Effect Of Lipid Oxidation Research Articles

Effect of lipid oxidation on glucose utilization in humans

The mechanisms responsible for the competition between glucose and fatty acids as oxidative fuels are not yet completely understood in humans. Maintenance of plasma fatty acid concentrations by means of lipid and heparin infusion during hyperinsulinemic, euglycemic clamps in humans first suppresses glucose oxidation and only later decreases nonoxidative glucose disposal; muscle pyruvate dehydrogenase activity is inhibited when plasma fatty acid concentrations are maintained during hyperinsulinemic, euglycemic clamps. The maintenance of plasma fatty acid concentrations impairs insulin-stimulated muscle glucose uptake only if fatty acid uptake by skeletal muscles is increased. The role of hyperglycemia in glucose-fatty acid competition has recently been emphasized. Fatty acid utilization by muscle is impaired in patients with type 2 diabetes mellitus during fasting hyperglycemia: both lipid oxidation and uptake of plasma fatty acids by skeletal muscle are impaired during postabsorptive conditions. Hyperglycemia indirectly activates pyruvate dehydrogenase, the rate-limiting enzyme for glucose oxidation. The ability of increased glucose availability to stimulate glucose oxidation and reduce lipid oxidation by skeletal muscle can be considered a corollary of the Randle glucose-fatty acid cycle. It can be concluded that within a reasonable range of carbohydrate-to-fat ratios, the addition of fat to a meal does not decrease postprandial carbohydrate oxidation. Furthermore, high-fat meals do not promote fat oxidation leading to fat storage in adipose tissue.

LIPID OXIDATION IN MUTTON: SPECIES-RELATED AND WARMED-OVER FLAVORS

Effects of lipid oxidation in cooked mutton on species-related flavor and warmed-over flavor (WOF) intensities were studied using various additive treatments and post-cooking storage (versus no additive/no storage) as means to produce samples of varied lipid oxidation. Ground mutton was treated with 200 ppm sodium nitrite, 0.5% sodium tripolyphosphate, 0.05% sodium ascorbate, 3% sodium lactate, 0.002% propyl gallate, or water only (control), cooked to 74C, and aerobically stored at 4C for 0, 2, or 4 days. Nitrite-treated samples showed the least lipid oxidation as determined by the 2-thiobarbituric acid reactive substances (TBARS) and had more intense species-related (muttony) flavor than all other treated samples. Some samples exhibited high TBARS after 4 days but were still rated “slight” for WOF intensity, probably due to the strong species-related flavor that could have made WOF less perceivable. Accordingly, correlations, although statistically significant, were low between TBARS and WOF intensity or between species flavor intensity and WOF intensity.

Effect of lipid oxidation on the regulation of glucose utilization in obese patients.

The effect of changes in lipid oxidation on glucose utilization (storage and oxidation) was studied in seven nondiabetic obese patients. They participated in three protocols in which: (1) Intralipid (to raise plasma FFA concentrations), (2) beta-pyridylcarbinol [a precursor of nicotinic acid, to lower plasma free fatty acids (FFA) concentrations], or (3) isotonic saline were infused over 2 h. Thereafter, these infusions were discontinued, and a 2-h euglycemic, hyperinsulinemic clamp was performed to measure glucose uptake. All studies were carried out in combination with indirect calorimetry to measure oxidative and nonoxidative glucose disposal (glucose storage). The high plasma FFA concentrations (1024 +/- 57 mumol/l) and lipid oxidation rates (1.1 +/- 0.1 mg/kg.min) found at the end of the Intralipid infusion and the low plasma FFA concentrations (264 +/- 26 mumol/l) and lipid oxidation rates (0.7 +/- 0.1 mg/kg.min) found at the end of the beta-pyridylcarbinol infusions resulted in significantly different rates of total and nonoxidative glucose disposal during the insulin clamp. The values were 2.6 +/- 0.6 mg/kg.min after Intralipid and 4.1 +/- 1.0 mg/kg.min after beta-pyridylcarbinol for total glucose disposal, and 0.4 +/- 0.4 and 1.6 +/- 0.8, respectively for nonoxidative glucose disposal. In conclusion, these observations show that changes in lipid oxidation rates preceding a glucose load influence glucose disposal and glycogen storage in obese subjects.

Effect of free fatty acids on insulin receptor binding and tyrosine kinase activity in hepatocytes isolated from lean and obese rats.

