Disease relevance of Lipogenesis

• As a citrate cleavage enzyme that may play an essential role in de novo lipogenesis inhibition, G cambogia is claimed to lower body weight and reduce fat mass in humans [1].
• Insulin action was studied in rats with CCl4/phenobarbital-induced cirrhosis of the liver using the euglycemic hyperinsulinemic clamp technique coupled with isotopic measurement of individual tissue glucose uptake, glycogen formation, and lipogenesis [2].
• However, synthetic LXR ligands have also been shown to induce lipogenesis and hypertriglyceridemia in mice, raising questions as to the net effects of these compounds on the development of cardiovascular disease [3].
• S14 expression provides a pathophysiological link between two prognostic indicators in breast cancer: enhanced lipogenesis and 11q13 amplification [4].
• Stimulation of S14 mRNA and lipogenesis in brown fat by hypothyroidism, cold exposure, and cafeteria feeding: evidence supporting a general role for S14 in lipogenesis and lipogenesis in the maintenance of thermogenesis [5].

High impact information on Lipogenesis

• M. tuberculosis differs radically from other bacteria in that a very large portion of its coding capacity is devoted to the production of enzymes involved in lipogenesis and lipolysis, and to two new families of glycine-rich proteins with a repetitive structure that may represent a source of antigenic variation [6].
• LXR also induces the sterol response element binding protein-1c that regulates lipogenesis [7].
• However, in adipocytes from homozygous Brattleboro rats oxytocin is incapable of stimulating lipogenesis or pyruvate dehydrogenase activity, although insulin stimulation of both processes is normal and the antilipolytic activity of oxytocin is normal [8].
• Oxytocin has insulin-like activity in that it stimulates lipogenesis and increases pyruvate dehydrogenase activity [8].
• Oral administration of T0901317 to mice and hamsters showed that LXR activated the coordinate expression of major fatty acid biosynthetic genes (lipogenesis) and increased plasma triglyceride and phospholipid levels in both species [9].

Chemical compound and disease context of Lipogenesis

• This suggests that in freshly isolated Morris Hepatoma 7777 cells, citrate export from the mitochondria for cholesterogenesis and lipogenesis is a minor fate of substrate carbon entering the mitochondria for oxidation [10].
• Hypertriglyceridemia in lecithin-cholesterol acyltransferase-deficient mice is associated with hepatic overproduction of triglycerides, increased lipogenesis, and improved glucose tolerance [11].
• The hyperlipidemia associated with obesity and type 2 diabetes is caused by an increase in hepatic triglyceride synthesis and secretion that is secondary to an increase in de novo lipogenesis, a decrease in fatty acid (FA) oxidation, and an increase in the flux of peripherally derived FA to the liver [12].
• These finding suggest that metabolism of ethanol increased hepatic lipogenesis by activating SREBP-1 and that this effect of ethanol may contribute to the development of alcoholic fatty liver [13].
• We conclude that in STZ-D, ketosis does not stimulate hepatic lipogenesis via cytosolic activation of acetoacetate [14].

Biological context of Lipogenesis

• 15-19% of the increased caloric intake was channeled through lipogenesis, assuming glucose to be the sole substrate for lipogenesis [15].
• Thyroid hormone, acting through several nuclear hormone receptors, plays important roles in thermogenesis, lipogenesis and maturation of the neonatal brain [16].
• Lipid metabolism was estimated by Oil Red O staining of intracellular lipids, mRNA expression of fatty acid synthase and adipocyte lipid binding protein 2, and insulin activation of lipogenesis [17].
• A regulatory role for intracellular Ca2+ ([Ca2+]i) in adipocyte lipogenesis, lipolysis and triglyceride accumulation has been demonstrated [18].
• Its effects on lipogenesis, substrate cycling, peroxisome proliferation, mitochondrial respiration, protein synthesis, and thyroid hormone function have been reported [19].

Anatomical context of Lipogenesis

• The results suggest that calcitonin lowers serum lipid levels and lipogenesis in hepatocytes in a calcium/calmodulin-dependent way [20].
• In the transition between the fasting state (low rates of lipogenesis) and fasting/re-feeding (high rates), the fraction of total cytosolic plus microsomal acetyl-CoA carboxylase in the microsomes increases from 6% to 43%, whereas the microsomal proportion of total fatty acid synthetase and ATP-citrate lyase remains approximately 10% [21].
• Because insig-1 binds sterol regulatory element-binding protein cleavage-activating protein in the endoplasmic reticulum, thereby blocking proteolytic processing required for sterol regulatory element-binding protein activation, we tested its influence on lipogenesis [22].
• The administration of a single injection of tumor necrosis factor (TNF) produces a variety of acute and sustained biological effects, including hyperlipidemia, stimulation of hepatic lipogenesis, decreases in adipose tissue lipoprotein lipase activity, and anorexia with weight loss [23].
• The oligonucleotides did not significantly affect lipogenesis in a rat hepatoma cell line that does not express detectable spot 14 mRNA or protein [24].

Associations of Lipogenesis with chemical compounds

• In agreement with reports from some laboratories, but contrary to popular belief, glucose was not taken up efficiently by the cells and was thus a poor substrate for eigher glycogen synthesis or lipogenesis [25].
• In transgenic mice overexpressing a protein that regulates SREBP activation, lipogenesis is more sensitive to cholesterol and less sensitive to insulin [26].
• The best precursor for glycogen formation was fructose, whereas lactate (pyruvate) was most efficient in lipogenesis [25].
• Tumor necrosis factor-alpha stimulates hepatic lipogenesis in the rat in vivo [27].
• In conclusion, portacaval shunting lowered blood triacylglycerol and cholesterol levels in fa/fa rats, and this was due, at least partially, to reduction in hepatic lipogenesis and cholesterologenesis [28].

Gene context of Lipogenesis

• ATF6 modulates SREBP2-mediated lipogenesis [29].
• Corticotropin-releasing hormone: an autocrine hormone that promotes lipogenesis in human sebocytes [30].
• Polyunsaturated fatty acids (PUFAs) are not only ligands for peroxisome proliferator-activated receptor (PPAR) alpha but are also negative regulators of hepatic lipogenesis, which is thought to be mediated by the repression of sterol regulatory element-binding protein (SREBP)-1 [31].
• Fatty acid synthase (FAS) plays a central role in de novo lipogenesis in mammals [32].
• These results indicate that the LXR signaling pathway modulates FAS expression through distinct but complementary mechanisms and suggest that the FAS gene may be a critical target in the control of lipogenesis by LXRs [33].

Analytical, diagnostic and therapeutic context of Lipogenesis

• CONCLUSIONS: The addition of high-performance inulin to a moderately high-carbohydrate, low-fat diet has a beneficial effect on plasma lipids by decreasing hepatic lipogenesis and plasma triacylglycerol concentrations [34].
• Flutamide inhibition of flank organ weight paralleled the drug effect on lipogenesis [35].
• To obtain a measure of sebaceous lipogenesis, the class composition of the lipid was determined by quantitative thin-layer chromatography and the ratio of wax esters/[cholesterol + cholesterol esters] (WE/[CH + CE]) was calculated [36].
• However, only in the intact control group did training promote a higher basal and isoproterenol-stimulated lipolysis, increase the incorporation of palmitate (esterification), decrease the incorporation of acetate (lipogenesis) into lipids and diminish circulating leptin levels [37].
• Plasma testosterone levels were determined by radioimmunoassay (RIA) of blood samples and sebaceous lipogenesis was determined by measurement of the incorporation of a lipid precursor, 14C-acetate, in ear skin biopsy samples [38].

References