Lipogenesis cells

The citric acid cycle is the final common pathway for the aerobic oxidation of carbohydrate, lipid, and protein because glucose, fatty acids, and most amino acids are metabolized to acetyl-CoA or intermediates of the cycle. It also has a central role in gluconeogenesis, lipogenesis, and interconversion of amino acids. Many of these processes occur in most tissues, but the hver is the only tissue in which all occur to a significant extent. The repercussions are therefore profound when, for example, large numbers of hepatic cells are damaged as in acute hepatitis or replaced by connective tissue (as in cirrhosis). Very few, if any, genetic abnormalities of citric acid cycle enzymes have been reported such ab-normahties would be incompatible with life or normal development. 

The pathway has an oxidative phase, which is irreversible and generates NADPH and a nonoxidative phase, which is reversible and provides ribose precursors for nucleotide synthesis. The complete pathway is present only in those tissues having a requirement for NADPH for reductive syntheses, eg, lipogenesis or steroidogenesis, whereas the nonoxidative phase is present in all cells requiring ribose. 

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... 

Glucocorticoids inhibit the uptake of glucose by fat cells, resulting in increased lipolysis. The increased insulin secretion in response to hyperglycaemia also stimulates lipogenesis and ultimately increase in fat deposition. 

Glucocorticoids increase serum glucose levels and thus stimulate insulin release and inhibit the uptake of glucose by muscle cells, while they stimulate hormone sensitive lipase and thus lipolysis. The increased insulin secretion stimulates lipogenesis and to a lesser degree inhibits lipolysis, leading to a net increase in fat deposition combined with increased release of fatty acids and glycerol into the circulation. 

Endocrine Influences. A number of hormones are known to influence carbohydrate metabolism in the mammal. Insulin seems to increase oxidation of glucose, lipogenesis. and glycogenesis. Its primary mode of action may be io facilitate the entry of glucose into the cell. 

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. 

MetabolicaUy, biotin is of central importance in lipogenesis, gluconeogen-esis, and the catabolism of branched-chain (and other) amino acids. There are two well-characterized biotin-responsive inborn errors of metabolism, which are fatal if untreated holocarboxylase synthetase deficiency and biotinidase deficiency. In addition, biotin induces a number of enzymes, including glu-cokinase and other key enzymes of glycolysis. Biotinylation of histones may be important in regulation of the cell cycle. 

Lipogenesis, the synthesis of lipids from carbohydrate via acetyl-CoA, occurs almost exclusively in the liver cells and the fatty tissue, (s. fig. 3.9) According to lipid topogenesis (4), the enzymes involved in triglyceride and phospholipid synthesis are localized on the cytoplasmic surface of the endoplasmic reticulum. The level of hepatic synthesis is regulated primarily by the insulin-glucagon quotient, as described by R.H. Unger in 1971. 

Effects of Natural Products isolated from Medicinal Plants and Foodstuffs on Lipolysis and Lipogenesis in Fat Cells... 

We also reported that propranolol, a p-blocker, inhibited both catecholamine-induced lipolysis and insulin-stimulated lipogenesis from glucose in fat cells [3]. In contrast to p-blockers, adenosine and... 

Fig. (4). and Fig. (5). Effects of adenosine and pyroglutamic acid isolated from Ginseng roots on lipogenesis from glucose in rat fat cells... 

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