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)

1. The growth of the gastric mucosa during pregnancy and afterwards has been studied by comparing the stomachs of rats, killed at weekly intervals after impregnation, with the stomachs of virgin rats of the same age and starting weight. The rate of growth of the gastric mucosa in both groups was determined from the changes observed in the weight of the whole stomach, the weight and surface area of the fundus, the volume (mass) of the fundic mucosa and the total parietal and total peptic cell populations.2. Hyperplasia of the gastric mucosa occurred during pregnancy and lactation, the effect being characterized by increases in the surface area and volume (mass) of the gastric mucosa, and in the total parietal and total peptic cell populations.3. The data suggest that the effect developed shortly after conception. Hyperplasia of the gastric mucosa continued throughout pregnancy and reached maximal values after the second week of lactation and waned thereafter; the maximal changes obtained for individual observations such as surface area and the total parietal and total peptic cell populations represented increases of the order of 40% above corresponding control values.4. From the observations that were made on food intake it seemed unlikely that the hyperplasia of the gastric mucosa was due to hyperphagia. It also seemed unlikely that the effect could be accounted for by the increase that occurred in body weight during pregnancy.
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PMID:Hyperplasia of the gastric mucosa during pregnancy and lactation in the rat. 557 50

Expression of the obese hyperglycaemic (bo/ob) syndrome in mice is modified by the background genome. The Aston colony carries the ob gene on a mixed background which produces a unique combination of different features shown by ob/ob mice on other backgrounds. The maximum body weight of Aston ob/ob mice exceeded that of other colonies, possibly reflecting a trait for higher growth rate in the background genome. The hyperphagia, marked hyperinsulinaemia and moderate hyperglycaemia observed during the development of the syndrome receded in old mice. Plasma glucagon concentrations in the fed state were similar to +/+ mice and did nor Vary throughout life. Hyperplasia of the B-cells increased inordinately during the development of the syndrome, but declined in older mice coincident with progressive intercellular vacuolation and the appearance of acinar-like cells within the islets. A-cell hyperplasia was greater in young mice, and A-cells became relocated throughout the islets of older mice. The distinct pattern of age-related changes in ob/ob mice indicates that experiments using this gene type should define clearly their age as well as genetic background.
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PMID:Influence of genetic background and age on the expression of the obese hyperglycaemic syndrome in Aston ob/ob mice. 704 Feb 65