Insulin’s actions on plasma free fatty acids are normal in patients with stage 2 to 3 chronic kidney disease

Abstract

Resistance to insulin’s action to suppress plasma nonesterified fatty acids (NEFA) is implicated in the hypertension and hyperlipidemia characterizing the metabolic syndrome. It is unknown whether insulin resistance to NEFA suppression is linked to hypertension and dyslipidemia in patients with mild chronic kidney disease (CKD). Eight patients with nonnephrotic, nondiabetic stage 2 to 3 CKD (I 125–iothalamate clearances of 56 ± 6 mL/min) and 7 hypertensive (HT) and 8 normotensive (NT) subjects with normal kidney function matched for age, gender, race, and percent body fat were studied. Plasma oleate, linoleate, palmitate, and stearate were measured during a 2–stage euglycemic hyperinsulinemic clamp procedure. Insulin suppressed plasma linoleate and oleate similarly in CKD (81%, 84%) and NT subjects (84%, 85%, respectively; P = NS) but less in HT patients (67%, 70%, P < .05 vs. CKD and NT). Likewise, the sum of NEFA were equally suppressed in the CKD and NT groups ( P = NS) but not in HT subjects ( P < .01 both vs. CKD and NT). Percent body fat correlated highly with NEFA suppression in the CKD and NT groups but not in HT subjects. Impairment of insulin’s antilipolytic actions is not involved in the early pathogenesis of dyslipidemia and hypertension in patients with mild to moderated renal dysfunction.