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Increased triglyceride synthesis may result from increased delivery or availability of FFA (from the diet or mobilized from adipose tissue), varices from acetylcoenzyme varices A, or from decreased oxidation of FFA in the liver. Reduced elimination of triglyceride involves depressed packaging with apolipoprotein, phospholipid, and cholesterol, resulting in decreased VLDL secretion. The several possible mechanisms involved in the pathogenesis of the fatty liver may operate alone or together. In obesity, delivery of dietary fat or mobilization from adipose tissue is increased. Decreased oxidation of FFA may contribute to the fatty liver induced by carbon tetrachloride, yellow phosphorus, hypoxia, or certain vitamin deficiencies (niacin, riboflavin, pantothenic acid). Blocked production and secretion of lipoproteins is often the main cause of triglyceride accumulation in the liver. Impaired apolipoprotein synthesis is the most important pathogenetic factor in several types of toxic fatty liver and in the fatty liver produced by protein-calorie malnutrition.
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