Overview of nutrition and lipogenesis

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Lipogenesis encompasses the processes of fatty acid synthesis and subsequent triacylglycerol synthesis, mainly from excess carbohydrate in the diet. The main sites of lipogenesis are liver and adipose tissue. A detailed overview of lipogenesis and other processes of lipid metabolism is presented in Chapter 1 and here only some specific aspects will be addressed.

In humans, the main site of de novo synthesis of fatty acids is the liver. Fatty acid synthesis requires NADPH, acetyl coenzyme A (CoA) and ATP, all of which are obtained by the liver in the postprandrial state (i.e. after meals), mainly from glucose metabolism (through the pentose phosphate pathway, glycolysis plus the pyruvate dehydrogenase reaction, and complete oxidation, respectively) (Fig. 4.3). Newly synthesized fatty acids (as acyl-CoA) are esterified to glycerol-3-phosphate, forming triacylglycerols that, to a large extent, abandon the liver as part of liver-born lipoproteins (mainly very low density lipoproteins, VLDL). These fatty acids eventually would reach adipocytes for storage. Therefore, enhanced lipogenesis over fatty acid oxidation in the liver may favor WAT enlargement.

In human WAT, de novo synthesis of fatty acids is quantitatively less important than in the liver. Rather, in the postprandial state, adipocytes synthesize triacylglycerol from fatty acids - derived from the action of lipoprotein lipase (LPL) on the lipoprotein (chylomicron, VLDL)-containing triacylglycerols - and glucose, which enters the adipocyte through insulin-regulated glucose transporter GLUT4 and whose intracellular metabolism produces the glycerol-3-phosphate needed for triacylglycerol synthesis (Fig. 4.3). Triacylglycerols are stored in the adipocytes,



Fig. 4.3 Overview of lipogenesis in hepatocytes and adipocytes. See Section 4.3 for details. PEPCK, phosphoenolpyruvate carboxykinase; ACC, acetyl-CoA carboxylase; FAS, fatty acid synthase; GLUT4, glucose-transporter 4.

contributing to adipocyte hypertrophy, and are mobilized in situations of energy deficit, such as fasting.

The traditional view is that low activity of the enzyme glycerol kinase in adipocytes ensures that triacylglycerol formation in these cells is dependent on an optimal supply of glucose, avoiding re-esterification under conditions in which fatty acids are to be exported, such as fasting. However, cycles of triacylglycerol hydrolysis and re-esterification do occur within the adipo-cytes, even during fasting, because glycerol-3-phosphate can be produced from precursors (other than glucose or glycerol) through glyceroneogene-sis, which is an abbreviated version of gluconeogenesis that occurs both in liver and adipose tissue.50'51 Disregulation of glyceroneogenesis in WAT can contribute to obesity (reviewed in reference 52). Overactivity, due to WAT-specific overexpression of the rate-limiting enzyme of the pathway (phos-phoenolpyruvate carboxykinase, PEPCK), results in obesity without insulin resistance in transgenic mice.52,53

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