The significance of solute carrier group of genes in the pathogenesis and treatment of diabetic microvascular complications

K. Singh, T. Yuzvenko



Aim- To study the impact of the solute carrier group of genes on the mechanisms involved in hyperglycemia induced tissue damage and its implication on the treatment of diabetic microvascular complications.

Introduction – the estimated figure of people suffering from diabetes worldwide in 2019 was 9.3% (463 million people) and the projected estimates for 2030 is an alarming figure of approximately 578 million people [1]. Various pathological processes are responsible for the development of diabetes, the irreversible factor is the destruction of β-cells in the pancreas leading to insulin insufficiency, or other factors such as obesity and abnormal carbohydrate and fat metabolism which leads to insulin resistance and diminished tissue response to insulin. Defects in insulin secretion and insulin action frequently coexist in diabetics [2].

The damaging effects of hyperglycemia are classified into microvascular complications - diabetic retinopathy, neuropathy and nephropathy, and macrovascular complications - coronary artery disease, peripheral artery disease and stroke [3]. The effects of hyperglycemia are not seen in all cells of the body, but are distinct only in certain types of cells: neurons and Schwann cells in peripheral nerves, capillary endothelial cells, mesengeal cells in the renal glomerulus due to their inability to effectively maintain a constant level of glucose, in contrast most cells are able to reduce the transport of glucose when exposed to hyperglycemia [4, 5, 6].


solute carrier family; transketolase; PPP; thiamine transporter; diabetic peripheral neuropathy

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