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  • Review
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6 November 2026

13 Pages

Obesity-Related Dyslipidemia and the Impact of Novel Therapeutics on the Atherogenic Profile

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Bruce & Robbi Toll Heart and Vascular Institute, Thomas Jefferson University Hospital, Philadelphia, PA 19107, USA
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Author to whom correspondence should be addressed.
Lipidology2026, 3(4), 28;https://doi.org/10.3390/lipidology3040028
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Abstract

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.

1. Obesity-Associated Dyslipidemia

It is estimated that, in the United States, over 40% of adults suffer from obesity, defined as a body mass index (BMI) greater than 30 kg/m2 [1]. Obesity is both an independent and causal risk factor for heart failure, atrial fibrillation, stroke, hypertension, and sudden cardiac death [2]. Patients who suffer from obesity, namely those with marked central adiposity, experience systemic inflammation as well as changes to lipid profiles, insulin resistance, and endothelial dysfunction—all of which contribute to accelerating atherosclerosis [3]. Therefore, it is important to study how weight loss by any mechanism, whether via bariatric surgery, with medication, or solely through diet/lifestyle, may improve cardiovascular disease (CVD) risk. Does the weight loss associated with the use of these drugs impact coronary atherosclerosis and risk of adverse cardiac events? In this review, the authors use extensive literature search to investigate prior prospective randomized clinical trials, animal models, and meta-analyses to summarize what is known about obesity’s effects on lipid profiles and atherogenicity as well as the effects of weight loss to determine if there is indeed a “reversibility” of the inflammatory atherogenic process.
The research reviewed includes studies published over the past fifty years. Search terms included limitations on date published for therapeutic options to include pivotal trials from no earlier than the 2000s, but basic science and animal model research on atherogenesis included articles as far back as the 1970s, a time when coronary atherogenesis mechanistic research was robust. Single-center observational trials were excluded.
This review first describes the effect of obesity on atherogenesis, followed by the effect of weight loss on atherogenic particles, and concludes with current and future medical and surgical methods to achieve both weight loss and improved atherogenic profile.

Lipid Profile Changes with Obesity

In the setting of obesity, lipid levels typically change in a pattern characterized by elevated triglycerides (TG), reduced high-density lipoprotein cholesterol (HDL-C), increased non-HDL cholesterol, elevated apolipoprotein B (apoB), and a greater proportion of small, dense low-density lipoprotein (LDL) particles (Table 1) [4]. One mechanism thought to be responsible for these changes is a decrease in adiponectin levels seen in those with obesity, specifically those with higher central adiposity and visceral fat [5]. Adiponectin is a hormone secreted by adipose tissue and is responsible for enhancing insulin sensitivity by promoting glucose uptake and fatty acid oxidation in skeletal muscle and suppressing hepatic glucose production. It also increases HDL cholesterol and decreases triglycerides by upregulating ATP-binding cassette transporter A1 and lipoprotein lipase while reducing hepatic lipase (LPL) activity, which is associated with decreased HDL production. Its anti-inflammatory and anti-atherogenic properties include inhibition of macrophage activation, reduction of pro-inflammatory cytokines, and promotion of cholesterol efflux from vascular cells [6]. However, for patients with excessive visceral fat, hypertrophied visceral adipocytes and low-level inflammation lead to decreased gene expression of adiponectin, leading to decreased insulin sensitivity, worsening of dyslipidemia, and increased cardiometabolic risk [7].
Table 1. Lipid Changes in Obesity and Impact of Weight Loss.
Cholesterol was measured (concentration, the standard lab value obtained clinically). ApoB level reflects the number of circulating atherogenic lipoproteins and is a more accurate marker of cardiovascular risk in this population [8,9]. The relationship between obesity and apoB is further influenced by fat distribution, with central (visceral) adiposity showing a stronger correlation with elevated apoB than peripheral fat depots [10].
Another mechanism by which obesity alters lipid profile is via increased cholesteryl ester transfer protein (CETP) level. Adipose tissue is a major source of CETP production, and expansion of adipose mass in obesity upregulates CETP synthesis and secretion [11]. With increased levels of CETP, HDL particles lose cholesterol esters in exchange for TG, which then gets catabolized by hepatic lipase, lowering circulating HDL-C. In addition to decreased adiponectin and increased CETP, the atherogenic milieu associated with obesity is enhanced by insensitivity to insulin caused by the metabolic syndrome [4].
When insulin loses its effect on adipose tissue, the normal antilipolytic effect is impaired, resulting in increased release of free fatty acids (FFAs) into the circulation [12]. These FFAs are taken up by the liver, where they serve as substrates for hepatic triglyceride synthesis and drive overproduction of very low-density lipoprotein (VLDL) particles, leading to elevation in triglyceride (TG) levels [4,13]. Increased de novo synthesis of TGs coupled with decreased activity of lipoprotein lipase (LPL) to break down circulating TG leads to even higher levels for the patient with obesity and insulin resistance.
Though adiposity is associated with the metabolic syndrome and insulin insensitivity, it also has direct effects on creating atherogenic lipid profiles and facilitating an environment that promotes coronary atherosclerosis. Adipocytes and infiltrating immune cells in obese adipose tissue secrete increased levels of proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), interleukin-1β (IL-1β), and monocyte chemoattractant protein-1 (MCP-1) [14,15]. These cytokines promote local and systemic inflammation, endothelial dysfunction, and contribute to the development and progression of coronary artery disease (CAD) by facilitating atherogenesis and plaque instability [15].

