Abstract:
:High concentrations of glucose induce insulin resistance and impair insulin secretion in a manner that mirrors type 2 diabetes, a phenomenon known as glucose toxicity. High concentrations of hexosamines mimic these effects, leading to the hypothesis that cells use hexosamine flux as a glucose- and satiety-sensing pathway. Overexpression of the rate-limiting enzyme for hexosamine synthesis (glutamine:fructose-6-phosphate amidotransferase, GFA) in muscle and fat results in insulin resistance and hyperleptinemia. GFA overexpression targeted to liver results in hyperlipidemia and to the beta cell in increased insulin secretion. Thus, excess hexosamine flux leads to a coordinated response whereby fuel is shunted toward long-term storage, mirroring the "thrifty phenotype". The results suggest a mechanism by which chronic overnutrition leads to the phenotype of type 2 diabetes.
journal_name
Ann N Y Acad Scijournal_title
Annals of the New York Academy of Sciencesauthors
Cooksey RC,McClain DAdoi
10.1111/j.1749-6632.2002.tb04268.xsubject
Has Abstractpub_date
2002-06-01 00:00:00pages
102-11eissn
0077-8923issn
1749-6632journal_volume
967pub_type
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