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Why can't fatty acids be converted directly to glucose
Hormones play an important role in lipid metabolism (Figure 3). Fatty acid synthesis is regulated by phosphorylation-dephosphorylation reactions. Insulin stimulates the dephosphorylation of acetyl-CoA carboxylase, activating fatty acid synthesis. Phosphorylation of acetyl-CoA carboxylase by the hormones epinephrine, norepinephrine, and glucagon result in the inactivation of this enzyme, inhibiting synthesis of fatty acids from acetyl-CoA.
N2 - Glucose disposal induces a signal that modulates the transcriptional regulation of genes involved in the glycolysis and lipogenesis pathways. To investigate the role of glucose metabolism on hepatic gene expression independently from insulin action, we overexpressed glucokinase, the limiting enzyme in the glycolysis pathway, in the liver of streptozotocin-induced type 1 diabetic rats. By microarray analysis, we observed that critical genes such as liver-type pyruvate kinase, malic enzyme, fatty acid synthase, and stearoyl-CoA desaturase 1 were enhanced multiple-fold, whereas genes involved in mitochondrial fatty acid oxidation and the Krebs cycle were downregulated. Despite the increase in expression of fatty acid synthesis genes and the presence of steatosis, no major alterations to the levels of genes involved in VLDL assembly and secretion, such as diacylglycerol acyltransferases 1 and 2 and microsomal triglyceride transfer protein, were observed. Overall, our data suggest that the gene expression pattern induced by glucose metabolism favors fatty acid storage in the liver rather than secretion into the circulation.
There can therefore be no net conversion of fatty acids into glucose.
About 40% of the bodies caloric intake is derived from lipids and almost all of these calories come from fats, the . The fatty acid composition in terms of saturation (oxidation forms) is not uniform but varies with the origin. Plant fats contain more polyunsaturated fatty acids and animal fats contain more saturated fatty acids as well as cholesterol. Polyunsaturated fats are essential for humans because animals are not able to synthesize those on their own. Most lipids, however, have metabolic functions contributing to membrane structures and signaling. (C20:4) is a fatty acid which plays a central role as precursor for prostaglandin synthesis. Phospholipids are synthesized from diacylgycerolphosphate, a negatively charged phospholipid precursor and signaling molecule itself, carrying various hydrophilic and/or charged headgroups that determine the surface charge and chemical properties of biological membrane surfaces.
At the beginning of the 20th Century, it would have been hard to imagine that as we approach the end of the millenium, obesity, rather than hunger, would be a major public health problem for much of the developed world. The condition of being overweight affects 58 million Americans who spend $30 billion a year fighting excess pounds, often futilely. However, obesity is not just a problem in the U.S., it is an international health problem. Now recognized as a chronic disease, obesity is second only to smoking as a contributor to illness and premature death throughout the world. Complications that result from obesity include hypertension, hyperlipidemia, cardiovascular disease, diabetes, and cancer (1). By understanding and developing pharmacological agents that regulate fatty acid metabolism, the huge medical, social, and financial toll that obesity causes could be reduced.
The pathway for fatty acid synthesis occurs in the cytoplasm, ..
The rate of fatty acid synthesis is controlled by the equilibrium between the monomeric and polymeric acetyl-CoA carboxylase. Control of the acetyl-CoA carboxylase enzyme involves phosphorylation-dephosphorylation reactions (3). Metabolically, this conformational change is enhanced by citrate and is inhibited by long-chain fatty acids (i.e. palmitoyl-CoA). The accumulation of citrate in the cytosol of adipose cells shifts equilibrium to the polymeric acetyl-CoA carboxylase, thus activating fatty acid biosynthesis. Palmitoyl-CoA promotes polymer disaggregation and is a primary feedback inhibitor of fatty acid synthesis.
The level of food intake has profound effects on the rate of incorporation of lipogenic precursors into fatty acids in ruminant adipose tissue (4, 5). Smith et al. (4) demonstrated that graded increases in the level of food intake markedly increased de novo lipogenesis. Smith and Prior (6) suggested that ATP-citrate lyase is rate limiting to the incorporation of lactate into fatty acids because of the high correlation between the intracellular concentration of citrate and the rate of lipogenesis from lactate. Studies conducted using chickens demonstrated that short-term fasting reduces lipogenesis (7), while meal size increased the proportion of glycogen synthesized by rats (8).
