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Fatty acid
About: Fatty acid is a research topic. Over the lifetime, 74521 publications have been published within this topic receiving 2244818 citations. The topic is also known as: fatty acids.
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TL;DR: It is shown that to accommodate the increased requirement for hepatic fatty acid oxidation, PPAR α mRNA is induced during fasting in wildtype mice, indicating that PPARα plays a pivotal role in the management of energy stores during fasting.
Abstract: Prolonged deprivation of food induces dramatic changes in mammalian metabolism, including the release of large amounts of fatty acids from the adipose tissue, followed by their oxidation in the liver. The nuclear receptor known as peroxisome proliferator-activated receptor alpha (PPARalpha) was found to play a role in regulating mitochondrial and peroxisomal fatty acid oxidation, suggesting that PPARalpha may be involved in the transcriptional response to fasting. To investigate this possibility, PPARalpha-null mice were subjected to a high fat diet or to fasting, and their responses were compared with those of wild-type mice. PPARalpha-null mice chronically fed a high fat diet showed a massive accumulation of lipid in their livers. A similar phenotype was noted in PPARalpha-null mice fasted for 24 hours, who also displayed severe hypoglycemia, hypoketonemia, hypothermia, and elevated plasma free fatty acid levels, indicating a dramatic inhibition of fatty acid uptake and oxidation. It is shown that to accommodate the increased requirement for hepatic fatty acid oxidation, PPARalpha mRNA is induced during fasting in wild-type mice. The data indicate that PPARalpha plays a pivotal role in the management of energy stores during fasting. By modulating gene expression, PPARalpha stimulates hepatic fatty acid oxidation to supply substrates that can be metabolized by other tissues.
1,535 citations
TL;DR: Modifications necessary to the theory of Martin & Synge (1941) to allow for the compressibility of the mobile phase are presented and the application of the gas-liquid partition chromatogram to the separation of volatile fatty acids is described.
Abstract: Industry has long used charcoal or other solid absorbents in columns for cleaning gas streams or for solvent recovery, and more recently Turner (1943), Claesson (1946), Glueckauf, Barker & Kitt (1949), Phillips (1949) and Turkel'taub (1950) have used charcoal in gas chromatograms for the analysis of hydrocarbons and esters. Gas-liquid scrubbing columns have been used in industry for many years but, though Martin & Synge (1941) suggested the use of gas-liquid partition chromatograms for analytical purposes, no work has been reported along these lines. This paper presents modifications necessary to the theory of Martin & Synge (1941) to allow for the compressibility of the mobile phase and describes the application ofthe gas-liquid partition chromatogram to the separation of volatile fatty acids. The separations obtainable by this method are essentially parallel to those obtainable by distillation, but good separations can be achieved much more easily and it is possible to work with very much smaller quantities. In fact, the lower limit of quantity of material used is determined only by the efficiency of detection. In general, far less trouble from azeotrope formation is to be expected, since the concentrations of the substances to be separated in the liquid phase are always low and it may be possible to choose a liquid phase which associates only with one component of the azeotrope. Work on a preparative scale, though theoretically possible, is likely to be inconvenient because of the bulk of the apparatus. The method of detection described here is acid-base titration, but many methods of detecting changes in the composition ofa gas stream could be used and it is intended in future publications to explore some of these, which should extend the range of application to all substances capable of being distilled at the pressure of a few mm. of mercury. In suitable cases the gas-liquid partition column has two principal advantages over the ordinary liquid-liquid partition column: (a) the low viscosity of the mobile phase allows relatively longer columns to be used with a corresponding gain in efficiency and (b) in general it is easier to detect changes in composition of a gas than of a liquid stream. A THEORY OF GAS-LIQUID PARTITION CHROMATOGRAPHY
1,513 citations
TL;DR: It is demonstrated that free fatty acids induce insulin resistance in humans by initial inhibition of glucose transport/phosphorylation which is then followed by an approximately 50% reduction in both the rate of muscle glycogen synthesis and glucose oxidation.
