Anti‐adipogenic Activity of Terminalia pallida

Abstract

Obesity rates are rising globally, with 1.5 billion overweight and 500 million obese worldwide. According to The Centers for Disease Control and Prevention, almost 2/3rds of the United States population is either overweight or obese. Growing obesity rates in children and adolescents makes the obesity pandemic more alarming and solutions more critical. Further, non‐Hispanic Black and Hispanic Americans are more prone to this disease/condition, making it also a health disparity. Obesity increases the risk for insulin resistance, diabetes mellitus, dyslipidemia, hypertension, sleep apnea, cardiovascular disease and certain types of cancer (4). Only limited obesity management options are available, including behavioral interventions, lifestyle modification and invasive surgeries.New drug development remain the cornerstone of anti‐obesity research due to the limited availability of drug treatments. Further, due to reduced costs, fewer side effects and cultural significance, many are opting for complementary treatments. Terminalia pallida (TP) is one such plant that is been used ethno‐botanically to treat metabolic diseases. Hence, here we investigated the anti‐adipogenic activity of TP. We used 3T3‐L1 embryonic fibroblast‐preadipocyte cells treated with or without adipogenic cocktail (1 μM dexamethasone, 10 μg/mL insulin and 0.5 mM 3‐isobutyl 1 methylxanthine) to induce adipogenesity. We treated the 3T3‐L1 cells with various concentrations of ethanolic extract of Terminalia pallida fruit (TP‐50, 25 and 10 μg/ml) or Simvastatin (1 μM), a known anti‐lipidemic drug. Ten days post‐adipogenic induction, the adipogenic cocktail‐treated 3T3‐L1 preadipocytes differentiated into adipocytes. However, TP‐treated groups showed significant inhibition of adipocyte formation. The Simvastatin‐treated group also showed anti‐adipogenic activity, as evidenced by the reduced size and number of adipocytes. Expression of the key adipogenic markers PPARγ2 and C/EBPα was decreased in the TP‐treated group compared to untreated control. We further investigated the cellular mechanisms by which TP elicit the antiadipogenic function. Our studies conclude that TP significantly decreased proliferation and elevated apoptosis in 3T3‐L1 adipocytes, indicating that partially TP shows its anti‐adipogenic function by regulating preadipocyte and adipocyte cell cycle.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.