Adipose tissue lipogenesis

Marshall CE, Watis DI, Sugden MC. 1983. Effects of hydrazine on liver and brown adipose tissue lipogenesis in 24-h starved rats. J Pharm Pharmacol 35 460-461. 

Clarke SD, Romsos DR, Leveille GA. Differential effects of dietary methyl esters of long chain saturated and polyunsaturated fatty acids on rat liver and adipose tissue lipogenesis. J Nutr 1977 107 1170-1180. Clarke SD, Armstrong MK, Jump DB. Nutritional control of rat liver fatty acid synthase and S14 mRNA... 

Fatty acids are synthesized by an extramitochondrial system, which is responsible for the complete synthesis of palmitate from acetyl-CoA in the cytosol. In the rat, the pathway is well represented in adipose tissue and liver, whereas in humans adipose tissue may not be an important site, and liver has only low activity. In birds, lipogenesis is confined to the liver, where it is particularly important in providing lipids for egg formation. In most mammals, glucose is the primary substrate for lipogenesis, but in ruminants it is acetate, the main fuel molecule produced by the diet. Critical diseases of the pathway have not been reported in humans. However, inhibition of lipogenesis occurs in type 1 (insulin-de-pendent) diabetes mellitus, and variations in its activity may affect the nature and extent of obesity. 

Insulin stimulates lipogenesis by several other mechanisms as well as by increasing acetyl-CoA carboxylase activity. It increases the transport of glucose into the cell (eg, in adipose tissue), increasing the availability of both pyruvate for fatty acid synthesis and glycerol 3-phosphate for esterification of the newly formed fatty acids, and also converts the inactive form of pyruvate dehydrogenase to the active form in adipose tissue but not in liver. Insulin also—by its ability to depress the level of intracellular cAMP—inhibits lipolysis in adipose tissue and thereby reduces the concentration of... 

Human adipose tissue may not be an important site of lipogenesis. There is no significant incorporation of glucose or pyruvate into long-chain fatty acids ATP-... 

Adipose tissue Storage and breakdown of triacylglyc-erol Esterification of fatty acids and lipolysis lipogenesis Glucose, lipoprotein triacylglycerol Free fatty acids, glycerol Lipoprotein lipase, hormone-sensitive lipase... 

Lipogenesis in liver and possibly adipose tissue, leading to increased synthesis of phospholipids and triacylglycerol. 

Very little data are available regarding effects of anabolic steroid implants on the lipid metabolism in growing ruminants. Lipogenic enzyme activity and fatty acid synthesis in vitro were elevated in subcutaneous adipose tissue from bulls implanted with estradiol (44), which may account for the increase in fat content of carcasses reported in some studies. TBA implants have no effect on lipogenesis in intact heifers, and only tend to reduce lipogenic enzyme activities in ovariectomized heifers (45). 

It has been reported also that epidermal growth factor stimulates fatty acid synthesis and the phosphorylation of ACC in rat liver and adipose tissues (Holland and Hardie, 1985) through phosphorylation of the I-peptide, suggesting that several peptide hormones sharing homology with insulin, such as IGF-1, could enhance lipogenesis similarly. 

Insulin is an antilipolytic hormone, and its effect on adipose tissue is to increase the transport of glucose into the fat cell, to stimulate lipogenesis and inhibit lipolysis. Thus, pyruvate dehydrogenase and acetyl-CoA carboxylase are activated, and the hormone-sensitive lipase is inactivated. In the normal, well-fed state insulin stimulates the deposition of fat. 

Taylor, W.M., D Costa, M., Angel, A., Halperin, M.L. (1977). Insulin-like effects of fluoroacetate on lipolysis and lipogenesis in adipose tissue. Can. J. Biochem. 55 982-7. 

Moreover, the relative sensitivity of the tissues was in the same order as the relative sensitivity of the three species to the hypoglycemic action of the biguanides. In another investigation, a number of the effects of phenformin on metabolism in rat adipose tissue,— Inhibition of glucose oxidation and lipogenesis, both basal and insulin stimulated— were traced to an inhibition of pyruvate oxidation, presumably resulting from interference with electron transport. 

Although the effects of insulin on postprandial metabolism are profound, other factors (e.g., substrate supply and allosteric effectors) also affect the rate and degree to which these processes occur. For example, elevated levels of fatty acids in blood promote lipogenesis in adipose tissue. Regulation by several allosteric effectors further ensures that competing pathways do not occur simultaneously for example, in many cell types fatty acid synthesis is promoted by citrate (an activator of acetyl-CoA carboxylase), whereas fatty acid oxidation is depressed by malonyl-CoA (an inhibitor of carnitine acyltransferase I activity). The control of fatty acid metabolism is described in Section 12.1. 

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