Abstract: To examine the mechanism by which lipids cause insulin resistance in humans, skeletal muscle glycogen and glucose-6-phosphate concentrations were measured every 15 min by simultaneous 13C and 31P nuclear magnetic resonance spectroscopy in nine healthy subjects in the presence of low (0.18 +/- 0.02 mM [mean +/- SEM]; control) or high (1.93 +/- 0.04 mM; lipid infusion) plasma free fatty acid levels under euglycemic (approximately 5.2 mM) hyperinsulinemic (approximately 400 pM) clamp conditions for 6 h. During the initial 3.5 h of the clamp the rate of whole-body glucose uptake was not affected by lipid infusion, but it then decreased continuously to be approximately 46% of control values after 6 h (P < 0.00001). Augmented lipid oxidation was accompanied by a approximately 40% reduction of oxidative glucose metabolism starting during the third hour of lipid infusion (P < 0.05). Rates of muscle glycogen synthesis were similar during the first 3 h of lipid and control infusion, but thereafter decreased to approximately 50% of control values (4.0 +/- 1.0 vs. 9.3 +/- 1.6 mumol/[kg.min], P < 0.05). Reduction of muscle glycogen synthesis by elevated plasma free fatty acids was preceded by a fall of muscle glucose-6-phosphate concentrations starting at approximately 1.5 h (195 +/- 25 vs. control: 237 +/- 26 mM; P < 0.01). Therefore in contrast to the originally postulated mechanism in which free fatty acids were thought to inhibit insulin-stimulated glucose uptake in muscle through initial inhibition of pyruvate dehydrogenase these results demonstrate that free fatty acids induce insulin resistance in humans by initial inhibition of glucose transport/phosphorylation which is then followed by an approximately 50% reduction in both the rate of muscle glycogen synthesis and glucose oxidation.
1,488 citations
TL;DR: It is shown that the saturated fatty acid palmitate, but not unsaturated oleate, induces the activation of the NLRP3-ASC inflammasome, causing caspase-1, IL-1β and IL-18 production, which affects insulin sensitivity through tumor necrosis factor–independent and dependent pathways.
Abstract: High-fat diet (HFD) and inflammation are key contributors to insulin resistance and type 2 diabetes (T2D). Interleukin (IL)-1b plays a role in insulin resistance, yet how IL-1b is induced by the fatty acids in an HFD, and how this alters insulin signaling, is unclear. We show that the saturated fatty acid palmitate, but not unsaturated oleate, induces the activation of the NLRP3-ASC inflammasome, causing caspase-1, IL-1b and IL-18 production. This pathway involves mitochondrial reactive oxygen species and the AMP-activated protein kinase and unc-51–like kinase-1 (ULK1) autophagy signaling cascade. Inflammasome activation in hematopoietic cells impairs insulin signaling in several target tissues to reduce glucose tolerance and insulin sensitivity. Furthermore, IL-1b affects insulin sensitivity through tumor necrosis factor–independent and dependent pathways. These findings provide insights into the association of inflammation, diet and T2D.
1,456 citations
TL;DR: All fatty acids elevated HDL cholesterol when substituted for carbohydrates, but the effect diminished with increasing unsaturation of the fatty acids, and that for monounsaturates was not.
Abstract: To calculate the effect of changes in carbohydrate and fatty acid intake on serum lipid and lipoprotein levels, we reviewed 27 controlled trials published between 1970 and 1991 that met specific inclusion criteria. These studies yielded 65 data points, which were analyzed by multiple regression analysis using isocaloric exchanges of saturated (sat), monounsaturated (mono), and polyunsaturated (poly) fatty acids versus carbohydrates (carb) as the independent variables. For high density lipoprotein (HDL) we found the following equation: delta HDL cholesterol (mmol/l) = 0.012 x (carb----sat) + 0.009 x (carb----mono) + 0.007 x (carb---- poly) or, in milligrams per deciliter, 0.47 x (carb----sat) + 0.34 x (carb----mono) + 0.28 x (carb----poly). Expressions in parentheses denote the percentage of daily energy intake from carbohydrates that is replaced by saturated, cis-monounsaturated, or polyunsaturated fatty acids. All fatty acids elevated HDL cholesterol when substituted for carbohydrates, but the effect diminished with increasing unsaturation of the fatty acids. For low density lipoprotein (LDL) the equation was delta LDL cholesterol (mmol/l) = 0.033 x (carb----sat) - 0.006 x (carb----mono) - 0.014 x (carb----poly) or, in milligrams per deciliter, 1.28 x (carb----sat) - 0.24 x (carb----mono) - 0.55 x (carb---- poly). The coefficient for polyunsaturates was significantly different from zero, but that for monounsaturates was not. For triglycerides the equation was delta triglycerides (mmol/l) = -0.025 x (carb----sat) - 0.022 x (carb----mono) - 0.028 x (carb---- poly) or, in milligrams per deciliter, -2.22 x (carb----sat) - 1.99 x (carb----mono) - 2.47 x (carb----poly).(ABSTRACT TRUNCATED AT 250 WORDS)
1,454 citations