Insulin resistance, hypertension and microalbuminuria in patients with type 2 (non-insulin-dependent) diabetes mellitus

• Published in: Diabetologia Vol. 36; no. 7; p. 642
• Main Authors: Groop, L, Ekstrand, A, Forsblom, C, Widén, E, Groop, P H, Teppo, A M, Eriksson, J
• Format: Journal Article
• Language: English
• Published: Germany 01.07.1993
• Subjects: Albuminuria; Blood Glucose - analysis; Blood Pressure; Body Mass Index; C-Peptide - blood; Cholesterol - blood; Cholesterol, HDL - blood; Diabetes Mellitus, Type 2 - blood; Diabetes Mellitus, Type 2 - physiopathology; Diabetes Mellitus, Type 2 - urine; Diabetic Angiopathies - blood; Diabetic Angiopathies - physiopathology; Diabetic Angiopathies - urine; Fasting; Fatty Acids, Nonesterified - blood; Glucagon; Glucose - metabolism; Glycated Hemoglobin A - analysis; Humans; Hypertension - blood; Hypertension - physiopathology; Hypertension - urine; Insulin - blood; Insulin Resistance; Lipids - blood; Liver - metabolism; Middle Aged; Reference Values; Triglycerides - blood
• ISSN: 0012-186X
• DOI: 10.1007/BF00404074

We examined the impact of hypertension and microalbuminuria on insulin sensitivity in patients with Type 2 (non-insulin-dependent) diabetes mellitus using the euglycaemic insulin clamp technique in 52 Type 2 diabetic patients and in 19 healthy control subjects. Twenty-five diabetic patients had hypertension and 19 had microalbuminuria. Hypertension per se was associated with a 27% reduction in the rate of total glucose metabolism and a 40% reduction in the rate of non-oxidative glucose metabolism compared with normotensive Type 2 diabetic patients (both p < 0.001). Glucose metabolism was also impaired in normotensive microalbuminuric patients compared with normotensive normoalbuminuric patients (29.4 +/- 2.2 vs 40.5 +/- 2.8 mumol.kg lean body mass-1.min-1; p = 0.012), primarily due to a reduction in non-oxidative glucose metabolism (12.7 +/- 2.9 vs 21.1 +/- 2.6 mumol.kg lean body mass-1.min-1; p = 0.06). In a factorial ANOVA design, however, only hypertension (p = 0.008) and the combination of hypertension and microalbuminuria (p = 0.030) were significantly associated with the rate of glucose metabolism. The highest triglyceride and lowest HDL cholesterol concentrations were observed in Type 2 diabetic patients with both hypertension and microalbuminuria. Of note, glucose metabolism was indistinguishable from that in control subjects in Type 2 diabetic patients without hypertension and microalbuminuria (40.5 +/- 2.8 vs 44.4 +/- 2.8 mumol.kg lean body mass-1.min-1). We conclude that insulin resistance in Type 2 diabetes is predominantly associated with either hypertension or microalbuminuria or with both.