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Stimulatory effect of insulin on renal proximal tubule sodium transport is preserved in type 2 diabetes with nephropathy
Ist Teil von
Biochemical and biophysical research communications, 2015-05, Vol.461 (1), p.154-158
Ort / Verlag
United States: Elsevier Inc
Erscheinungsjahr
2015
Link zum Volltext
Quelle
MEDLINE
Beschreibungen/Notizen
Our previous study indicates that hyperinsulinemia in metabolic syndrome in the absence of nephropathy may promote hypertension by stimulating renal proximal tubule (PT) sodium transport via insulin receptor substrate (IRS) 2/phosphoinositide 3-kinase pathway. In the present study we showed that the stimulatory effect of insulin on the Na+-HCO3- cotransporter NBCe1 in isolated PTs was completely preserved in type 2 diabetic rats with overt nephropathy. Furthermore, the IRS2 expression and insulin-induced Akt phosphorylation in kidney cortex were preserved in these rats. By contrast, the IRS1 expression in kidney cortex was markedly reduced, which might be relevant to enhanced renal gluconeogenesis consistently reported in diabetes. The stimulatory effect of insulin on NBCe1 was preserved also in a human type 2 diabetic patient with advanced nephropathy. These results revealed that insulin can stimulate PT sodium transport even in type 2 diabetes with overt nephropathy. In addition to hypoglycemia, insulin-induced renal sodium retention might also play a role in increased cardiovascular risk associated with intensive glycemic control in type 2 diabetic patients with nephropathy.
•Insulin stimulates Na–HCO3 cotransporter NBCe1 in diabetic nephropathy.•The expression of IRS1 but not IRS2 is reduced in diabetic nephropathy.•High doses of insulin may cause sodium retention in diabetic nephropathy.