Search

A decrease of the basal glucose metabolism with sensescence in the isolated rat adipose tissue has been demonstrated. In the presence of insulin, the oxidation of (U14C)-D-glucose and its incorporation into triglycerides are significantly increased at all ages studied. No significant difference between groups of animals was noted when the insulin-stimulating effect was related to basal metabolism. The synthesis of fatty acids from glucose is highly enhanced by insulin at 6 weeks, poorly at 6 months and no more at 24 months. It is concluded that the insulin sensitivity of the rat adipose tissue is not affected by ageing. Nevertheless, as far as fatty acid synthesis is concerned, a different metabolic pathway could be involved.

The aim of the present investigation was to study the effect of aging upon the metabolism and the responsiveness to insulin of epididymal adipose tissue from rats (6 weeks, 6 and 24 months). Basal glucose metabolism by these tissues and adipocytes was positively related to cell size, for each age group. But age per se plays an important role: for the same diameter, the U-14C-glucose oxidation to CO2 and its incorporation into triglycerides described markedly between 6 weeks and 6 months, as reported peviously, and decreased still further between 6 months and 24 months, for any diameter. In contrast, insulin responsiveness of adipose tissue fragments and fat cells was negatively correlated to adipose cell size, when we analyzed the role of cell diameter for a group of given age. When comparing the sensitivity to hormone for a given cell volume but at different ages, it appeared that insulin resistance increased considerably between 6 weeks and 6 months and was still more marked in old age. The mechanisms underlying these facts have been discussed.

Physical training (forced swimming for 6 weeks) led in resting adult rats modifications of circulating hormones, fuels and substrates, of epididymal adipose tissue composition and of its glucose metabolism. Plasma concentrations of free fatty acids, cholesterol and insulin were decreased by training. The weight of the epididymal fat pad, its triglyceride content and the mean cell size of adipocytes were significantly diminished. Twenty four hours after the end of the final exercise period, incorporation of D-U-14C-glucose into triglycerides was reduced (P less than 0.01) but the response to insulin was greatly enhanced for swimming rats both for oxidation of labelled glucose (P less than 0.001) and its incorporation into lipids (P less than 0.001) (respectively 215 and 225%). This enhancement of insulin sensitivity by training persisted and became more marked one week after the end of the exercise period (respectively 258 and 363%).

No modification in basal radioglucose metabolism by isolated rat diaphragm could be seen with senescence. Insulin increased the production of 14CO2 only in growing animals. On the opposite, incorporation of radioglucose into glycogen is enhanced in the different age groups; nevertheless, the response in 3-month-old animals was lower than in 6-week-old ones. No significant difference has been detected between the adult and the old rats. Therefore, it is concluded that a diminution of insulin sensitivity appeared during the period of transition between growing up and maturity without any further modification during old age.

In the male rat a diet rich in beef fat facilitates the occurrence of hyperinsulinemia after a glucose load whereas fats rich in linoleic acid produce no such effect. The combination of saturated fat and saccharose facilitates the occurrence of hypertriglyceridemia in the male rat, no such effect is produced by the combination of fats rich in linoleic acid and saccharose. Linoleic acid prevents natrium chloride from provoking hypertriglyceridemia in male and in female rats subjected to a diet enriched in saccharose and fat. Estrogen-induced hypertriglyceridemia in castrated animals is strongly inhibited if the diet is rich in linoleic acid. Physical effort can prevent saccharose combined with saturated fats from inducing hypertriglyceridemia.