Increased beta-cell secretory capacity as mechanism for islet adaptation to nicotinic acid-induced insulin resistance.

摘要: To determine whether prolonged nicotinic acid (NA) administration produces insulin resistance and, if so, how the normal pancreatic islet adapts to resistance, we administered incremental doses of NA 11 men for 2 wk, ending at g/day. Insulin sensitivity was measured with Bergman's minimal model. Islet function evaluated by measurement acute (AIR) and glucagon (AGR) responses arginine three glucose levels. demonstrated quantified a marked drop in index (Sl) from 6.72 +/- 0.77 2.47 0.36 x 10(-5) min-1/pM (P less than .0001) resulted doubling basal immunoreactive levels (from 75 7 157 21 pM, P .001) no change fasting (5.5 0.1 vs. 5.7 mM). Proinsulin also increased 9 1 15 .005), but ratio proinsulin did not (12.7 1.9 10.3 1.9%). beta-Cell changes were characterized increases AIR 548 829 .005) level 431 54 788 164 .05). At maximal hyperglycemia represents beta-cell secretory capacity, this 2062 267 2630 363 .05).(ABSTRACT TRUNCATED AT 250 WORDS)