Estradiol Determine Liver Lipid Deposition in Ratsfed Standard Diets Unbalanced with Excess Lipid or Protein
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The ingestion of excess fat often produces an increased body weight, because of higher adiposity and accumulation of fat in the liver. However, modulation of diet energy partition may affect differently the body metabolic responses and the extent of lipid deposition. Ten-week-old male and female rats were fed with either standard rat chow (SD), standard diet enriched with coconut oil (high-fat diet, HF), standard diet enriched with protein (high-protein diet, HP) or a self-selected “cafeteria” diet (CAF) for one month. Both HF and CAF diets provided the same lipid-derived percentage of energy (40%) HP diet protein-energy derived was twice (40%) than those of the SD diet. After the treatment, CAF groups showed significant weight increases. Hepatic lipid content also showed sex-related differences; triacylglycerol accumulation was significant in HF and CAF fed males. Cholesterol content was higher only in the CAF male group. Plasma estradiol in HF and HP males was higher than in CAF. Circulating cholesterol was inversely correlated with estradiol levels, which were proportional to lactate levels. These changes agreed with the differences found in the expression of key hepatic enzymes of lipid and energy metabolism. The protective effect of estrogens preventing excess liver lipid deposition, is also effective in males with ‘normal’ diets unbalanced by lipid or protein, but is not sufficient to protect males from the massive changes produced by a markedly obesogenic cafeteria-type diet. Estradiol protective effects are exerted at the root of energy metabolism, on the partition of substrates distributed from or entering the liver.