Effects of long-term high-sucrose and dexamethasone on fat depots, liver fat, and lipid fuel fluxes through the retroperitoneal adipose tissue and splanchnic area in rats.

In affluent societies high caloric intake and chronic stress are currently associated with upper body fat. We investigated the effects of a high-sucrose (S) diet and dexamethasone (DEX) on fat depots (experiment 1) and lipid fuel fluxes (experiment 2) in male Wistar rats. In experiment 1, a liquid diet of commercial powdered milk containing 31% calories as carbohydrate or an isocaloric S diet (80% calories as carbohydrate) was offered to male rats. One half of the rats on each diet received a daily dose of 3 microg DEX in their diet. Intake was measured daily and body weight 3 times a week. Rats were killed after 7 weeks, and fat depot weights and carcass lipid were determined. In a second experiment, other rats received only the S diet with or without DEX. After 7 weeks, under pentobarbital anesthesia, arterial, portal, and iliolumbar vein blood was drawn, and the liver was extracted. Plasma concentration of triacylglycerides (TAG), nonesterified fatty acids (NEFA), glycerol (GOL), and lactate (L) and liver TAG were measured. Rats on the S diet ingested less and gained less weight. DEX treatment significantly reduced body weight gain. All fat depots as percentage of body weight were increased only in the S-DEX group. The S-DEX group had more liver TAG and less arterial NEFA and GOL than the S group. TAG determinations showed unexpected results: portal levels in the S-DEX group and iliolumbar levels in both groups were significantly higher than in the arterial plasma. This fact, together with high NEFA/GOL ratios in these veins, may signify incomplete TAG hydrolysis by lipoprotein lipase. L levels were higher in the S-DEX group and higher in arterial versus venous blood in both groups, indicating L uptake both in the splanchnic area and the retroperitoneal fat. These results show that, in rats, a long-term high-sucrose diet has peculiar effects on L turnover, and when associated with DEX, it also increases fat depots, induces liver steatosis, and, presumably, inhibits complete hydrolysis of TAG by lipoprotein lipase (LPL).