Mentor: Paul Harding, Ph.D.

Over one-half of the global population is expected to be obese by 2030 [1]. Obesity is a physically and psychologically debilitating cycle that is positively correlated with depression symptoms and incidental depression, implying that further weight gain will only worsen symptoms [2]. These sorts of mental health implications further the notion that obesity is not only a physically debilitating condition, but a psychological one as well. While causes of obesity and excessive weight gain may vary, the symptoms and biological markers are rather consistent. Grossly excess white adipose tissue composition is the primary factor relating to the function and potential remedial effects of BAT reprogramming [3]. Furthermore, hypertension, inflammation, and insulin resistance should be noted as telling symptoms associated with obesity. Brown adipocytes are known to host an increased number of mitochondria, especially relative to white adipocytes [4]. The function of the mitochondria in this instance varies slightly from their “quintessential'' function, as these organelles operate to produce heat via non-shivering thermogenesis. Attenuation of ATP synthesis is due to a principal gene, uncoupling protein 1 (UCP-1), one whose products dissipate the coordination of the electron transport chain [5]. By rerouting protons through a channel alternative to ATP synthase, energy produced via oxidative phosphorylation is dissipated as heat as opposed to generating ATP. Furthermore, BAT activity is stimulated by cold temperatures and norepinephrine [6]. Our lab has previously demonstrated that co-expression of HB-EGF and ADAM 12S in mammalian cells results in reprogramming of the cells into brown adipose tissue (BAT)-like cells. Reprogramming white adipose tissue (WAT) into BAT-like cells may serve as a potential combatant for obesity and type II diabetes.

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