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In the present study, the effect of long-term fructose feeding on skeletal muscle mitochondrial energetics was investigated. Measurements in isolated tissue were coupled with the determination of whole-body energy expenditure and insulin sensitivity. A significant increase in plasma NEFA, as well as in skeletal muscle TAG and ceramide, was found in fructose-fed rats compared with the controls, together with a significantly higher plasma insulin response to a glucose load, while no significant variation in plasma glucose levels was found. Significantly lower RMR values were found in fructose-fed rats starting from week 4 of the dietary treatment. Skeletal muscle mitochondrial mass and degree of coupling were found to be significantly higher in fructose-fed rats compared with the controls. Significantly higher lipid peroxidation was found in fructose-fed rats, together with a significant decrease in superoxide dismutase activity. Phosphorylated Akt levels normalised to plasma insulin levels were significantly lower in fructose-fed rats compared with the controls. In conclusion, a fructose-rich diet has a deep impact on a metabolically relevant tissue such as skeletal muscle. In this tissue, the consequences of high fructose feeding are altered glucose tolerance, elevated mitochondrial biogenesis and increased mitochondrial coupling. This latter modification could have a detrimental metabolic effect by causing oxidative stress and energy sparing that contribute to the high metabolic efficiency of fructose-fed rats.

The present study investigated the effect of 2 weeks of energy restriction on whole body, liver and skeletal muscle energy handling. We measured whole-body oxygen consumption, as well as mitochondrial protein mass, respiratory capacity and energetic coupling in liver and skeletal muscle from food-restricted (FR) rats, age- and weight-matched controls. We also assessed markers of oxidative damage and antioxidant defences. The present results show that, in response to energy restriction, an adaptive decrease in whole-body energy expenditure is coupled with structural and functional changes in mitochondrial compartment, both in liver and skeletal muscle. In fact, liver mitochondrial mass per g of liver significantly increased, whereas total hepatic mitochondrial oxidative capacity was lower in FR than in control rats, because of a significant decrease in liver contribution to total body weight. In skeletal muscle, sub-sarcolemmal (SS) mitochondrial respiratory capacity, as well as SS and inter-myofibrillar (IMF) mitochondrial protein mass per g of tissue, was significantly lower in FR rats, compared to controls. Finally, a decrease in oxidative damage was found in liver but not in skeletal muscle mitochondria from FR rats, whereas an increase in antioxidant defence was found in both tissues. From the present results, it appears that skeletal muscle is involved in the decrease in energy expenditure induced by energy restriction. Energy sparing is achieved through changes in the activity (SS), mass (SS and IMF) and efficiency (IMF) of mitochondrial compartment.

The changes in metabolic efficiency, body composition, and nutrient partitioning induced by high-fat feeding were evaluated in adult rats (90 d of age). The alterations in serum free triiodothyronine, insulin, and leptin levels, as well as in hepatic and skeletal muscle metabolism, were also assessed. Rats were fed either a low- or a high-fat diet for 2 weeks. Relative to the low-fat feeding, energy intake and expenditure, as well as body-energy gain, lipid gain, and energetic efficiency, were increased by the high-fat feeding. Increased serum leptin levels accompanied these variations. A positive correlation between serum leptin levels and percentage of body fat was found in the rats fed the low- or high-fat diet, with a significant divergence between the slope of the regression lines. Furthermore, a negative correlation between serum leptin level and energy intake was found in the rats fed the low-fat diet, while a positive correlation was found in the rats fed the high-fat diet. Finally, the high-fat feeding decreased the hepatic and skeletal muscle mitochondrial oxidative capacity. It is concluded that, in adult rats, a nutritional factor such as a high level of fat in the diet induces obesity, leptin resistance, and impairment of mitochondrial capacity, all phenomena typical of unrestrained aged rats.

The purpose of this work was to study the effect of early long-term high-fat feeding on energy balance and liver oxidative activity. To this end, rats aged about 30 d were fed a high-fat or a low-fat diet for 15, 30 or 60 d. Full energy balance and energy partitioning measurements were carried out. In addition, we measured hepatic mitochondrial and peroxisomal oxidative capacities. Serum levels of free triiodothyronine (T3) and leptin were also determined. Rats fed a high-fat diet showed an increase in metabolizable energy intake as well as in energy expenditure, while lipid gain over the whole period was lower than that expected due to a decrease in metabolic efficiency. An increase in serum free T3 levels was also found in rats fed a high-fat diet after 15 and 30 d. Statistically significant correlations between serum leptin levels and body fat mass were found after 15, 30 and 60 d of high-fat feeding. Finally, no variation in hepatic mitochondrial and peroxisomal fatty acid oxidation capacity was found in rats fed a high-fat diet for 15, 30 or 60 d. In conclusion, the results of the present study show that young Wistar rats fed a high-fat diet for up to 60 d are able to counteract, at least in part, obesity development.