PHARMACEUTICAL AGENTS-MEDIATED LIVER TOXIC DAMAGE AND OBESITY

Studies have shown that drug-induced liver injury, which involves the parent drug or a reactive metabolite generated through cytochromes P450, Microvesicular steatosis, a potentially severe liver lesion usually associated with liver failure and profound hypoglycemia, is due to a major inhibition of mitochondrial fatty acid oxidation (FAO). Moreover, recent investigations suggest that some drugs could favor lipid deposition in the liver through primary alterations of white adipose tissue (WAT) homeostasis. Numerous factors could favor drug-induced mitochondrial and metabolic toxicity, such as the structure of the parent molecule, genetic predispositions (in particular those involving mitochondrial enzymes), alcohol intoxication, hepatitis virus C infection, and obesity. In obese and diabetic patients, some drugs may induce acute liver injury more frequently. World many countries are facing an epidemic of obesity that can be explained, at least in part, by a sedentary life style and calorie overconsumption. This poses a major issue for public health since obesity primarily enhances the risk of various illnesses such as type 2 diabetes, coronary heart disease, some cancers and non-alcoholic fatty liver disease (NAFLD). Consequently, obese patients are consuming on average more drugs than non-obese individuals, some medications in obese individuals can cause severe liver damage [1]