Stella Kim, PhD

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Stella Kim, PhD

In an insulin resistant state such as obesity, a reduction in insulin action due to decreased sensitivity of insulin responsive tissues is generally compensated by a rise in plasma insulin levels. This compensatory rise in the plasma concentration of insulin is essential for the maintenance of glucose homeostasis in face of chronic insulin resistance. Plasma insulin concentration is determined by pancreatic beta-cell secretion and by its clearance, which includes both first-pass hepatic and peripheral insulin uptake and degradation. Although it is often assumed that increased pancreatic secretion is largely responsible for hyperinsulinemia, previous studies in the laboratory of Stella Kim, PhD, examined both first-pass hepatic insulin extraction and insulin secretion in a longitudinal manner. It was found that changes in hepatic extraction occurred in a synchronous pattern with increased beta cell secretion during the development of insulin resistance with obesity. This suggested that decreased hepatic extraction might allow the beta-cell "rest," which may in turn preserve beta-cell function and perhaps delay or prevent the development of Type 2 diabetes. Current work of the lab is now focused on the role of hepatic insulin clearance as a primary mechanism by which insulin is upregulated during insulin resistance. It is hoped that exploiting the liver’s ability to modulate insulin levels may provide an alternate therapeutic mechanism by which insulin can be increased to offset developing insulin resistance.

  • Undergraduate: UCLA, 1998
  • Doctorate: Keck School of Medicine of USC, 2007
  • Kim SP, Ellmerer M, Kirkman EL, Bergman RN. Beta-cell "rest" accompanies reduced first-pass hepatic insulin extraction in the insulin-resistant, fat-fed canine model. Am J Physiol Endocrinol Metab. 2007;292:E1581-1589.
  • Kim SP, Catalano KJ, Hsu IR, Chiu JD, Richey JM, Bergman RN. Nocturnal free fatty acids are uniquely elevated in the longitudinal development of diet-induced insulin resistance and hyperinsulinemia. Am J Physiol Endocrinol Metab. 2007;292:E1590-1598.
  • Ader M, Stefanovski D, Kim SP, Richey JM, Ionut V, Catalano KJ, Hucking K,Ellmerer M, Van Citters G, Hsu IR, et al. Hepatic insulin clearance is the primary determinant of insulin sensitivity inthe normal dog. Obesity (Silver Spring). 2014;22(5):1238-1245.
  • Bergman RN, Stefanovski D, Kim SP. Systems analysis and the prediction and prevention of Type 2 diabetes mellitus. Curr Opin Biotechnol. 2014;28:165-170.
  • Kim SP, Woolcott OO, Hsu IR, Stefanovski D, Harrison LN, Zheng D, Lottati M, Kolka C, Catalano KJ, Chiu JD, et al. CB(1) antagonism restores hepatic insulin sensitivity without normalization of adiposity in diet-induced obese dogs. Am J Physiol Endocrinol Metab. 2012;302:E1261-1268.

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