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1 Department of Internal Medicine, Division of Endocrinology, Metabolism and Nutrition, Mayo Clinic & Foundation, Rochester, MN, USA
2 Department of Anesthesia, Division of Research, Mayo Clinic & Foundation, Rochester, MN, USA
* To whom correspondence should be addressed. E-mail: rizza.robert{at}mayo.edu.
To determine whether in the presence of constant insulin concentrations, a change in glucose concentrations results in a reciprocal change in endogenous glucose production (EGP), glucagon (~130 ng/L) and insulin (~65 pmol/L) were maintained at constant "basal" concentrations while glucose clamped at ~5.3 mM (euglycemia), ~7.0 mM (sustained hyperglycemia; n=10) or varied to create a "post-prandial" profile (profile; n=11). EGP fell slowly over the 6 hrs of the euglycemia study. In contrast, an increase in glucose to 7.13 ± 0.3 mmol/L resulted in prompt and sustained suppression of EGP to 9.65 ± 1.21 µmol/kg/min. On the profile study day, glucose increased to a peak 11.2 ± 0.5 mmol/L and EGP decreased to a nadir of 6.79 ± 2.54 µmol/kg/min by 60 minutes. Thereafter, the fall in glucose was accompanied by a reciprocal rise in EGP to rates that did not differ from those observed on the euglycemic study day (11.31 ± 2.45 vs. 12.11 ± 3.21 µmol/kg/min). Although the pattern of change of glucose differed markedly on the sustained hyperglycemia and profile study days, by design, the area above basal did not. This resulted in equivalent suppression of EGP below basal (-1952 ± 204 vs. -1922 ± 246 mmol/kg per 6 hrs). These data demonstrate that in the presence of constant basal insulin concentration, changes in glucose within the physiologic range, rapidly and reciprocally regulate EGP.
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