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#Gastroenterology #Hepatology #Multispeciality
Obesity is related with an increased risk of nonalcoholic fatty liver disease (NAFLD). Steatosis or fatty liver, a hallmark feature of NAFLD is caused when the rate of hepatic fatty acid uptake from plasma and de novo fatty acid synthesis is more than the rate of fatty acid oxidation and export. This pathological mechanism produces an excessive amount of intrahepatic triglyceride which thus, shows a state of an imbalance between different complex metabolic events. Moreover, fatty liver is correlated with a various adverse reactions undergoing in glucose, fatty acid and lipoprotein metabolism.
Plethora of evidences suggest that abnormalities in fatty acid metabolism, in combination with adipose tissue, hepatic, and systemic inflammation, are important pathological process implicated in the development of insulin resistance, dyslipidemia and other cardiometabolic risk factors related with NAFLD.
Evidence based observations also suggest that obesity is correlated with multiple metabolic risk factors for cardiovascular disease, such as insulin resistance, diabetes, and dyslipidemia. About 30% of obese adults are termed as metabolically normal, which is characterized by some measure of insulin sensitivity or having ≤1 cardiometabolic abnormality. Moreover, pathologic increased production of intrahepatic triglyceride (IHTG) content in obese persons is a considered to be a key marker of metabolic abnormalities such as insulin resistance in liver, muscle and adipose tissue, alterations in free fatty acid metabolism, and increased VLDL-TG secretion rate, which is independent of BMI, percent body fat, and visceral fat mass. On the contrary, obese persons with normal IHTG content have not shown any inclination of developing obesity-related metabolic complications. However, more research is required to assess whether NAFLD is a cause or a consequence of metabolic dysfunction.
Source: Fabbrini E, Sullivan S, Klein S. Obesity and nonalcoholic fatty liver disease: biochemical, metabolic, and clinical implications. Hepatology. 2010;51(2):679-689.