2. Weight Loss and Lipid Metabolism

2.1. Overall Lipid Profile Changes with Weight Loss

Obesity is strongly associated with dyslipidemia, characterized by elevated triglycerides (TG) and apoB, increased very-low-density lipoprotein (VLDL) secretion, and elevated non-HDL-C levels while high-density-lipoprotein cholesterol (HDL-C) and APO A-I are reduced [16,17,18]. While LDL levels typically demonstrate a mild elevation in obesity, there is a shift from large LDL particles to small dense LDL particles, which are regarded as more pro-atherogenic [16,17,18]. These findings collectively form a lipid profile that promotes atherosclerosis and cardiovascular disease. Excess visceral adiposity increases free-fatty-acid flux to the liver, stimulating hepatic TG synthesis and apoB-containing lipoprotein production while reducing clearance [19]. Weight reduction reverses these disturbances by improving insulin sensitivity, decreasing hepatic de novo lipogenesis, and up-regulating skeletal–muscle lipoprotein–lipase activity [20,21]. Meta-analyses demonstrate that each kilogram of weight loss lowers TG by approximately 4 mg/dL, LDL-C by 1.28 mg/dL, and raises HDL-C by 0.46 mg/dL [22]. Although the relationship is dose dependent, even modest 5–10% weight reduction reduces overall CVD risk, even if only marginal changes in lipid profiles occur [23,24].

2.2. Effect of Weight Loss on Triglycerides

Among the major lipid subgroups, TG concentrations are the most sensitive to weight loss. Caloric restriction and exercise reduce hepatic TG synthesis and VLDL secretion while enhancing lipoprotein-lipase-mediated clearance of TG-rich remnants [25]. A 5–10% body weight reduction lowers fasting TG by roughly 15–20%, and losses of 10–15% may reduce TG by more than 25% [23,26]. Progressive improvements occur across interventions—from dietary programs to bariatric surgery—with the steepest decline appearing beyond 7.5–12.5% total-body-weight loss seen after laparoscopic adjustable gastric banding [27]. Randomized trials show that low-carbohydrate diets yield greater TG reduction than low-fat regimens, likely because of lower hepatic VLDL output and improved insulin sensitivity [28,29]. Aerobic exercise independently decreases TG and potentiates diet-induced effects through enhanced fatty-acid oxidation and up-regulation of lipoprotein–lipase activity [30,31,32]. Pharmacologic weight loss agents such as glucagon-like peptide-1 receptor agonists (GLP-1 RAs) produce parallel lipid effects, lowering TG and total cholesterol in individuals with obesity even without diabetes [33]. Overall, the TG response to weight loss appears to be dose dependent, reflecting both reduced hepatic TG synthesis and increased peripheral clearance.

