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Postprandial metabolism in health and type 2 diabetes

hisulin resistance is a characteristic halhnark of type 2 diabetes and contributes to impaked glucose disposal and utilization in insulin-sensitive tissues (liver, skeletal muscle and fat) and inadequate suppression of postprandial hyperglycaemia. Elevated hepatic and intramuscular triglyceride (TG) content in type 2 diabetes has been postulated to underpin the insulin resistance seen in each of these issues. The reasons for this increased tissue TG content is poorly understood. Reduction in liver TG content with weight loss normalizes basal rates of EGP. Likewise peroxisome proliferator activated receptor-7 agonists (PPAR-y) and peroxisome proliferator activated receptor-a agonists (PPAR-a) also decrease liver TG content, but their effects on EGP is unclear. A mutation in PPP1R3A, the gene encoding muscle-specific glycogen-regulating subunit, a key regulator of muscle glycogen metabolism has recently been reported. The physiological implication of this genetic variant on human muscle glycogen metabolism is unknown.

Identiferoai:union.ndltd.org:bl.uk/oai:ethos.bl.uk:500958
Date January 2008
CreatorsBalasubramanian, Ravikumar
PublisherUniversity of Newcastle Upon Tyne
Source SetsEthos UK
Detected LanguageEnglish
TypeElectronic Thesis or Dissertation

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