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Treatment with a glucagon-like peptide-1 receptor agonist exenatide decreases albuminuria in overweight type 2 diabetic patients

There is evidence from animal studies that glucagon-like peptide-1 (GLP-1) receptor agonist exenatide exert protective role in diabetic nephropathy with mechanisms that seem to be independent of their glucose-lowering effect. The aim of this study was to investigate effects of exenatide therapy on renal function parameters in overweight T2DM. A total of 43 overweight T2DM with normal, mildly or moderate decreased (estimated GFR > 30 mlmin-11.73m2) renal function were included in this study and followed for 22 months (age 57±7 years, 22M/21F, body mass index (BMI) 36.4±5.1 kg/m2, weight 114±18 kg, HbA1c 8.6±1.2%, duration of diabetes 11±6 years, serum creatinine 74±23 umol/L, estimated GFR 89±18 mlmin-11.73m2, urinary albumin excretion rate (UAE) 19.5 (2.5-2455.2 mg/24h). UAE was measured from at least two 24-h urine samples. Estimated GFR was calculated using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) formula. Treatment with exenatide caused, as expected, a significant decrease in HbA1c from 8.6±1.2 to 8.0±1.3% (p=0.01), BMI from 38±5 to 36±5 kg/m2 (p<0.001), weight from 114±18 to 106±18 kg (p<0.001), and in waist circumference from 119±12 to 115±11 cm (p<0.001). However, the 22- month administration of exenatide caused a significant decrease in UAE from 19.5 (2.5-2455.2) to 17.2 (3.4-1851.2) mg/24h (p=0.02), while serum creatinine (from 74±23 to 73±23 umol/L (p=0.1)) and estimated GFR (from 89±18 to 90±17 mlmin- 11.73m2 (p=0.2)) did not significantly changed. The results of our study suggest that therapy with exenatide may significantly reduce UAE in overweight T2DM. It has been suggested that exenatide protective action in glomerular endothelial cells is partly mediated via its own receptor by the activation of protein kinase A. However, the exact mechanisms need to be further explored.

type 2 diabetes; glucagon-like peptide-1; renal function; albuminuria

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