2.3. Effect of Weight Loss on HDL Cholesterol

HDL-C generally increases with sustained weight loss, though absolute changes are relatively small, and studies have demonstrated both improvement [23,26] and no change/mild decrease [34]. Improvements are thought to result from decreased cholesteryl-ester-transfer-protein (CETP) activity, reduced TG enrichment of HDL particles, and enhanced apoA-I turnover, which stabilize HDL and enhance reverse cholesterol transport [35,36]. Exercise is believed to play a greater role in increasing HDL-C levels when compared to dietary interventions, and even with the addition of dietary interventions to an exercise regimen, HDL-C levels did not further improve. These findings from Khalafi et al. show that clinically meaningful changes to HDL are more likely driven by aerobic exercise [31]. Exercise also improves HDL-C functionality—reflected in improved cholesterol efflux capacity and antioxidative potential—and appears to contribute to cardiovascular benefit even when serum changes are small [37,38]. Surgical and intensive lifestyle interventions sustain higher HDL-C levels for years even as weight gain gradually returns, further contributing to a decreased atherogenic profile [39].

2.4. Effect of Weight Loss on LDL Cholesterol

LDL-C concentrations generally decline modestly with weight reduction, but qualitative changes in particle size and composition substantially lessen atherogenicity. Weight loss shifts LDL from small, dense subclasses toward larger, buoyant particles less prone to oxidation and endothelial retention [27,40]. Modest (5–10%) weight loss often lowers LDL-C by only 3–5%, whereas reductions exceeding 10–15% can yield declines of 10–20 mg/dL [22,23,24]. Bariatric surgery achieves even greater effects, resulting in average LDL-C reductions of about 22 mg/dL one year post-operatively [39]. GLP-1 RAs also modestly lower LDL-C while improving TG and HDL-C, reinforcing the lipid benefits of pharmacologic weight loss [33]. Importantly, even when absolute LDL-C reduction is limited, decreases in apolipoprotein B and remnant cholesterol reflect fewer circulating atherogenic particles [23,41]. Thus, modest weight loss produces a less atherogenic lipid phenotype overall—marked by lower TG, higher HDL-C, and larger LDL particles—thereby reducing cardiovascular risk even if LDL-C concentrations remain within baseline ranges.

3. Therapeutic Approaches to Dyslipidemia in Obesity

Traditional treatments for dyslipidemia, including HMG-CoA reductase inhibitors (statins), fenofibrates, and omega-3 fatty acids found in fish oil, have myriad evidence of their beneficial effects on lipid profiles. Statins primarily lower LDL-C and modestly reduce TG, fenofibrates are most effective at lowering TG and can increase HDL-C, and omega-3 fatty acids mainly reduce TG with minimal impact on LDL-C [42]. These effects are well established in the medical literature and reflected in current US guidelines [42]. However, other, newer therapies are showing promise as an adjunct—or in some cases, replacement therapy—to optimize atherogenic profile, especially for patients with obesity.

