OBJECTIVEMedium-chain fatty acids (MCFAs) have been reported to be less obesogenic than long-chain fatty acids (LCFAs); however, relatively little is known regarding their effect on insulin action. Here, we examined the tissue-specific effects of MCFAs on lipid metabolism and insulin action.RESEARCH DESIGN AND METHODSC57BL6/J mice and Wistar rats were fed either a low-fat control diet or high-fat diets rich in MCFAs or LCFAs for 4–5 weeks, and markers of mitochondrial oxidative capacity, lipid levels, and insulin action were measured.RESULTSMice fed the MCFA diet displayed reduced adiposity and better glucose tolerance than LCFA-fed animals. In skeletal muscle, triglyceride levels were increased by the LCFA diet (77%, P < 0.01) but remained at low-fat diet control levels in the MCFA-fed animals. The LCFA diet increased (20–50%, P < 0.05) markers of mitochondrial metabolism in muscle compared with low-fat diet–fed controls; however; the increase in oxidative capacity was substantially greater in MCFA-fed animals (50–140% versus low-fat–fed controls, P < 0.01). The MCFA diet induced a greater accumulation of liver triglycerides than the LCFA diet, likely due to an upregulation of several lipogenic enzymes. In rats, isocaloric feeding of MCFA or LCFA high-fat diets induced hepatic insulin resistance to a similar degree; however, insulin action was preserved at the level of low-fat diet–fed controls in muscle and adipose from MCFA-fed animals.CONCLUSIONSMCFAs reduce adiposity and preserve insulin action in muscle and adipose, despite inducing steatosis and insulin resistance in the liver. Dietary supplementation with MCFAs may therefore be beneficial for preventing obesity and peripheral insulin resistance.

The effects of feeding two levels of rice bran oil (RBO) on the growth, lipid parameters, and fatty acid composition of the plasma and liver of rats (Wistar strain) were compared with those produced on animals which had been fed the same levels of peanut oil (PNO). The control animals were fed synthetic diets containing 5 and 20% peanut oil (PNO) and the experimental groups were fed similar diets, containing the same level of rice bran oil (RBO). There was no significant difference with respect to the organ weights between the control and the experimental groups. In general, groups fed 20% oil gained more weight than groups fed 5% oil. The animals which received rice bran oil in their diet had, in general, comparatively lower levels of cholesterol, triglycerides and phospholipids. On the other hand, animals receiving 20% rice bran oil in their diet, showed an increase of 20% in high density lipoproteins (HDL-C), within 18 weeks (p < 0.05), when compared to the animals fed with peanut oil. Similarly, low density lipoprotein cholesterol (LDL-C) and very low density lipoprotein cholesterol (VLDL-C) were lower in RBO-fed groups, than in the PNO-fed groups. There was, however, no significant differences in the cholesterol/phospholipid (C/P) ratio of the two groups. Analysis of plasma and of liver fatty acids indicated, in a general way, the type of fat consumed. There were no significant difference in the P/S ratio, nor any in the oleic/linoleic, oleic/stearic, palmitoleic/palmitic, oleic/palmitic, and oleic/palmitoleic ratios.(ABSTRACT TRUNCATED AT 250 WORDS)

1. l-alphagamma-Diaminobutyric acid is metabolized in Xanthomonas sp. to aspartic beta-semialdehyde, aspartic acid and oxaloacetic acid. 2. Aspartic beta-semialdehyde is formed from diaminobutyric acid by a pyruvate-dependent gamma-transamination. 3. The transaminase has a pH optimum of 9 and exhibits a high degree of substrate specificity, as analogues of diaminobutyric acid and pyruvate are inert in the system. The transaminase is inhibited by carbonyl-binding agents such as hydroxylamine. 4. Aspartic acid is formed from aspartic beta-semialdehyde by an NAD(+)-dependent dehydrogenation. 5. The dehydrogenase has a pH optimum of 8.5 and is a thiol enzyme. It is specific for aspartic beta-semialdehyde but analogues of NAD(+) such as 3-acetylpyridine-adenine dinucleotide and deamino-NAD are partly active in the system. 6. The significance of these reactions is discussed in relation to diaminobutyric acid metabolism in plants and mammalian systems.

Three different groups of infants were fed with different formulae based on milk fat. Group I received cow's milk fat formulae with 20% butter fat whereas groups II and III received a formulae which was supplemented with 50 and 33% of peanut oil supplementation in 20% milk fat respectively. Anthropometric measurements, cholesterol, triglyceride, lipoproteins and plasma fatty acids were followed up to a period of 6 months. The results indicated that cow's milk-fed infants had higher cholesterol levels (P < 0.01) than the other two groups. No significant differences with respect to high-density lipoproteins (HDLs) were found, whereas low-density lipoproteins (LDLs) and very low-density lipoproteins (VLDls (VLDls) were found to be increasing up to a period of 6 months. No significant differences were observed with respect to saturated fatty acids and oleic acid (18:1) levels whereas linoleic acid (18:2) clearly showed a proportional relationship between the intake and plasma levels, indicating a positive correlation. Arachidonic acid (20:4) did not, however, show a proprotionate relationship with respect to linoleic acid (18:2) intake. The triene/tetraene, oleic/linoleic, linoleic/arachidonic and total n6 fatty acids were all normal indicating normal activity of desaturase and elongase enzymes for the optimal utilisation of linoleic acid. Thus, the present study suggests that a vegetable oil such as peanut oil could be used in milk fat to improve the essential fatty acid (EFA) status of infants.

1. The activities of the enzymes histidase, urocanase and histidine-pyruvate transaminase were studied in rats under conditions of protein malnutrition. Urocanase and histidase activities in liver were markedly lowered in experimental protein malnutrition, but the activity of histidine-pyruvate transaminase was unaffected. There is a metabolic control in vivo of the enzymes involved in the catabolism of histidine. 2. Significant changes in the urinary excretion of histidine, composition of liver and serum were apparent in the protein-malnourished rat. 3. The changes in the activities of the enzymes and other parameters were of a reversible nature and dependent on the nature of the dietary protein. 4. The significance of these findings is discussed in relation to abnormal histidine metabolism in kwashiorkor.