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1 Physiology and Biophysics, Keck School of Medicine of the University of Southern California, Los Angeles, California, United States
2 Physiology and Biophysics, Keck School of Medicine of the University of Southern California, 90033, California, United States
* To whom correspondence should be addressed. E-mail: rbergman{at}usc.edu.
Obesity is strongly associated with hyperinsulinemia and insulin resistance, both primary risk factors for Type 2 diabetes. It has been thought that increased fasting free fatty acids (FFA) may be responsible for the development of insulin resistance during obesity, causing an increase in plasma glucose levels which would then signal for compensatory hyperinsulinemia. But when obesity is induced by fat-feeding in the dog model, there is development of insulin resistance and a marked increase in fasting insulin despite constant fasting FFA and glucose. Here, we examined the 24-hour plasma profiles of FFA, glucose and other hormones to observe any potential longitudinal postprandial or nocturnal alterations that could lead to both insulin resistance and compensatory hyperinsulinemia induced by a high fat diet in eight normal dogs. We found that after six weeks of a high fat, hypercaloric diet, there was development of significant insulin resistance and hyperinsulinemia as well as accumulation of both subcutaneous and visceral fat without a change in either fasting glucose or postprandial glucose. Moreover, although there was no change in fasting FFA, there was a highly significant increase in the nocturnal levels of FFA which occurred as a result of fat-feeding. Thus enhanced nocturnal FFA, but not glucose, may be responsible for development of insulin resistance and fasting hyperinsulinemia in the fat fed dog model.
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