There is growing evidence that soy protein improves the blood lipid profiles of animals and humans. We compared the effects of fish protein hydrolysate (FPH), soy protein, and casein (control) on lipid metabolism in Wistar rats and genetically obese Zucker (fa/fa) rats. In Zucker rats, FPH treatment affected the fatty acid composition in liver, plasma, and triacylglycerol-rich lipoproteins. The mRNA levels of Delta 5 and Delta 6 desaturases were reduced by FPH and soy protein feeding compared with casein feeding. In Zucker rats both FPH and soy protein treatment reduced the plasma cholesterol level. Furthermore, the HDL cholesterol:total cholesterol ratio was greater in these rats and in the Wistar rats fed FPH and soy protein compared with those fed casein. Although fecal total bile acids were greater in soy protein-fed Zucker rats than in casein-fed controls, those fed FPH did not differ from the controls. However, the acyl-CoA:cholesterol acyltransferase activity was reduced in Zucker rats fed FPH and tended to be lower (P = 0.13) in those fed soy protein compared with those fed casein. Low ratios of methionine to glycine and lysine to arginine in the FPH and soy protein diets, compared with the casein diet, may be involved in lowering the plasma cholesterol concentration. Our results indicate that the effects of FPH and soy protein on fatty acid metabolism are similar in many respects, but the hypocholesterolemic effects of FPH and soy protein appear to be due to different mechanisms. FPH may have a role as a cardioprotective nutrient.

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It has previously been demonstrated that soya protein, which contains isoflavones and low methionine-glycine and lysine-arginine ratios, has a hypocholesterolaemic effect. In the present study, the hypocholesterolaemic effects of an isoflavone-enriched casein diet (HDI) and a single-cell protein-based diet (SCP) devoid of isoflavones but with low methionine-glycine and lysine-arginine ratios were investigated in obese Zucker rats after 6 weeks of feeding. The control diet contained casein, which has high ratios of methionine-glycine and lysine-arginine. HDI and SCP feeding reduced the concentrations of total cholesterol and cholesteryl esters in plasma and liver, and changed the fatty acid composition of the hepatic cholesteryl esters. Faecal cholesterol and bile acid levels were markedly higher in SCP-fed rats than in controls, whereas HDI feeding had only minor effects. However, both HDI and SCP feeding increased the hepatic gene expression of cholesterol 7a hydroxylase. In contrast, the hepatic acyl-CoA synthetase and acyl-CoA:cholesterol acyltransferase activities and the gene expression of the LDL receptor were increased by HDI, but not by SCP feeding. The present results suggested that the cholesterollowering effect of SCP was related to the enterohepatic circulation, whereas HDI seemed to lower the plasma cholesterol via the circulation. Plasma homocysteine level was reduced in rats fed HDI and SCP compared to rats fed casein. In summary, diets enriched in isoflavones or containing proteins with low methionine-glycine and lysine-arginine ratios lowered the plasma cholesterol and homocysteine levels, changing the plasma profile from atherogenic to cardioprotective.

We evaluated the effects of partly substituting lard with marine n-3 fatty acids (FA) on body composition and weight, adipose tissue distribution and gene expression in five adipose depots of male Wistar rats fed a high-fat diet. Rats were fed diets including lard (19·5 % lard) or n-3 FA (9·1 % lard and 10·4 % Triomare) for 7 weeks. Feed consumption and weight gain were similar, whereas plasma lipid concentrations were lower in the n-3 FA group. Magnetic resonance imaging revealed smaller visceral (mesenteric, perirenal and epididymal) adipose depots in the n-3 FA-fed animals (35, 44 and 32 % reductions, respectively). n-3 FA feeding increased mRNA expression of cytokines as well as chemokines in several adipose depots. Expression of Adipoq and Pparg was enhanced in the mesenteric adipose depots of the n-3 FA-fed rats, and fasting plasma insulin levels were lowered. Expression of the lipogenic enzymes Acaca and Fasn was increased in the visceral adipose depots, whereas Dgat1 was reduced in the perirenal and epididymal depots. Cpt2 mRNA expression was almost doubled in the mesenteric depot and liver. Carcass analyses showed similar body fat (%) in the two feeding groups, indicating that n-3 FA feeding led to redistribution of fat away from the visceral compartment.

Lowering of plasma triglyceride levels by hypolipidemic agents is caused by a shift in the liver cellular metabolism, which become poised toward peroxisome proliferator-activated receptor (PPAR) ␣-regulated fatty acid catabolism in mitochondria. After dietary treatment of rats with the hypolipidemic, modified fatty acid, tetradecylthioacetic acid (TTA), the energy state parameters of the liver were altered at the tissue, cell, and mitochondrial levels. Thus, the hepatic phosphate potential, energy charge, and respiratory control coefficients were lowered, whereas rates of oxygen uptake, oxidation of pyridine nucleotide redox pairs, ␤-oxidation, and ketogenesis were elevated. Moderate uncoupling of mitochondria from TTA-treated rats was confirmed, as the proton electrochemical potential (⌬p) was 15% lower than controls. The change affected the ⌬ component only, leaving the ⌬pH component unaltered, suggesting that TTA causes induction of electrogenic ion transport rather than electrophoretic fatty acid activity. TTA treatment induced expression of hepatic uncoupling protein 2 (UCP-2) in rats as well as in wild type and PPAR␣-deficient mice, accompanied by a decreased double bond index of the mitochondrial membrane lipids. However, changes of mitochondrial fatty acid composition did not seem to be related to the effects on mitochondrial energy conductance. As TTA activates PPAR␦, we discuss how this subtype might compensate for deficiency of PPAR␣. The overall changes recorded were moderate, making it likely that liver metabolism can maintain its function within the confines of its physiological regulatory framework where challenged by a hypolipemic agent such as TTA, as well as others.Administration of 3-thia fatty acids to rats leads to hypolipidemia. The metabolism and biological effects of these nonoxidizable fatty acid analogues, of which tetradecylthioacetic acid (TTA) 1 is the most studied, have been reviewed (1-4). A considerable body of evidence points to shifts in the liver cellular metabolism, resulting in channeling of fatty acids to an enhanced mitochondrial ␤-oxidation, at the expense of triacylglyceol synthesis. Simultaneously, there is up-regulation of the inner carnitine palmitoyltransferase II, 2,4-dienoyl-CoA reductase, and mitochondrial 3-hydroxy-3-methyl-CoA synthase. The outer carnitine palmitoyltransferase-I is not affected, suggesting that the rate control of ␤-oxidation and ketogenesis resides in steps beyond acyl group translocation into the matrix (4 -6). Modulation of lipid metabolism with TTA seems at least in part to be related to the role of TTA as a regulator for members of the peroxisome proliferator-activated receptor (PPAR) family of nuclear receptors. TTA has been demonstrated to function as a ligand and activator of the PPAR subtypes PPAR␣, PPAR␦, and PPAR␥ (4, 7-9). PPAR␣ is the predominant subtype in the liver where it controls transcription of genes involved in fatty acid metabolism, such as the genes for peroxisomal acyl-CoA oxidase and fatty acid transport protein, which ...

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