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Dyslipidemia (high LDL and triglycerides; low HDL), insulin acute pancreatitis resistance, and other components of the metabolic syndrome (see sidebar, on p.56, “The Syndrome X Connection”) increasingly are recognized as being associated with NAFLD. Adding weight to the theory that insulin resistance plays a leading role in the development of a fatty liver is that high insulin levels have acute pancreatitis been shown to block the oxidation (burning off) of fat in liver cells (hepatocytes), contributing to the buildup of harmful fatty acids and triglycerides in the organ.13-15 In fact, triglyceride fat is acute pancreatitis the very type of fat stored in tiny sacs inside a fatty liver.7 High concentrations of fatty acids (which help produce the triglycerides that can build up in the liver) are not only toxic to liver cells, but also may be directly tied to the oxidative stress that leads to the inflammation and scarring in the second stage of NAFLD.13,16
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