3.1. The Use of GLP-1/GIP Receptor Agonists

It is widely accepted that obesity and dyslipidemia are tightly intertwined with a chronic low-grade pro-inflammatory state that accelerates atherogenesis and vascular injury. Adipose tissue acts as an active endocrine organ, releasing pro-inflammatory cytokines and adipokines such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-1 (IL-1), and monocyte chemoattractant protein-1 (MCP-1) [43]. GLP-1 receptor agonists (GLP-1 RAs) appear to counteract several of these inflammatory processes through both direct and indirect mechanisms. Experimental and clinical studies demonstrate that GLP-1 signaling suppresses nuclear factor-κB (NF-κB) activation; reduces circulating levels of C reactive protein (CRP), IL-6, and TNF-α; and decreases expression of adhesion molecules such as vascular cell adhesion protein 1 (VCAM-1) and intracellular adhesion molecule 1 (ICAM-1) in vascular endothelium [44].
The convergence of these effects provides a plausible biological explanation for the cardiovascular benefits observed in the landmark SELECT (Semaglutide Effects on Cardiovascular Outcomes in People With Overweight or Obesity) trial. This trial evaluated once-weekly subcutaneous semaglutide 2.4 mg versus placebo in 17,604 adults (mean age ~62 yrs, BMI ≥ 27 kg/m2) with established atherosclerotic cardiovascular disease but without diabetes over a median follow-up of ~40 months [45]. The trial demonstrated a 20% relative risk reduction in the primary composite endpoint of cardiovascular death, non-fatal myocardial infarction, or non-fatal stroke (hazard ratio 0.80, 95% CI 0.72–0.90) compared to placebo. Importantly, this cardiovascular benefit emerged early during treatment, suggesting that mechanisms beyond the weight loss effect (mean ~9.4% of body weight) and modest lipid improvements may have contributed.
Mechanistically, semaglutide is thought to exert pleiotropic cardioprotective effects: direct improvements in endothelial function (via enhanced nitric oxide bioavailability and reduced oxidative stress), suppression of vascular inflammation and immune activation, amelioration of adipose tissue dysfunction (especially visceral and epicardial fat) with favorable shifts in adipokine and cytokine milieu, and modulation of thrombogenic pathways (for example, increased secretion of the antithrombotic protein gelsolin from epicardial adipose tissue and reduction of fatty-acid-binding protein-4 [FABP4]) [46]. However, these proposed mechanisms have not been established as direct mediators of the cardiovascular event reduction observed in clinical outcome trials.
The SELECT trial was particularly noteworthy because it was conducted in individuals with obesity and established cardiovascular disease but without diabetes, suggesting that the cardiovascular benefits observed with GLP-1 receptor agonist therapy could extend beyond just glucose control, reflecting favorable effects on inflammation, endothelial function, and adipose tissue biology rather than glycemic modulation alone.
Importantly, the mechanisms underlying the cardiovascular benefit observed in SELECT remain uncertain and should not be attributed to any single pathway. SELECT was designed to determine whether semaglutide reduces cardiovascular events, but not to determine which of its many biological effects were responsible for this benefit. Semaglutide simultaneously produces changes in body weight and several cardiovascular risk factors; therefore, the relative contributions of weight loss, reductions in blood pressure and systemic inflammation, changes in glycemia and lipid parameters, renal effects, and potential direct vascular actions remain unresolved. Although the relatively early separation of the event curves has raised the possibility that mechanisms beyond weight loss alone may contribute, this temporal relationship does not establish causality. Thus, the mechanistic effects described should be viewed as biologically plausible contributors to, rather than proven explanations for, the cardiovascular benefit observed with semaglutide.
