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• W2161567465 abstract "ABSTRACT: Animals with genetically or nutritionally induced insulin resistance and Type 2 diabetes comprise two groups: those with resilient β‐cells, e.g., ob/ob mice or fa/fa rats, capable of longstanding compensatory insulin hypersecretion and those with labile β‐cells in which the secretion pressure leads to β‐cell degranulation and apoptosis, e.g., db/db mice and Psammomys gerbils (sand rats). Psammomys features low insulin receptor density; on a relatively high energy diet it becomes hyperinsulinemic and hyperglycemic. In hyperinsulinemic clamp the hepatic glucose production is only partially suppressed by insulin, even in the normoglycemic state. The capacity of insulin to activate muscle and liver receptor tyrosine kinase is nearly abolished. GLUT4 content and mRNA are markedly reduced. Hyperinsulinemia was also demonstrated to inhibit insulin signaling and glucose transport in several other species. Among the factors affecting the insulin signaling pathway, phosphorylation of serine/threonine appears to be the prominent cause of receptor malfunction as inferred from the finding of overexpression of PKCɛ isoforms in the muscle and liver of Psammomys . The insulin resistance syndrome progressing in animals with labile β‐cells to overt diabetes and β‐cell failure is a “thrifty gene” characteristic. This is probably also true for human populations emerging from food scarcity into nutritional affluence, inappropriate for their metabolic capacity. Thus, the nutritionally induced hyperinsulinemia, associated with PKCɛ activation may be looked upon from the molecular point of view as “PKCɛ overexpression syndrome.”" @default.
• W2161567465 created "2016-06-24" @default.
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• W2161567465 date "1999-11-01" @default.
• W2161567465 modified "2023-09-27" @default.
• W2161567465 title "Nutritionally Induced Insulin Resistance and Receptor Defect Leading to beta-Cell Failure in Animal Models" @default.
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• W2161567465 doi "https://doi.org/10.1111/j.1749-6632.1999.tb07798.x" @default.
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