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A 4-week diet containing 1% of the conjugated trans-10,cis-12 linoleic acid (CLA2) induces, in C57BL/6 mice, a lipodystrophy, a liver steatosis and a reduction of plasma triglycerides. We demonstrate that, first, hepatic lipid accumulation is not due to an in vivo alteration of lipoprotein production. Fates of CLA2 relative to ß-oxidation reactions are then studied in mitochondrial fractions isolated from liver of control animals and the data indicate not only that the CLA is poorly oxidised but also that it modifies the oxidation of usual fatty acids. We also demonstrate that oxidation capacities are increased by CLA2 treatment concomitantly to carnitine palmitoyltransferase I (CPT I) activity. Besides, the increases in acetyl-CoA carboxylase activity and malonyl-CoA concentration in the liver of CLA2 treated mice provide evidence of a high rate of lipogenesis. The increased CPT I sensibility to malonyl-CoA inhibition due to the treatment suggests that the whole fatty acid ß-oxidation is finally reduced in vivo. The mechanisms implicated in the setup of the hepatic steatosis and in the reduction of the lipaemia despite the increased VLDL secretion are discussed.

Feeding mice the trans-10, cis-12 (t10c12) conjugated linoleic acid (CLA) isomer is associated with lipodystrophy, insulin resistance, hyperinsulinemia, and liver steatosis. It has been hypothesized that CLA-induced liver steatosis is the result of increased hepatic lipogenesis stimulated by high insulin levels. We studied the effects of a 12-d t10cl 2CLA treatment (1 g/100 g diet) on liver carbohydrate and lipid metabolism in control and streptozotocin (STZ)-injected mice. STZ mice were characterized by insulin deficiency, hypertriglyceridemia, and depletion of liver triglyceride and glycogen. Remarkably, feeding t10c12CLA to diabetic mice (STZ-CLA) normalized these variables. Reconstitution of fat stores in the livers of STZ-CLA mice was associated with lower fatty acid (FA) oxidation rates and greater malonyI-CoA concentration than in STZ mice. FA translocase and VLDL receptor mRNA levels were greater in STZ-CLA than in STZ mice, suggesting that t10c12CLA increased liver lipid uptake. Phosphoenolpyruvate carboxykinase mRNA levels and AMP kinase phosphorylation were lower in STZ-CLA than in STZ mice, indicating that t10c12CLA may reduce glucogenic activity and promote glycogenesis in diabetic mice. Because glycemia and glucokinase expression were not modified by t10c12CLA treatment, we postulated that glycogen accumulation is likely not the result of an effect of t10c12CLA on plasma glucose utilization, but rather is due to the contribution of lactate, the concentration of which was higher in muscle of STZ-CLA mice. The results demonstrate that t10c12CLA stimulates liver lipid accumulation in the absence of insulin and, thus, suggest that t10c12CLA can improve liver carbohydrate and lipid metabolism in type I diabetic mice.

These studies were designed to investigate the lymph absorption of a lipid emulsion in rats prefed different long-term high-fat diets. Particular emphasis was placed on the consequences of endogenous fatty acid alteration on the lymph recovery of two labeled fatty acids. Male Wistar rats were fed a standard diet (LF) containing 3.5 g/100 g fat or high-fat diets containing 15 g/100 g sunflower oil (HSFO), menhaden oil (HMO) or medium-chain triglyceride oil (HMCT) for 4 wk. The lymph was collected for 3 h before and after the intraduodenal infusion of a 90[[micro]mol] lipid emulsion (30[[micro]mol] monopalmitin, 30[[micro]mol] oleic acid, 25[[micro]mol] linoleic acid, 5[[micro]mol] arachidonic acid) labeled with [3H] oleic (OA) and [14C] arachidonic (AA) acids. The [3H] OA and [14C] AA lymph recoveries were measured and the lymph samples were tested for fatty acid, phospholipid and triglyceride content. Prefeeding an HSFO or HMO diet led to a 65 or 32% greater total lymph fatty acid output, respectively, compared with rats prefed the LF diet. In rats prefed both the HSFO and HMO diets, lymph fatty acid characteristics provided evidence of a dilution of exogenous fatty acids coming from the emulsion by endogenous fatty acids. In rats prefed the HMCT diet, the total lymph fatty acid output after the infusion of the lipid emulsion was not greater than that of starved rats. Nevertheless, 27% [3H] OA and 21% [14C] AA were recovered in the lymph, suggesting a limited dilution of exogenous fatty acids by endogenous fatty acids. In rats prefed the HMCT diet, some exogenous long-chain fatty acids must have been transported by the portal vein in response to low biliary phopholipid production, as indicated by the proportions of [3H] OA and [14C] AA taken up by the mucosa and not recovered in the lymph. Thus we demonstrated that during absorption of a single long-chain fatty acid meal a dilution of exogenous fatty acids by endogenous fatty acids occurred. The nature and the quantity of these endogenous fatty acids could alter the absorption efficiency of long-chain fatty acids by the lymphatic pathway and modify the fatty acid characteristics of lymph lipoprotein. KEY WORDS: lymphatic absorption oleic acid arachidonic acid high-fat diets rats

Research was conducted to examine the effects of dietary oil intake and fatty acid infusions on the expression of intestinal and liver fatty acid-binding proteins (I-FABP and L-FABP, respectively) on the small intestine of mice. L-FABP mRNA and protein levels in duodenum and proximal jejunum were increased after a daily force-feeding for 7 days with 0.2 ml sunflower oil. Results indicate that long-chain fatty acids are strong inducers of L-FABP gene expression in the small intestine.

l-Carnitine is essential for mitochondrial β-oxidation and has been used as a lipid-lowering feed additive in humans and farmed animals. d-Carnitine is an optical isomer of l-carnitine and dl-carnitine has been widely used in animal feeds. However, the functional differences between l- and d-carnitine are difficult to study because of the endogenous l-carnitine background. In the present study, we developed a low-carnitine Nile tilapia model by treating fish with a carnitine synthesis inhibitor, and used this model to investigate the functional differences between l- and d-carnitine in nutrient metabolism in fish. l- or d-carnitine (0·4 g/kg diet) was fed to the low-carnitine tilapia for 6 weeks. l-Carnitine feeding increased the acyl-carnitine concentration from 3522 to 10 822 ng/g and alleviated the lipid deposition from 15·89 to 11·97 % in the liver of low-carnitine tilapia. However, as compared with l-carnitine group, d-carnitine feeding reduced the acyl-carnitine concentration from 10 822 to 5482 ng/g, and increased lipid deposition from 11·97 to 20·21 % and the mRNA expression of the genes involved in β-oxidation and detoxification in the liver. d-Carnitine feeding also induced hepatic inflammation, oxidative stress and apoptosis. A metabolomic investigation further showed that d-carnitine feeding increased glycolysis, protein metabolism and activity of the tricarboxylic acid cycle and oxidative phosphorylation. Thus, l-carnitine can be physiologically utilised in fish, whereas d-carnitine is metabolised as a xenobiotic and induces lipotoxicity. d-Carnitine-fed fish demonstrates increases in peroxisomal β-oxidation, glycolysis and amino acid degradation to maintain energy homeostasis. Therefore, d-carnitine is not recommended for use in farmed animals. [ABSTRACT FROM AUTHOR]