Key result
Inactivation of growth hormone action in liver IGF-1-deficient mice via a growth hormone antagonist transgene restored insulin sensitivity, increasing the glucose infusion rate during clamping to 291 µmol/kg/min compared to 109 µmol/kg/min in LID mice.
Why the study?
Does inactivation of growth hormone action improve insulin sensitivity in liver IGF-1-deficient mice?
Does inactivation of growth hormone action improve insulin sensitivity in liver IGF-1-deficient mice?
Absolute Event Rate: 291% vs 109%
p-value: p=<0.05
Inactivating growth hormone action improves insulin sensitivity in liver IGF-1-deficient mice, suggesting that chronic elevation of growth hormone plays a major role in insulin resistance.
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No immediate clinical implications; leaves open translation of GH antagonism benefits to human insulin resistance.
Yakar et al. (2004) studied Insulin resistance in liver IGF-1 deficiency. Growth hormone antagonist (GHa) transgene vs. LID mice (without GHa) and control mice was evaluated on Glucose infusion rate during hyperinsulinemic-euglycemic clamp (µmol/kg/min) (p=<0.05). Inactivation of growth hormone action in liver IGF-1-deficient mice via a growth hormone antagonist transgene restored insulin sensitivity, increasing the glucose infusion rate during clamping to 291 µmol/kg/min compared to 109 µmol/kg/min in LID mice.
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