Triglycerides increased synthesis

Alterations in the composition of the plasma lipids caused by estrogens are characterized by an increase in the high-density lipoproteins (HDL), a slight reduction in the low-density lipoproteins (LDL), and a reduction in total plasma cholesterol levels. Plasma triglyceride levels are increased. Estrogens decrease hepatic oxidation of adipose tissue lipid to ketones and increase synthesis of triglycerides. 

Increased synthesis of lipid or uptake. Increased synthesis of lipid may be the cause of fatty liver after hydrazine administration as this compound increases the activity of the enzyme involved in the synthesis of diglycerides. Hydrazine also depletes ATP and, however, inhibits protein synthesis. Large doses of ethanol will cause fatty liver in humans, and it is believed that this is partly due to an increase in fatty acid synthesis. This is a result of an increase in the NADH/NAD"1" ratio and therefore of the synthesis of triglycerides. Changes in the mobilization of lipids in tissues followed by uptake into the liver can also be another cause of steatosis. 

In six patients with renal transplants treated with sirolimus, mean total plasma cholesterol, triglyceride, and apolipoprotein concentrations increased (1067). The authors suggested that sirolimus increases lipase activity in adipose tissue and reduces lipoprotein lipase activity, resulting in increased hepatic synthesis of triglycerides, increased secretion of VLDL, and increased hypertriglyceridemia. 

Synthesis of fatty acids and triglycerides Increase Liver, adipose tissue... 

Insulin inhibits lipid breakdown by a number of mechanisms and increases synthesis of glycogen, fetty acids, triglycerides, and proteins. Insulin reduces the level of cyclic AMP. It also promotes the transport of glucose into cells, especially fet cells, where glucose can be converted and stored as triglyceride. 

Inhibits HMG-Co-A reductase, the enzyme that catalyzes the early step in cholesterol synthesis. Decreases LDL cholesterol, VLDL cholesterol, and plasma triglycerides, increases HDL cholesterol. 

Intolerance to intravenous lipid emulsion (IVFE), evidenced by increased serum triglyceride concentrations, is common in ARE Hypertriglyceridemia is thought to be caused by decreased catabolism of triglycerides and increased synthesis from free fatty acids (FFAs). Hepatic triglyceride lipase and peripheral lipoprotein lipase activ-... 

Many of (he effects of chronic alcohol abuse arc due either to the toxicity of acetaldehyde and/or the failure of one or more of the many homeostatic and synthetic mechanisms in the liver. One of the earliest signs of chronic alcohol abuse is hepatomegaly. This results from the accumulation of triglyceride due to increased synthesis from the carbohydrate load and reduced protein synthesis. Continued high ethanol intake may cause the following sequelae ... 

A multitude of genetic defects lead to an increased synthesis and/or a decreased catabolism of cholesterol or LDL. A well characterized although rare defect is the LDL-receptordefect. Ascorbate deficiency unmasks these inherited metabolic defects and leads to an increased plasma concentration of cholesterol-rich lipoproteins, e.g. LDL, and their deposition in the vascular wall. Hypercholesterolemia increases the risk for premature CVD primarily when combined with elevated plasma levels of Lp(a) or triglycerides. 

Triglyceride accumulation in the liver (i.e. fatty livers) can be brought about by agents which will cause an increased synthesis of triglycerides, decreased oxidation, increased uptake of triglycerides or fatty acids from the blood, decreased secretion of triglycerides by the liver, or a combination of any of these factors. 

A molecular variation of plasma membrane has been reported by Puccia et al. Reduction of total lipids (XL) content and significant variations of triglyceride (TG) and phospholipids (PL) fractions were observed as a consequence of exposure of C. intestinalis ovaries to TBTCl solutions. In particular, an evident TG decrease and a PL increase were observed, which probably provoked an increment in membrane fluidity, because of the high concentration of long chain fatty acids and, as a consequence, PL. This could be a cell-adaptive standing mechanism toward the pollutants, as observed in Saccharomyces cerevisiae. Also the increase in the content of the polyunsaturated fatty acids (PUPA), important in the synthesis of compounds such as prostaglandin which are present in the ovary in a stress situation, was probably a consequence of a defense mechanism to the stress provoked by the presence of TBTCl. 

Gemfibrozil reduces the synthesis of VLDL and, to a lesser extent, apolipoprotein B with a concurrent increase in the rate of removal of triglyceride-rich lipoproteins from plasma. Clofibrate is less effective than gemfibrozil or niacin in reducing VLDL production. 

Several studies have been conducted on calcium-fat interactions in human infants (64-70). Low synthesis of bile salts and low pancreatic lipase activity may be responsible for poorer fat utilization in infants than in adults (63,71). Fat from infant formulas may be lower than that from human milk because of the lack of a bile-stimulated lipase in the former (72). In infants, fat absorption tends to decrease with increase in fatty acid length, with lower degree of saturation, and with increase of total fat (3). Triglyceride structure may also influence fat absorption in the infant and, thus, indirectly, might also affect calcium absorption in the infant. 

Il.f.l.1. Insulins. Insulin is the most effective of diabetes medications. Insulin has profound effects on carbohydrate, protein, fat metabolism and electrolytes. It has anabolic and anticatabolic actions. In a state of insulin deficiency, glycogenesis, glucose transport, protein synthesis, triglyceride synthesis, LPL activity in adipose tissue, cellular potassium uptake all decrease on the other hand, gluconeogene-sis, glycogenolysis, protein degradation, ketogene-sis, lipolysis increase. 

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