By Aresh J. Anwar MD, MRCP, Anthony H. Barnett MD, FRCP, Sudhesh Kumar MD, FRCP (auth.), Michael T. Johnstone MD, CM, FRCP(C), Aristidis Veves MD, DSC (eds.)
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Nature 1994;372:425-432. 90. Halaas JL, Gajiwala KS, Maffei M, et al. Weight reducing effects of the plasma protein encoded by the obese gene. ScienceI995;269:543-546. 91. Stephens TW, Basinski M, Bristow PK, et al. The role of neuropeptide Y in the antiobesity action of the obese gene product. Nature 1995;377:530-532. 22 Anwar, Barnett, and Kumar 92. Erickson JC, Clegg KE, Palmiter RD. Attenuation of the obesity syndrome of ob/ob mice by loss of neuropeptide Y. Science1996;274: 1704-1707. 93. Shimabukuro M, Koyama K, Chen G, et al.
Fractional sodium excretion fell by 20-30% in response to euglycemic hyperinsulinemia with insulin levels of 50-60 IlU/mL, well in the physiologic range. Reductions in potassium and uric acid excretion in response to insulin were of similar magnitude (31). Based on animal studies (32), it was thought that insulin exerts the antinatriuretic effect at the level of the distal tubule, where the highest density of insulin receptors is found, but it may be that the proximal tubule is the more likely site of insulin's antinatriuretic action in humans (33).
Heart rate was also found to rise in a dose-dependent fashion in response to hyperinsulinemia in type 2 diabetics. Since stroke volume and heart rate did not change in our obese group (Fig. 3C), cardiac output did not change either. However, other studies report a significant 15% increment in obesity (69). In type 2 diabetes, data on changes in cardiac output in response to hyperinsulinemia are not available. Nevertheless, since heart rate has been reported to increase in diabetics in response to hyperinsulinemia, it is reasonable to assume that cardiac output may increase as well.