Key result
Short-term, sustained euglycemic hyperinsulinemia in rats increased abdominal skeletal muscle blood flow (0.11 vs. 0.05 mL/min/g; p<0.02) but had no effect on cardiac output or splanchnic circulation.
Why the study?
Does sustained euglycemic hyperinsulinemia alter systemic and splanchnic hemodynamics in male rats?
Does sustained euglycemic hyperinsulinemia alter systemic and splanchnic hemodynamics in male rats?
Absolute Event Rate: 0.11% vs 0.05%
p-value: p=<0.02
Short-term sustained euglycemic hyperinsulinemia in rats increases skeletal muscle blood flow without affecting cardiac output or splanchnic hemodynamics.
May warrant caution against extrapolating rat muscle flow data to humans; leaves open translation of insulin's regional hemodynamic effects.
Insulin, in addition to its metabolic function, was found to induce skeletal muscle vasodilatation after acute administration. The vasoactive effects of sustained euglycemic hyperinsulinemia, especially in the splanchnic circulation, are less well known. The aim of this study was to evaluate the systemic and splanchnic hemodynamic effects of sustained euglycemic hyperinsulinemia. Hyperinsulinemia was induced by a sustained-release insulin implant in the scurf area of male rats (release rate -1 U/day). Beginning on the 3rd day, the study group was fed a glucose-rich diet. Hemodynamic studies were performed on the 5th day using the radioactive microsphere technique. Serum insulin was measured by radioimmunoassay. At the time of the hemodynamic measurements, plasma insulin level was higher in the insulin-treated (n=8) compared to control rats (n=8) (23.6 +/- 4.7 vs. 13.2+/-3.9 microu/mL, respectively; p<0.001). Plasma glucose level of the two groups was similar (5.43 +/- 1.07 vs. 5.83 +/- 1.44 mmol/L, respectively). Abdominal skeletal muscle blood flow was higher in the insulin-treated group (0.11 +/- 0.05 vs. 0.05 +/- 0.04 mL x min(-1) x g(-1), respectively; p<0.02). No significant changes were observed in cardiac output and renal blood flow. In the splanchnic circulation: stomach, pancreatic, intestinal, splenic, hepatic arterial and total hepatic blood flow were also not significantly different. In summary, short-term, sustained euglycemic hyperinsulinemia in rats increased blood flow to skeletal muscle but had no hemodynamic effects on cardiac output or splanchnic circulation.
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Hilzenrat et al. (2001) studied Healthy (n=16). Sustained euglycemic hyperinsulinemia (insulin implant + glucose-rich diet) vs. Control was evaluated on Abdominal skeletal muscle blood flow (mL x min(-1) x g(-1)) (p=<0.02). Short-term, sustained euglycemic hyperinsulinemia in rats increased abdominal skeletal muscle blood flow (0.11 vs. 0.05 mL/min/g; p<0.02) but had no effect on cardiac output or splanchnic circulation.
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