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)

Parenteral progesterone injections into different mammalian species induce hyperinsulinemia, pancreatic islet hypertrophy, and exaggerated insulin secretion in vitro in response to glucose. The primary effect of progesterone by itself on carbohydrate metabolism appears to be the diversion of glucose utilization away from muscle and fat to other tissues, and the promotion of more storage of glycogen in the liver. On lipid metabolism, the 1 effect of progesterone is to favor storage of depot fat in adipose and breast tissue and to partially reduce the hypertriglyceridemic action of estrogens. On protein metabolism, it has been suggested that progesterone may have a catabolic action in man, and that the basic effects may be a lowering of several plasma amino acids and an increased total urinary nitrogen excretion without an associated aminoaciduria. On ketone body metabolism, progesterone partially suppresses the estrogen effect on liver triglyceride formation while promoting ketogenesis. The metabolic effects of progesterone are most relevant to pregnancy. The hormonal milieu of early to midgestation favors the stimulation of hyperphagia, pancreatic islet hypertrophy, hyperinsulinemia, and body fat and glycogen deposition. This period promotes maternal tissue accretion and weight gain. During the later half of pregnancy, progesterone acts simultaneously with prolactin and other hormones to prepare the breasts for lactation by promoting hyperinsulinemia and fuel storage and by helping to condition the liver in elaborating ketones more promptly to meet the demands of advancing pregnancy.
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PMID:Metabolic effects of progesterone. 703 19