DEXAMETHASONE-INDUCED INSULIN RESISTANCE ENHANCES B-CELL RESPONSIVENESS TO GLUCOSE LEVEL IN NORMAL MEN
DEXAMETHASONE-INDUCED INSULIN RESISTANCE ENHANCES B-CELL RESPONSIVENESS TO GLUCOSE LEVEL IN NORMAL MEN
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DOI:
10.1152/ajpendo.1984.247.5.e592
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发表时间:
1984-01-01
影响因子:
--
通讯作者:
PORTE, D
中科院分区:
文献类型:
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作者:
BEARD, JC;HALTER, JB;PORTE, D
To determine whether islet adaptation during insulin resistance involves incresaed responsiveness to the level of plasma glucose, insulin resistance was induced in 9 normal men by giving dexamethasone (Dex) (3 mg twice daily for 2 days). Plasma insulin and acute insulin responses (AIR) to isoproterenol were measured at 3 different glucose levels under control and Dex conditions. During Dex there were elevations above control levels of basal glucose (104 .+-. 2 vs. 94 .+-. 3 mg/dl) and insulin (21 .+-. 3 vs. 13 .+-. 2 .mu.U/ml, both P < 0.03). When glucose levels were raised stepwise by matching amounts using glucose clamps, AIR to isoproterenol rose as a linear function of glucose level under both conditions but rose more steeply during DEX. The potentiating effect of glucose (.DELTA.AIR/.DELTA.glucose) was greater during Dex: 1.3 .+-. 0.2 vs. 0.8 .+-. 0.2 (P < 0.01). Similarly, matched increments in glucose level produced greater increments in prestimulus insulin level during DEX (P < 0.03). Apparently 48 h of Dex raises the "gain" of the potentiating effect of glucose. Because the direct effect of glucocorticoids on B cell function has been reported inhibitory, the observed stimulation is likely to be a result of the insulin resistance caused by Dex.