Fenofibrate And Pioglitazone On Liver Fat Deposition And Insulin Resistance Study Of The Mechanism Of Action

Part Ⅰ Effect of fenofibrate and pioglitazone on energyhomeostasis and adipose distribution in high fat-fedand high starch-fed SD ratsObjective: To investigate effect of PPAR a and y agonists on energy homeostasis and adipose distribution in high fat-fed and high starch-fed SD rats.Methods: PPAR a agonist fenofibrate and PPAR y agonist pioglitazonewere administrated 8 — 10 weeks to SD rats which were simultaneously induced with high fat-feeding or high starch-feeding to insulin resistance model. Then body weight change, food intake, feed efficiency and adipose distribution were compared.Results: High fat-feeding and high starch-feeding increased FBG, TG, TCand FFA, decreased plasma level of adiponectin. Fenofibrate and pioglitazone protected metabolic homeostasis from influence of high fat-feeding and high starch-feeding on FBG and lipid. In addition they raise the level of adiponectin. Fenofibrate decreased food intake and body weight gain but pioglitazone increased food intake and body weight gain than diet-matched vehicle-treated rats. PPAR y agonist increased feed efficiency, whereas PPAR a agonist treatment decreased feed efficiency. The tendency toincrease the ratio of subcutaneous fat volume to visceral fat volume evaluated by CT scan was shown in pioglitazone-treated groups.Conclusions: High fat-feeding and high starch-feeding influence glucoseand lipid metabolism. Fenofibrate and pioglitazone inhibited those influences. Fenofibrate may mediate negative energy balance, whereas pioglitazone may favor positive energy balance and subcutaneous fat distribution.