Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Blood glucose, plasma insulin and glucagon, as well as pancreatic insulin, glucagon and somatostatin contents, were measured in control (C group, 18% casein), deprived (D group, 5% casein) and pair-fed (PF) rats at seven intervals during 23 wk after weaning (wk 0). In C rats, plasma and pancreatic insulin showed parallel variations, in D rats, plasma insulin increased normally until wk 3 after weaning, dropped from wk 3 to 8 and was higher in wk 16 and 23 than in wk 8, while pancreatic insulin increased linearly after a significant drop between wk 0 and 1. Insulin variations in D rats were related to protein deficiency until wk 5, but only to energy deficiency thereafter. Circulating and pancreatic glucagon dropped identically for the three groups until wk 5: its role in adaptation to malnutrition is quite irrelevant, although a dysregulation of its secretion was noted. Protein-energy malnutrition induced an increase of pancreatic somatostatin content that was due to the energy deficiency. On the basis of the insulin-to-glucagon ratio, three phases of adaptation to protein-energy malnutrition appeared. From wk 0 to 3, the metabolic priority was growth, whereas glucose homeostasis was secondary, accounting for the early hypoglycemia. From wk 3 to 8 survival was the main priority. After wk 8, the various biochemical parameters stabilized, and growth was parallel to that of normal animals. Protein-energy malnutrition was responsible for a dissociated adaptation of pancreatic hormones.
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PMID:Progressive adaptation of the endocrine pancreas during long-term protein deficiency in rats: effects on blood glucose homeostasis and on pancreatic insulin, glucagon and somatostatin concentrations. 286 38

Immune responses result in a variety of metabolic adjustments that are mediated by cytokines of leukocytic origin. Of the dozens of cytokines released during an immune response, interleukin-1 (IL-1), tumor necrosis factor alpha (TNF alpha) and interleukin-6 (IL-6) are the major mediators of intermediary metabolism. These three cytokines act in concert to decrease food intake, increase resting energy expenditure, gluconeogenesis, glucose oxidation, and hepatic synthesis of fatty acids and acute phase proteins, decrease fatty acid uptake by adipocytes and alter the distribution of zinc, iron and copper. Most of these activities result from direct interactions between the cytokine and the responding cells. IL-1, TNF alpha and IL-6 also affect changes in metabolism by changing levels of circulating insulin, glucagon and corticosterone. The nutritional impact of these metabolic changes is dependent upon age. In growing animals, increases in energy expenditure and oxidation of amino acids are balanced by lower needs associated with growth. In adult animals, energy and amino acid requirements are increased by an amount similar to the increased basal metabolic rate and amino acid oxidation. Nutrition also influences the release of cytokines and consequently affects regulation of the immune response. For example, protein deficiency results in decreased IL-1 release and impaired tissue responses to IL-1.
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PMID:Nutritional aspects of leukocytic cytokines. 306 44