Similar Insulin Sensitivity in NIDDM Patients With Normo- and Microalbuminuria

Abstract

OBJECTIVE To investigate whether insulin resistance and microalbuminuria are associated in non-insulin-dependent diabetes mellitus (NIDDM). RESEARCH DESIGN AND METHODS Insulin sensitivity was assessed using a hyperinsulinemic euglycemic clamp in 11 normoalbuminuric and 9 microalbuminuric NIDDM patients matched for sex, age, body composition, glycemic control, diabetes duration, and therapy. RESULTS Isotopically determined glucose disposal was similar in normo- and microalbuminuric patients in the basal state (mean ± SD; 3.30 ± 1.01 vs. 3.46 ± 0.82 mg·kg lean body mass [LBM]−1 · min−1; NS) and during hyperinsulinemia (7.16 ± 2.65 vs. 6.63 ± 2.88 mg·kg LBM−1 · min−1;NS). No difference was observed in nonoxidative glucose disposal or lipid oxidation. Endogenous glucose production was equally suppressed by insulin (−0.08 ± 0.99 vs. 0.30 ± 1.12 mg·kg−1 LBM·min−1; NS). Glucose oxidation tended to be lower in the normoalbuminuric patients in the basal state (1.16 ± 0.37 vs. 1.41 ± 0.36 mg·kg LBM· min−1) and during hyperinsulinemia (2.35 ± 0.72 vs. 2.90 ± 0.77 mg·kg LBM· min−1; both P < 0.15). Urinary albumin excretion rate correlated with the insulin-stimulated glucose oxidation rate (r = 0.59, P = 0.0064), and a similar trend was seen in the basal state (r = 0.42, P = 0.063). Protein oxidation was higher in normoalbuminuric patients (1.6 ± 0.5 vs. 1.0 ± 0.4 mg·kg LBM · min−1; P = 0.017) and correlated inversely with albuminuria (r = −0.70, P = 0.0007). Serum growth hormone increased during insulin infusion; however, the increase was significantly greater in microalbuminuric patients. Plasma lipoproteins, maximal aerobic capacity, and 24-h ambulatory blood pressure were similar in the two groups. CONCLUSIONS Basal and insulin-stimulated glucose uptakes are comparable in carefully matched normo- and microalbuminuric NIDDM patients, and glucose oxidation may be positively related to albuminuria. The inverse relation between protein oxidation and albuminuria may be due to higher growth hormone levels during daily life perturbations in glucose in microalbuminuric patients.