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(Diabetes Mellitus)

- 2-7% (30% !)(~ 220 . ; ~220 . ) ( ) (N0 5 )

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I 95% (; I) (; II)MODY - Maturity-Onset Diabetes of the Youth ( )II 5%

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; - (7, 12 20) - ( II)

1 kg 5%

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- >7 mmol/l, >11.1 mmol/l 7-11.1 mmol/l, TT (75 g ) >7.8 mmol/l (>6.1*)

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***Insulin actions in peripheral tissues. Protein phosphorylation is required to mediate insulin action. After receptor autophosphorylation, the subunit becomes active as a tyrosine-specific kinase and catalyzes phosphorylation of several intracellular proteins. This event promotes the multifaceted actions of insulin. Insulin stimulates glucose turnover by favoring its transport across the plasma membrane followed either by oxidative or nonoxidative disposal, the latter being associated with glycogen synthesis. The effect of insulin on glucose transport is observed only in skeletal muscle, adipose cells, and heart. Insulin promotes protein synthesis in almost all tissues by virtue of a combined effect on gene transcription, messenger RNA translation, and amino acid uptake. Insulin also has a mitogenic effect that is mediated through increased DNA synthesis and prevention of programmed cell death, or apoptosis. In addition, insulin stimulates ion transport across the plasma membrane of multiple tissues. Finally, insulin stimulates lipid synthesis in fat cells, skeletal muscle, and liver while preventing lipolysis by inhibiting hormone-sensitive lipase. There is increasing evidence for a direct role of insulin, acting through the insulin or insulin-like growth factor (IGF) receptors, to regulate pancreatic -cell growth, survival, and insulin release from the pancreatic cells [],[]. Different tissues are known to respond differently to insulin. While tissue sensitivity to insulin correlates with the levels of insulin receptors expressed on the plasma membrane, it is clear that the assembly of different components of the insulin signaling pathway also confers specificity of insulin signaling on target cells. Thus, insulin-dependent glucose transport is only observed in skeletal muscle and adipose cells because these cells possess the insulin-dependent glucose transporter GLUT4. Likewise, the effect of insulin to inhibit gluconeo-genesis is specific to liver and kidney. In contrast, the effects on gene expression and protein synthesis might be ubiquitous.

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