Risk and mechanism of dexamethasone-induced deterioration of glucose tolerance in non-diabetic first-degree relatives of NIDDM patients

摘要: We tested the hypothesis that glucose intolerance develops in genetically prone subjects when exogenous insulin resistance is induced by dexamethasone (dex) and investigated whether steroid-induced due to impairment of beta-cell function alone and/or resistance. Oral tolerance (OGTT) intravenous tests with minimal model analysis were performed before following 5 days dex treatment (4 mg/day) 20 relatives non-insulin-dependent diabetic (NIDDM) patients matched control (age: 29.6 +/- 1.7 vs 1.6 years, BMI: 25.1 1.0 0.9 kg/m2). Before dex, was similar both groups (2-h plasma concentration (PG): 5.5 0.2 [range: 3.2-7.0] [3.7-7.4] mmol/l). Although sensitivity (Si) significantly lower reduced a level during (0.30 0.04 0.34 10(-4) min(-1) per pmol/l, NS). During variation OGTT 2-h PG greater (8.5 0.7 [3.9-17.0] 7.5 0.3 [5.7-9.8] mmol/l, F-test p < 0.05) which, inspection data, caused seven higher than maximal value seen (9.8 These "hyperglycaemic" had diminished first phase secretion (O1) compared "normal" (pre-dex O1: 12.6 3.6 26.4 4.2 24.6 (p 0.05), post-dex 22.2 6.6 48.0 7.2 46.2 respectively pmol x l(-1) mg/dl). However, Si (0.65 0.10 0.54 pmol/l) suppressed similarly 0.07 0.30 0.06 pmol/l). Multiple regression confirmed unique importance low pre-dex subsequent development high levels (R2 = 0.56). In conclusion, will induce impaired or those genetic NIDDM who have (retrospectively) prior exposure. are therefore unable enhance their response order match dex-induced resistant state.