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We Really Can Make Glucose From Fatty Acids After All
Several pioglitazone (1) derivatives have been tested as antidiabetic TZDs for possible clinical development (Tanis et al., ). PNU-91325 (2) was found to be the most effective TZD and proved to have greater binding to mitoNEET. Thus modification of mitoNEET function may, at least in part, contribute to lowering circulating lipid levels and glucose in the KKAy mouse model of human type-2 diabetes. Evidence has recently been presented suggesting that the insulin sensitizing effects of thiazolidinediones may correlate with modification of mitochondrial function rather than activation of PPARγ (Colca, ). Changes in mitochondrial function may alter the usage of cellular metabolites (e.g., sugars and fatty acids) in a way that favors insulin sensitivity.
Metabolic Actions of Insulin and Glucagon: Fatty acid ..
Thiazolidinedione (TZD) compounds are used for the treatment of type 2 diabetes and are believed to exert their beneficial effects by increasing glucose-derived fatty acid synthesis secondary to the increased degradation of long chain fatty acids through the activation of the nuclear receptor peroxisome proliferator-activated receptor-gamma (PPARγ). Studies with a tritiated photo-affinity labeled pioglitazone (1) analog identified a novel saturable TZD binding site also in mitochondria (Colca et al., ). The binding correlated with a et al., ).
Fatty Acid Synthesis: Activation, Steps and Control
Human liver hepatocellular (epithelial) carcinoma HepG2 cells (ATCC CRL11997) were purchased from American Type Culture Collection (ATCC, Manassas, VA, USA). HepG2 cells have an average doubling time of 34 h in DMEM with 10% fetal bovine serum and 2.5% horse serum (Gibco/BRL, Gaitersburg, MD) in the presence of antibiotics. The cells were incubated at 37 °C, 5% CO2 and 95% humidity and passed by using trypsin 0.25% (Gibco/BRL) no more than three times after receipt from the ATCC and prior to use in this study. HepG2 cells have previously been used in both in vitro and in vivo experiments and responded to treatment with troglitazone and other compounds with characteristic metabolic profile changes showing altered macromolecule synthesis and fatty acid cycling (Lee et al., ). Tracer-labeled parallel cultures of HepG2 cells were used in this study as controls to compare vehicle (DMSO) treated cell cultures to rosiglitazone (3), pioglitazone (1) and PNU-91325 (2) treatment in an escalating regime of drug treatment.
How Free Fatty Acids Inhibit Glucose Utilization in Human Skeletal ..
Alterations in substrate metabolism and mitochondria during the development of heart failure (HF). Bold lines indicate pathways reported to be activated. Thin lines represent pathways reported decreased. The question marks imply unknown changes or inconsistent observations. A, Fatty acid oxidation is impaired in cardiac hypertrophy and failure, leading to reduced ATP production. B, Most evidence suggests that glucose oxidation is unchanged in compensated hypertrophy and decreased in HF, but discrepancies exist. In contrast, several non–ATP-generating pathways of glucose metabolism (HBP, PPP, anaplerosis) are induced. C, Increased generation of mitochondrial reactive oxygen species (ROS; perhaps because of changes in the electron transport chain) causes direct mitochondrial damage, which may further increase mitochondrial ROS production to create a vicious cycle. Mitochondrial damage results in ATP deficiency. Mitochondrial ROS may also cause oxidative damage to other cellular components and may contribute to adverse structural remodeling. BCAA indicates branched-chain amino acid; CoA, coenzyme A; CPT, carnitine palmitoyltransferase; FAT, fatty acid transporter; G6P, glucose 6-phosphate; GLUT, glucose transporter; HBP, hexosamine biosynthetic pathway; IMS, mitochondrial intermembrane space; PPP, pentose phosphate pathway; and TG, triglyceride. Illustration Credit: Ben Smith. 
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