorexigenic neuropeptides pro-opiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART) did not differ among females raising small, medium and large litters. Leptin levels in lactation may only reflect a state of energy balance rather than being the prime driver of hyperphagia. Some hypothalamic neuropeptides, such as NPY, POMC and CART, may be involved in the limits to the SusEI during lactation.
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PMID:Plasticity in gastrointestinal morphology and enzyme activity in lactating striped hamsters (Cricetulus barabensis). 2694 87