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The effect of surgical stress on insulin sensitivity, glucose effectiveness and acute insulin response to glucose load

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Abstract

Hyperglycemia after stress is a very common clinical phenomenon. It is generally hypothesized that the underlying cause is a neuroendocrine-mediated deterioration in glucose metabolism. However, the detailed roles of insulin sensitivity, glucose effectiveness and acute insulin response to glucose load in response to stress have not been well established. Hernioplasty was used as a minor stress model for studying stressinduced hyperglycemia. Eleven healthy young men were enrolled voluntarily in this study. Their mean age was 22.0±0.9 yr and BMI 23.3±0.6 kg/m2. Frequently sampled iv glucose tolerance tests were performed one day before and one day after the surgery. Insulin sensitivity (SI), glucose effectiveness (EG) and area under acute insulin response (AIR) were calculated from “minimal model“ algorithms. We also measured fasting concentrations of human GH, ACTH and F on the days of the test.

Compared to the pre-operation data, levels of ACTH and F did not change significantly after the surgery. Only GH levels were marginally significant. On the other hand, the SI (0.75±0.1, 0.52±0.9x10−5 min-1/pmol, p=0.04), EG (0.023±0.03, 0.016±0.003 min-1, p=0.01) and AIR (6738.5±1111.6, 5130.0±1047.2 pmol, p=0.005) were all significantly decreased after surgery. The percentages of decrease were 16.3±15.5, 32.1±10.3 and 17.8±10.3%, respectively. Finally, only the changes of EG positively correlate with the changes of ACTH before and after surgery. No significant changes were noted among other stress hormones and the changes of SI, EG and AIR. In conclusion, hernioplasty results in reduced SI, EG and AIR. Among them, although not statistically significant, the EG showed the most distinct decrease after the surgery, which has not been found in previous literature.

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Pei, D., Chen, TW., Kuo, YL. et al. The effect of surgical stress on insulin sensitivity, glucose effectiveness and acute insulin response to glucose load. J Endocrinol Invest 26, 397–402 (2003). https://doi.org/10.1007/BF03345193

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