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1 Department of Kinesiology, University of Montreal, Montreal, Quebec, Canada
2 Department of Pathology and Cellular Biology, University of Montreal, Montreal, Quebec, Canada
* To whom correspondence should be addressed. E-mail: jean-marc.lavoie{at}umontreal.ca.
The purpose of the present study was to assess the effect of an exercise training programme conducted concurrently with a high-fat diet regimen on the induction of hepatic steatosis. A novel tool was used to histologically quantify the accumulation of fat within hepatocytes, in terms of number and size of lipid vacuoles and, hence, to determine the type of steatosis (macrovesicular (> 1 um2 of surface area) and/or microvesicular (< 1 um2 of surface area). Two groups of rats were either fed a standard (SD) or a high-fat (HF; 40% kcal) diet for eight weeks and were additionally assigned either to a sedentary (SED) or a treadmill-trained (TR) group. Training (5 days/wk) was initiated at the same time of the high-fat diet and was progressively increased reaching 60 min at 26 m/min, 10% grade, for the last 4 weeks. Liver lipid infiltration was histologically quantified using an image analysis computing system (Northern Eclipse, Empix Imaging Inc.). At the end of the 8-wk period, HF-SED rats exhibited ~72% higher liver triacylglycerol concentration than SD-SED rats (X ± SE: 17.15 ± 1.5 vs 9.98 ± 1.0 mg/g; P < 0.01). Histological analysis revealed that although fat was mainly stored as microvesicles, the high-fat diet-induced hepatic steatosis occurred via the accumulation of macrovesicles. Concurrent exercise training completely prevented the high-fat diet-induced hepatic steatosis. The surface area of liver parenchyma infiltrated by lipid vacuoles was similar in HF-TR than in SD-SED rats (26.4 ± 1.8 vs 29.3 ± 5.9 x 103 µm2 / 200,000 µm2 of liver parenchyma; respectively; P > 0.05). The resorption of hepatic steatosis with training was mainly macrovesicular. The different states of liver lipid infiltration following the high-fat diet in SED and TR rats were associated with similar changes in plasma non-esterified fatty acids and glycerol, as well as with similar changes in fat pads weights but not with plasma triacylglycerol levels. It is concluded that following a high-fat diet regimen of eight weeks in rats, hepatic steatosis occurs primarily via the accumulation of lipid as macrovesicles. Exercise training pursued at the same time completely prevents the high-fat diet-induced macrovesicular hepatic steatosis.
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