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Figure 2 Pathophysiology of hyperglycaemia in T2DM

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1 Figure 2 Pathophysiology of hyperglycaemia in T2DM
Figure 2 | Pathophysiology of hyperglycaemia in T2DM. Insulin secretion from the β-cells in the pancreas normally reduces glucose output by the liver and increases glucose uptake by skeletal muscle and adipose tissue. Once β-cell dysfunction in the pancreas and/or insulin resistance in the liver, skeletal muscle or adipose tissue occur, hyperglycaemia develops, leading to an excessive amount of glucose circulating in the blood. The various factors listed at the top affect insulin secretion and insulin action. T2DM, type 2 diabetes mellitus. Zheng, Y. et al. (2017) Global aetiology and epidemiology of type 2 diabetes mellitus and its complications Nat. Rev. Endocrinol. doi: /nrendo


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