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

Abstract

Summary.We examined the impact of hypertension and microalbuminuria on insulin sensitivity in patients with Type 2 (non-insttlin-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 gmol. kg lean body mass -1. min-t; p = 0.012), primarily due to a reduction in non-oxidative glucose metabolism (12.7+2.9 vs 21.1+2.6btmol.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 gmol. kg lean body mass -1. rain 1). We conclude that insulin resistance in Type 2 diabetes is predominantly associated with either hypertension or microalbuminuria or with both.

Rosiglitazone enhances glucose uptake in glomerular podocytes using the glucose transporter GLUT1

“…Rosiglitazone increased glucose uptake in podocytes treated with palmitate Palmitate is the predominant circulating saturated fatty acid and it is increased in insulinresistant states such as type 2 diabetes [33]. We used palmitate to induce insulin resistance in podocytes.…”

Dissociation between albuminuria and insulinaemia in hypertensive and atherosclerotic men

“…22 Even in mechanistic experiments, 10-fold acute increments in circulating insulin left albumin excretion unchanged in normal subjects, 9 although acute or chronic hyperinsulinaemia might still behave differently in essential hypertensive subjects, for example by interacting specifically with other factors active on glomerular haemodynamics or permeability (eg, catecholamines, angiotensin II, glucagon, protein diet, sodium balance). Moreover, our negative conclusions cannot exclude that, as both in diabetic 23 and non-diabetic subjects, 16,19 renal excretion of albumin might be elevated in the presence of a greater degree of insulin resistance, perhaps because of its association with higher BP levels. 10 In fact, an exaggerated insulin response and lower tolerance to glucose load, somewhat increased body weight and hypertriglyceridaemia-in itself suggestive of insulin resistance 24 -characterised our patients.…”

Coronary artery disease, microalbuminuria and lipid profile in patients with non-insulin dependent diabetes mellitus

“…In the lipid analysis we did not use the criteria recommended by the Brazilian Consensus on Lipid Disorders 36 , since those criteria were not based on the Brazilian diabetic population. In our group the prevalence of hypertriglyceridemia and low HDL levels was similar to that reported in the literature 37,38 .…”