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Hepatic lipase (HL), also called hepatic triglyceride lipase (HTGL) or LIPC (for "lipase, hepatic"), is a form of lipase, catalyzing the hydrolysis of triacylglyceride. Hepatic lipase is coded by chromosome 15 and its gene is also often referred to as HTGL or LIPC . [ 5 ]
Liver function tests (LFTs or LFs), also referred to as a hepatic panel or liver panel, are groups of blood tests that provide information about the state of a patient's liver. [1] These tests include prothrombin time (PT/INR), activated partial thromboplastin time (aPTT), albumin , bilirubin (direct and indirect), and others.
According to NICE guidelines, statins can continue unless liver enzyme levels double within three months of starting statins. [66] Treatment with pentoxifylline is not recommended. [14] Omega-3 fatty acids may reduce liver fat and improve blood lipid profile but do not seem to improve liver histology (fibrosis, cirrhosis, cancer). [14]
Those with higher levels of HDL-C tend to have fewer problems with cardiovascular diseases, while those with low HDL-C cholesterol levels (especially less than 40 mg/dL or about 1 mmol/L) have increased rates for heart disease. [8] [needs update] Higher native HDL levels are correlated with lowered risk of cardiovascular disease in healthy people.
Lipoprotein lipase deficiency leads to hypertriglyceridemia (elevated levels of triglycerides in the bloodstream). [35] In mice, overexpression of LPL has been shown to cause insulin resistance, [36] [37] and to promote obesity. [30] A high adipose tissue LPL response to a high-carbohydrate diet may predispose toward fat gain.
Lipoprotein lipase deficiency is a genetic disorder in which a person has a defective gene for lipoprotein lipase, which leads to very high triglycerides, which in turn causes stomach pain and deposits of fat under the skin, and which can lead to problems with the pancreas and liver, which in turn can lead to diabetes.
Liver failure is the inability of the liver to perform its normal synthetic and metabolic functions as part of normal physiology. Two forms are recognised, acute and chronic (cirrhosis). [1] Recently, a third form of liver failure known as acute-on-chronic liver failure (ACLF) is increasingly being recognized. [2]
The complications are hepatic encephalopathy and impaired protein synthesis (as measured by the levels of serum albumin and the prothrombin time in the blood). The 1993 classification defines hyperacute as within 1 week, acute as 8–28 days, and subacute as 4–12 weeks; [ 1 ] both the speed with which the disease develops and the underlying ...