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Life sciences · Journal article
Lipidology · November 6, 2026
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Dyslipidemia associated with obesity is characterized by alterations in lipid metabolism, insulin resistance, and chronic inflammation, which contributes to progression of atherosclerotic cardiovascular disease. Evidence suggests that obesity promotes elevations in triglycerides, apolipoprotein B, LDL, non-HDL cholesterol, as well as reductions in HDL cholesterol through adiponectin deficiency, cholesteryl ester transfer protein (CETP) activity, insulin resistance, and inflammation. In this review, the authors examine the evidence for the underlying mechanism behind this phenomenon as well as the effects of weight loss and therapeutic modalities that may change the trajectory of atherogenesis in the obese population using meta-analyses, randomized clinical trials, and basic science research studies. A reduction in as little as 5-15% of total body weight has been shown to improve triglyceride levels, promote insulin sensitivity, and optimize lipoprotein concentrations. Glucagon-like peptide-1 receptor agonists and dual glucose-dependent insulinotropic polypeptide/glucagon-like peptide-1 agonists improve metabolic parameters, while semaglutide demonstrates cardiovascular event reduction. Emerging therapies targeting apolipoprotein C-III, cholesteryl ester transfer protein, ANGPTL3, and PCSK9 demonstrate promising lipid-lowering effects, although long-term cardiovascular outcomes remain uncertain. Obesity-associated dyslipidemia is a modifiable risk factor for pathologic changes to the atherogenic profile while weight reduction can reverse the process to some degree. Further investigation is necessary to establish long-term efficacy, safety, and to prove cardiovascular outcome benefit among those suggesting from obesity.