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)

To test the hypothesis that diabetes is a form of accelerated aging, the following observations were made. 1) The incidence rate of diabetes mellitus had its peak at around 50 years of age with a gradually decreasing rate thereafter. This was clearly different from the manner of incidence of such disease as arteriosclerosis which increased with advancing age. 2) 100g of the oral glucose tolerance test performed on elderly subjects aged 60 to 89 years revealed high incidence of abnormal tolerance, 21% diabetic and 53% borderline types. 3) The insulin secretory capacity to glucose load of subjects was not different from that of young and middle-aged subjects from 20 to 49 years old. Therefore, decreased tolerance to glucose load could not ba ascribed to deficient insulin secretion. 4) No abnormality of glucagon response to glucose load was found in the old. 5) Serum beta-N-acetylhexosaminidase activity was not increased in elderly subjects, again contrasting with the increased activity found in diabetics. 6) Both glycolytic and gluconeogenic enzyme activities were decreased in the liver of aged rats. 7) No specific abnromality in insulin secretory response was observed in Werner's syndrome which might be considered to be a model for aging. All the above observations do not support the aforementioned hypothesis. Abnormality of glucose tolerance frequently observed in elderly subjects appears to be caused by other pathogenesis than diabetes mellitus.
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PMID:[Aging and endocrine pancreas (author's transl)]. 34 Feb 93

Alcohol has been reported to increase the urinary excretion of dolichols, and urinary dolichols are suggested to be derived from the lysosomes of the renal cells. In the present study we examined the effects of alcohol and glucagon on the biliary excretion of dolichols in rats. Chronic ethanol treatment decreased both biliary dolichol and beta-hexosaminidase excretion. The absolute amount of dolichol excreted into the bile correlated highly significantly with the absolute amount of biliary beta-hexosaminidase. Our results indicate that biliary dolichols are--at least in part--derived from hepatic lysosomes. Decreased biliary dolichol output during chronic alcohol administration suggests that urinary and biliary dolichol excretions are regulated independently of each other.
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PMID:Biliary excretion of dolichols and beta-hexosaminidase--effect of ethanol and glucagon. 939 2