Fatty pathogenesis

Eaton S et al Multiple biochemical effects in the pathogenesis of fatty liver. EurJ Clin Invest 1997 27 719. 

Wilson DM, Binder LI. Free fatty acids stimulate the polymerization of tau and amyloid beta peptides. In vitro evidence for a common effector of pathogenesis in Alzheimer s disease. Am J Pathol 1997 150 2181-2195. 

Bays, H., Mandarino, L., and DeEronzo, R. A. (2004). Role of the adipocyte, free fatty acids, and ectopic fat in pathogenesis of type 2 diabetes mellitus Peroxisomal proleferator-activated receptor agonists provide a rational therapeutic approach. /. Clin. Endocrinol. Metab. 89, 463 78. 

Zieve L, Doizaki WM, Zieve FJ Synergism between mercaptans and ammonia or fatty acids in the production of coma A possible role for mercaptans in the pathogenesis of hepatic coma. J Lab Clin Med 83 16-28, 1974... 

Histone deacetylases are linked to the pathogenesis of malignancy from a mechanistic perspective. The capacity of HDAC inhibitors (HDACi) to interfere with the enzyme fimction has led to the observed prechnical and clinical activity in cancer therapy. Although the exact mechanism of anti-tumor activity is not fully elucidated, various cellular pathways have been shown to be involved. From the first chnical trials involving HDACi with short chain fatty acids to the newer generation hydroxamic acid derivatives and cychc tetrapeptides, a number of structurally diverse compounds have made the transition from the laboratory to the chnical arena. For purposes of this part of the discussion, HDACi are arbitrarily divided into the hydroxamates and nonhydroxamates. 

The pathogenesis of alcoholic liver disease is a multifactorial process involving metabolic repercussions of ethanol oxidation in the liver, dysregulation of fatty acid oxidation and synthesis, and activation of the innate immune system by a combination of direct effects of ethanol and its metabolites and by bacterial endotoxins that access the liver as a result of ethanol-induced changes in the intestinal tract. Tumor necrosis factor- , a proinflammatory cytokine that is consistently... 

In contrast to MPO, eosinophil peroxidase (EPO) prefers to oxidize plasma level bromide (20-100 pM) to hypobromous acid (HOBr) and several biological targets are implicated, including nucleic acids and nucleosides (1480, 1482, 2376), proteins (1812, 1813, 2377, 2378), unsaturated fatty acids (2379), and low-density lipoprotein (2380, 2381). This EPO-dependent bromination is suggested to be involved in the pathogenesis of asthma (2382). Accordingly, both 3-bromotyrosine and 3,5-dibromotyrosine (1812,1813) are produced by EPO-induced bromination of tyrosine residues in lung tissue (1813, 2382). 

Figure 14.1 Triglyceride cycle in the pathogenesis of fatty liver. = are metabolic blocks. (From S. A. Meyer, Introduction to Biochemical Toxicology, 3rd ed., Wiley, 2001.)...

Ghoshal AK, Porta EA, Hartroft WS. 1969. The role of lipoperoxidation in the pathogenesis of fatty livers induced by phosphorus poisoning in rats. Am J Pathol 54 275-291. 

Menendez JA, Lupu R (2007) Fatty acid synthase and the lipogenic phenotype in cancer pathogenesis. Nat Rev Cancer 7 763-777... 

Kumar CA, Das UN. Lipid peroxides, nitric oxide and essential fatty acids in patients with Plasmodium falciparum malaria. Prostaglandins Leukot Essent Eatty Acids 1999 61 255-258. Xiao L, Patterson PS, Yang C, Lai AA. Role of eicosanoids in the pathogenesis of murine cerebral malaria. Am. J. Trop. Med. Hyg. 1999 60 668-673. 

There is substantial evidence that indicates that dietary fat can influence significantly not only serum levels of cholesterol and triacylglycerols but also the lipid composition and content of Apoproteins (156-159). Much attention has been placed on the effects of diet on LDL levels, and saturated fatty acid and cholesterol itself have been identified as the major nutritional factors that can raise serum LDL-cholesterol levels. However, LDL cholesterol is only one of the many risk factors for atherosclerosis, and it is not known if oxidative modification of LDL is an equally or more important factor in the pathogenesis of atherosclerosis than total LDL cholesterol per se. More longitudinal studies are needed to answer these questions. If lipid peroxidation is a major risk factor for atherosclerosis, then excess consumption of highly unsaturated fats may not be advisable. 

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