Key result
Atherogenic dyslipidemia in nonalcoholic fatty liver disease is characterized by increased triglycerides, reduced HDL, and small dense LDL particles, largely driven by insulin resistance.
This review highlights the pathophysiology of atherogenic dyslipidemia in NAFLD, emphasizing the role of insulin resistance in driving lipid abnormalities that increase cardiovascular risk.
Alerts to elevated CV risk from dyslipidemia in NAFLD; leaves open targeted intervention trials.
Cardiovascular disease represents the most common cause of death in patients with nonalcoholic fatty liver disease (NAFLD). Patients with NAFLD exhibit an atherogenic dyslipidemia that is characterized by an increased plasma concentration of triglycerides, reduced concentration of high-density lipoprotein (HDL) cholesterol, and low-density lipoprotein (LDL) particles that are smaller and more dense than normal. The pathogenesis of NAFLD-associated atherogenic dyslipidemia is multifaceted, but many aspects are attributable to manifestations of insulin resistance. Here the authors review the structure, function, and metabolism of lipoproteins, which are macromolecular particles of lipids and proteins that transport otherwise insoluble triglyceride and cholesterol molecules within the plasma. They provide a current explanation of the metabolic perturbations that are observed in the setting of insulin resistance. An improved understanding of the pathophysiology of atherogenic dyslipidemia would be expected to guide therapies aimed at reducing morbidity and mortality in patients with NAFLD.
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Fisher et al. (2013) conducted a review in Nonalcoholic fatty liver disease (NAFLD). Atherogenic dyslipidemia in nonalcoholic fatty liver disease is characterized by increased triglycerides, reduced HDL, and small dense LDL particles, largely driven by insulin resistance.
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