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Abstract: TH-PO615

Effects of Gemfibrozil on Fatty Acid Induced Insulin Resistance in Adipocytes

Session Information

Category: Health Maintenance, Nutrition, and Metabolism

  • 1301 Health Maintenance, Nutrition, and Metabolism: Basic


  • Bose, Madhura, Texas Tech University, Lubbock, Texas, United States
  • Prabhakar, Sharma S., Texas Tech University Health Sciences Center, Lubbock, Texas, United States

Hyperlipidemia, specifically hypertriglyceridemia has been incriminated in contributing to insulin resistance in diabetes. However it is unclear if correcting hypertriglyceriemia improves insulin sensitivity and prevent diabetes in the context of metabolic syndrome. We hypothesized that reduction of lipid uptake by adipocytes using gemfibrozil would improve insulin signaling and facilitate glucose transport.


Mouse 3T3-L1 preadipocytes were differentiated into adipocytes by commercial differentiation cocktail and were stimulated with fatty acids 1 mM of palmitate (C16:0), oleate (C18:1), and linoleate (C18:2) for 24 hrs on 8th day of differentiation. The fatty acid treated adipocytes were labeled as obese while the fatty acid untreated cells were labelled as lean. The obese cells were further treated with Gemfibrozil (10 µM, 25 µM, 50 µM and 100 µM) for 72 hrs. Triglyceride assay and Oil red O staining were performed to determine lipid droplet accumulation. Cell lysates were used to study expression of insulin signaling proteins by western blot analysis. For determining the expression of GLUT4, membrane fraction was separated from the cytosolic fraction.


Upon incubation with fatty acid mixture, the lipid content in adipocytes significantly increased (obese cells) compared to untreated cells (lean cells). Gemfibrozil treatment decreased triglyceride content in the obese cells in a dose dependent manner with a significant change even at the lowest concentration of 25 μM. This data was further supported by reduction in lipid droplet accumulation in the obese cells as observed by Oil Red O staining. Western blot data revealed that gemfibrozil at 25 μM decreased IRS-1 phosphorylation at Ser 307 which is significantly increased in obesity and insulin resistance. Gemfibrozil also increased Akt phosphorylation which was decreased in the obese cells. GLUT 4 expression in whole cell lysate remain unchanged but increased in the membrane fraction of treated obese cells. Moreover investigation of upstream signaling showed that gemfibrozil reduced phosphorylation of IKK-β but not JNK.


We conclude that Gemfibrozil reversed insulin resistance in obese adipocytes by modulating phosphorylation of IRS-1, Akt and IKK-β and thereby facilitated insulin signaling.These observations may have implications for prevention and treatment of diabtetes in metabolic syndrome.


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