We demonstrated previously that high physiological concentrations of free fatty acids (FFA) rapidly decrease insulin binding, degradation, and action in isolated rat hepatocytes. In this study, hepatocytes from lean and obese Sprague-Dawley rats (Alab, Stockholm) were preincubated with or without 0.4 mM oleic acid, and the effect on insulin binding and tyrosine kinase activity was measured. In the absence of exogenous FFA, insulin binding was reduced in hepatocytes from obese compared with lean rats (mean +/- SE reduction 44 +/- 7%, n = 8, P less than 0.01). Furthermore, the inhibitory effect of oleic acid added to hepatocytes from lean rats (n = 8; 40 +/- 9%, P less than 0.01) was not seen in cells from obese rats. Treating obese rats with Etomoxir, a carnitine palmitoyl transferase I inhibitor, increased insulin binding to isolated hepatocytes by 41 +/- 13% (n = 5, P less than 0.05). There was no difference in total binding to partially purified insulin receptors from solubilized hepatocytes from lean and obese rats, whether cells were or were not preincubated with oleic acid. Tyrosine kinase activity of partially purified receptors from basal or insulin-stimulated cells was not affected by either obesity, treatment with Etomoxir, or preincubating the cells with oleic acid. Thus, both obesity and elevated ambient FFA levels are associated with impaired insulin cell surface binding to isolated hepatocytes, possibly through an effect of lipid oxidation on the internalization/recycling of the insulin-receptor complex without any perturbation of the receptor tyrosine kinase activity. The data suggest that the reduced insulin binding to hepatocytes from obese rats is due to elevated ambient FFA levels.

Pigment oxidation in ground veal: Influence of lipid oxidation, iron and zinc

The color stability of fresh ground veal from four different muscles ( biceps femoris, longissimus dorsi, psoas major and supraspinatus) was characterized, and the effects of lipid oxidation, iron and zinc on this degradative process were investigated. Samples were minced and prepared in a manner consistent with retail production and analyzed for pH, myoglobin concentration, total and nonheme iron, and zinc. Pigment and lipid oxidation were measured on days 0, 3 and 6 of 4°C storage. B. femoris demonstrated the greatest extent of lipid oxidation, and was more color-labile than p. major or supraspinatus ( P < 0·05), but no different from l. dorsi ( P > 0·05). Total iron and myoglobin concentrations were lowest for l. dorsi ( P<0·05). Zinc concentration in the four muscles followed the order supraspinatus ⩾ b. femoris ⩾ l. dorsi ⩾ p. major ( P < 0·05). Data analysis revealed that initial metmyoglobin formation (days 0 to 3) was significantly correlated with total iron ( r = 0·69) or nonheme iron ( r = 0·68) in b. femoris, but not any of the other muscles. Correlations between lipid and pigment oxidation in each of the four muscles were performed and the data support a strong relationship between these degradative processes in ground veal.

Effect of lipid oxidation on the functional and nutritional properties of washed chicken myofibrils stored at different water activities

Influence de la lyophilisation sur la solubilite des proteines de viande poulet et la stabilite de lipides ajoutes sous forme de linoleate de methyle. Effet de l'activite de l'eau et de la duree de stockage a 20 o C sur les proprietes suivantes de ces proteines: solubilite, viscosite, capacite de retention d'eau

Effect of Lipid Oxidation in "Kezuri-bushi" on the Flavor of Soup Stock.

Effect of Lipid Oxidation in "Kezuri-bushi" on the Flavor of Soup Stock.

Degenerative and Age-Related Changes in the X-Irradiated Kidney of the Rat

Exposure of rat kidney to a single dose of radiation (4000 rad) produced degenerative changes and accumulation of fluorescent granules after a latent period of approximately 8 weeks. The appearance of these fluorescent granules corresponded to the development of structural damage to the kidney. Radiation produced relatively minor changes in the lipid content of the kidney. The level of cholesteryl esters was increased, arachidonic acid content was decreased, and there was a progressive increase in fluorescent substances related to aging, as detected by thin layer chromatography, in chloroform-methanol extracts of the irradiated kidney. However, there was no apparent loss of vitamin E or ubiquinone and no increase in TBA values or diene conjugation as might be expected as effects of lipid oxidation. These changes were evident by the second month following irradiation and corresponded to the development of the morphological changes. The presence of lipofuscin substances, reduced arachidonic acid, and an increase in cholesteryl esters indicated an acceleration of aging in the radiation-exposed kidney. The relationship of lipid oxidation to the acceleration of aging and the production of acute renal lesions was not apparent.

Effects of lipids and their related compounds on the chloroplast functions.

Effects of lipids and their related compounds on the chloroplast functions were investigated. Whole lipids, i.e. methyl linolenate, monogalactosyidiglyceride, and lecithin induced only a slight effect on the photochemical activities; electron transport, H+ uptake, and cyclic photophosphorylation. Lecithin alone stimulated significantly O2 evolution. On the contrary, the lipid-hydrolysis products, i.e. linolenic acid, monogalactosylmonoglyceride, and lysolecithin caused a strong inhibition of all the photoactivities tested. They showed two different modes of inhibition, which arise probably from a situation whether the lipids affect coupling factor or not besides the membrane part in thylakoid. Peroxidized methyl linolenate and a-tocopherol were also examined and the effect of lipid oxidation was discussed.