BACKGROUND: Microalbuminuria (MA) clusters with metabolic derangements linked to the insulin resistance syndrome, and is associated with increased risk of cardiovascular disease in both diabetes and hypertension. This study questioned if MA, reflecting endothelial damage, is directly linked to impaired insulin action. METHODS: MA was measured in two 24-hour urine samples in 84 persons with untreated hypertension recruited from a population survey (diastolic blood pressures 90 to 105 mm Hg). Thirty-one percent had MA values>20 microg/min (MA group, N = 26), and these were matched according to age, gender, and body-mass index with hypertensive persons without MA (non-MA group, N = 32) for comparison of the metabolic profile. Insulin sensitivity was measured with clamp techniques. RESULTS: The MA and non-MA groups were similar in their fasting and post-load glucose and insulin levels, in the first (930 +/- 594 vs. 1097 +/- 707 pmol/L) and second (1111 +/- 662 vs. 1163 +/- 702 pmol/L) phases of insulin release during a hyperglycemic clamp, and in their insulin sensitivity indices (0.16 +/- 0.10 vs. 0.17 +/- 0.13, P> 0.3 for all). The MA group had higher systolic blood pressure (157 +/- 13 vs. 150 +/- 12 mm Hg, P = 0.05) and a higher serum level of circulating advanced glycation end products (AGEs; 11.0 +/- 3.0 vs. 7.9 +/- 3.5 U/mL, P = 0.05) than the controls. No associations were found between MA and the insulin sensitivity index, or glucose and insulin levels. Weak associations were found with systolic blood pressure (r = 0.25, P = 0.05), AGEs (r = 0.27, P = 0.05), and smoking habits (r = 0.39, P = 0.01). CONCLUSION: In hypertension, MA is not a determinant of insulin resistance, provided confounding factors such as degree of adiposity are carefully controlled.
BACKGROUND: Microalbuminuria (MA) clusters with metabolic derangements linked to the insulin resistance syndrome, and is associated with increased risk of cardiovascular disease in both diabetes and hypertension. This study questioned if MA, reflecting endothelial damage, is directly linked to impaired insulin action. METHODS: MA was measured in two 24-hour urine samples in 84 persons with untreated hypertension recruited from a population survey (diastolic blood pressures 90 to 105 mm Hg). Thirty-one percent had MA values>20 microg/min (MA group, N = 26), and these were matched according to age, gender, and body-mass index with hypertensivepersons without MA (non-MA group, N = 32) for comparison of the metabolic profile. Insulin sensitivity was measured with clamp techniques. RESULTS: The MA and non-MA groups were similar in their fasting and post-load glucose and insulin levels, in the first (930 +/- 594 vs. 1097 +/- 707 pmol/L) and second (1111 +/- 662 vs. 1163 +/- 702 pmol/L) phases of insulin release during a hyperglycemic clamp, and in their insulin sensitivity indices (0.16 +/- 0.10 vs. 0.17 +/- 0.13, P> 0.3 for all). The MA group had higher systolic blood pressure (157 +/- 13 vs. 150 +/- 12 mm Hg, P = 0.05) and a higher serum level of circulating advanced glycation end products (AGEs; 11.0 +/- 3.0 vs. 7.9 +/- 3.5 U/mL, P = 0.05) than the controls. No associations were found between MA and the insulin sensitivity index, or glucose and insulin levels. Weak associations were found with systolic blood pressure (r = 0.25, P = 0.05), AGEs (r = 0.27, P = 0.05), and smoking habits (r = 0.39, P = 0.01). CONCLUSION: In hypertension, MA is not a determinant of insulin resistance, provided confounding factors such as degree of adiposity are carefully controlled.
Authors: A Pätäri; P Karhapää; H Taipale; U Salmenniemi; E Ruotsalainen; P Vanninen; H Holthöfer; M Laakso Journal: Diabetologia Date: 2005-07-08 Impact factor: 10.122