Effects of high-intensity intermittent training on carnitine palmitoyl transferase activity in the gastrocnemius muscle of rats

We examined the capacity of high-intensity intermittent training (HI-IT) to facilitate the delivery of lipids to enzymes responsible for oxidation, a task performed by the carnitine palmitoyl transferase (CPT) system in the rat gastrocnemius muscle. Male adult Wistar rats (160-250 g) were randomly distributed into 3 groups: sedentary (Sed, N = 5), HI-IT (N = 10), and moderate-intensity continuous training (MI-CT, N = 10). The trained groups were exercised for 8 weeks with a 10% (HI-IT) and a 5% (MI-CT) overload. The HI-IT group presented 11.8% decreased weight gain compared to the Sed group. The maximal activities of CPT-I, CPT-II, and citrate synthase were all increased in the HI-IT group compared to the Sed group (P < 0.01), as also was gene expression, measured by RT-PCR, of fatty acid binding protein (FABP; P < 0.01) and lipoprotein lipase (LPL; P < 0.05). Lactate dehydrogenase also presented a higher maximal activity (nmol·min-1·mg protein-1) in HI-IT (around 83%). We suggest that 8 weeks of HI-IT enhance mitochondrial lipid transport capacity thus facilitating the oxidation process in the gastrocnemius muscle. This adaptation may also be associated with the decrease in weight gain observed in the animals and was concomitant to a higher gene expression of both FABP and LPL in HI-IT, suggesting that intermittent exercise is a "time-efficient" strategy inducing metabolic adaptation.

Heterogeneous response of adipose tissue to cancer cachexia

Cancer cachexia causes disruption of lipid metabolism. Since it has been well established that the various adipose tissue depots demonstrate different responses to stimuli, we assessed the effect of cachexia on some biochemical and morphological parameters of adipocytes obtained from the mesenteric (MES), retroperitoneal (RPAT), and epididymal (EAT) adipose tissues of rats bearing Walker 256 carcinosarcoma, compared with controls. Relative weight and total fat content of tissues did not differ between tumor-bearing rats and controls, but fatty acid composition was modified by cachexia. Adipocyte dimensions were increased in MES and RPAT from tumor-bearing rats, but not in EAT, in relation to control. Ultrastructural alterations were observed in the adipocytes of tumor-bearing rat RPAT (membrane projections) and EAT (nuclear bodies)

Fatty acid oxidation in lymphocytes from Walker 256 tumor-bearing rats

The oxidation of fatty acids in lymphocytes from the mesenteric lymph nodes of Walker 256 carcinosarcoma-bearing rats (TB) was studied, as well as the activity of the mitochondrial long-chain fatty acid transport system. Two-month old Wistar rats were subcutaneously implanted with 10(7) cells and after 2 weeks the tumor mass was 15-20 per cent of the carcass weight. The activity of camitine palmitoyltransferase (CPT) II was demonstrable in the lymphocytes of the TB group (8.2 ñ 5.6 nmol/min per mg mitochondria protein for 15 rats) and was not detected in the control, while that of CPT I was only slightly increased in the former. Similar rates of [1-14C]-palmitate decarboxylation were found for TB and control rat lymphocytes. However, when the rate of decarboxylation of [1-14C]-paimitate present in the intracellular pool of lipids was investigated in cultured lymphocytes, the cells of TB rats exhibited rates 17-fold higher than those of control animals in the presence of fetal calf serum (FCS). Decarboxylation in the presence of TB rat serum was 178-fold higher than obtained with normal rat serum, and 1.4-fold compared to FCS. These results suggest that, during cachexia, lymphocytes preferably oxidize intracellular lipids, and that this capacity is greatly enhanced by factors circulating in the serum of tumor-bearing rats.

Insulin and prostaglandins as signals between tumor and the host immune system

The development of malignant tissue in vivo is partially favored by the immunosuppression that occurs in cancer patients. However, the signals between tumor and immune tissues remain to be identified. We present evidence that prostaglandins may act as one of these signals by a direct action on cells of the immune system, or by inhibition of insulin secretion which in turn suppresses immune function, or both