Insulin resistance in chronic kidney disease
Insulin resistance (IR) refers to a state in which the biological effect of insulin on the target tissues is reduced. IR can be subdivided as either hepatic IR or peripheral IR. Hepatic IR is a state of impaired suppression of glucose synthesis in the liver, whereas peripheral IR refers to a reduced or blunted response to insulin in skeletal muscle or adipose tissue. As IR develops, there is a compensatory increase in the synthesis and secretion of insulin by β‐cells by the pancreatic islets, resulting in hyperinsulinaemia in order to maintain glycaemia in the normal range. However, if the secretion of insulin is inadequate, glucose intolerance with hyperglycaemia, and even type 2 diabetes, may follow.1 The function of β‐cells is to store and release insulin as well as C‐peptide. β‐cells can respond rapidly to the peaks of blood glucose levels by secreting insulin, while the concentration of C‐peptide is an estimate for the β‐cell mass. Because the β‐cell function seems to have not been greatly affected in uraemia,2 the main cause of IR in chronic kidney disease (CKD) and end‐stage renal disease (ESRD) is thought instead to be impaired by tissue insensitivity to insulin, most likely due to a post‐receptor defect in peripheral skeletal muscle.