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Meet our 2016 Locally Funded Researchers
Cynthia Hong, PhD (University of California, Los Angeles)
General Research Subject: Type 2 Diabetes
Focus: Complications, Complications\Diabetic Dyslipidemia, Complications\Macrovascular-Cellular Mechanisms of Atherogenesis in Diabetes
Research has revealed that many factors contribute to the development of diabetes. A key contributor is obesity; however, weight gain alone does not cause disease. Many diabetes patients also have atherosclerosis, yet the links between these conditions are not well understood. Epidemiology studies suggest an inverse association between lowered cholesterol levels and improved diabetic profiles, but the connection is unknown. The researchers are interested in the actions of cholesterol in fat and how cholesterol levels may be related to the development of diabetes. They identified a new mechanism for controlling cholesterol levels. In this pathway, a protein, IDOL, degrades receptors that clear cholesterol from the blood-the Low Density Lipoprotein Receptor (LDLR) and the Very Low Density Lipoprotein Receptor (VLDLR). The researchers have made mouse models that have more or less IDOL protein in their fat tissue in order to understand the importance of cholesterol content in fat to whole-body metabolism and diabetes. As predicted, preliminary analysis has confirmed that the levels of the cholesterol receptors, LDLR and VLDLR, are altered in these mice. This proposal will study cholesterol accumulation and the development of diabetes in these mouse models and endeavor to explain how cholesterol affects the function of adipose at the molecular level. Using cultured fat cells as a model system, the effects of cholesterol and IDOL on fat cell function will also be examined. Understanding the molecular mechanisms by which the IDOL pathway integrates cholesterol and triglyceride metabolism may lead to the development of novel therapeutics for diabetes.
Kathleen Page, MD (University of Southern California)
General Research Subject: Gestational Diabetes
Focus: Integrated Physiology, Integrated Physiology\Insulin Resistance, Integrated Physiology\Regulation of Food Intake, Obesity, Obesity\Pathogenesis
Children of mothers who had diabetes during pregnancy are at high risk for developing obesity and type 2 diabetes (T2DM). While the underlying mechanisms remain unclear, provocative studies in animal models suggest that fetal exposure to the altered metabolic environment of maternal diabetes leads to a reorganization of brain pathways that regulate energy homeostasis. These changes promote obesity, insulin resistance and T2DM. Analogous changes could contribute to the development of obesity and T2DM in humans. However, no studies have investigated the effects of intrauterine exposure to diabetes on brain circuitry in humans. The overall goal of this proposal is to test the hypothesis that in utero exposure to gestational diabetes mellitus (GDM) results in alterations in brain pathways involved in the regulation of energy and glucose homeostasis in humans. This proposal will use innovative neuroimaging techniques to compare brain pathways involved in the regulation of energy homeostasis between children exposed and children not exposed to GDM in utero. Through ongoing collaborative studies with Kaiser Permanente Southern California on the effects of intrauterine exposure to GDM on risk for obesity and T2DM, the investigators have access to thousands of offspring of mothers with and without a documented history of GDM. Preliminary data support findings of others demonstrating excess obesity and elevated fasting plasma glucose levels in the offspring exposed to GDM in utero. This proposal seeks to understand potential neuroendocrine mechanisms by which these intergenerational effects occur and to accelerate the development of targeted intervention strategies to prevent obesity and diabetes.