A growing body of evidence indicates that preventing atherosclerotic progression and plaque vulnerability depends not only on lowering LDL-cholesterol levels but more critically on modifying LDL particle characteristics and reducing vascular inflammation. Small, dense LDL particles are more atherogenic because they more readily penetrate the endothelial barrier, are more susceptible to oxidative modification, and persist longer in circulation, all of which enhance their capacity to drive foam-cell formation [47]. At the same time, chronic, low-grade inflammation amplifies this process by promoting endothelial dysfunction, increasing the expression of adhesion molecules, and sustaining the recruitment of inflammatory cells into the arterial wall. Thus, therapeutic strategies that shift LDL toward larger, more buoyant particles and attenuate systemic and vascular inflammation play a central role in stabilizing plaques and preventing the progression and destabilization that underlie acute atherosclerotic events [47]. GLP-1 RAs act on several of these same mechanistic pathways that drive atherogenesis. Preclinical and mechanistic studies suggest GLP-1 RAs reduce the burden of small, dense LDL particles by improving lipid metabolism and enhancing hepatic lipid clearance, thereby decreasing the substrate available for oxidative modification within the arterial wall. At the vascular level, GLP-1 receptor activation downregulates pro-inflammatory signaling, reduces oxidative stress, and improves endothelial function, each of which limits the recruitment and activation of monocytes and macrophages. Furthermore, GLP-1 RAs have been shown to shift macrophage polarization toward a less inflammatory phenotype, reduce foam-cell formation, and inhibit smooth muscle cell proliferation, collectively promoting a more stable plaque architecture [47]. These mechanistic effects align with recent clinical observations showing that GLP-1 RAs also produce favorable remodeling of the circulating lipid profile, including reductions in triglycerides, VLDL, free fatty acids, and apoB-containing lipoproteins, alongside modest improvements in LDL-C and HDL-C [48]. By reducing the atherogenic lipid burden that fuels the formation of small, dense LDL particles and macrophage-driven inflammation, GLP-1 RA therapy may complement its proposed vascular actions to further limit the progression of atherosclerotic plaque [48]. Through their integrated metabolic, lipid-modifying, and anti-inflammatory actions, GLP-1 RAs counteract the upstream drivers of atherogenesis and the downstream pathways of plaque growth and vulnerability, reinforcing their role as therapeutic agents that extend well beyond glucose control and weight loss. Although these findings provide biological plausibility for anti-atherosclerotic effects of GLP-1 RAs, much of the evidence supporting effects on plaque biology, macrophage function, and vascular inflammation remains mechanistic or preclinical.
GIP RAs represent an emerging class of metabolic therapies that complement and amplify the vascular and metabolic effects of GLP-1 receptor agonists. While pure GIP agonists are still largely experimental, dual GIP/GLP-1 receptor agonists, such as tirzepatide, have demonstrated robust effects on weight reduction, insulin sensitivity, and lipid remodeling. GIP activation enhances adipose tissue function, reduces free fatty acid flux, and lowers the production of atherogenic apolipoproteins, thereby decreasing the substrate for small, dense LDL formation and foam-cell development. In addition, GIP exerts anti-inflammatory and immunomodulatory effects, including reduced pro-inflammatory cytokine release and promotion of a less inflammatory macrophage phenotype, which complement the endothelial-protective actions of GLP-1 RAs [49].

3.2. Interventions to Lower Triglycerides

Two recent studies have added to growing evidence that beyond LDL-lowering, novel therapies can robustly reduce triglycerides and improve lipid-related risk in patients with severe hypertriglyceridemia. The first, Olezarsen (published in 2025), demonstrated in a large randomized trial that monthly Olezarsen injections substantially lowered triglycerides—many patients achieved levels below 500 mg/dL—and reduced apolipoprotein C-III, non–HDL cholesterol, and remnant cholesterol [50]. The second, a phase 2 trial of a novel triple-receptor agonist, DR10624, which targets the FGF21, glucagon, and GLP-1 receptors, achieved median fasting triglyceride reductions of ~66–75% over 12 weeks, with nearly 90% of treated patients reaching triglyceride levels below 500 mg/dL. In addition, DR10624 markedly reduced liver fat content (up to ~63%) and improved other atherogenic lipids [51]. These findings point to promising alternatives to traditional agents like fibrates or omega-3s.

3.3. The Use of a CETP Inhibitor

A recent study published in the Journal of the American College of Cardiology evaluated Obicetrapib, a selective CETP inhibitor, for its impact on lipid levels and cardiovascular events in high-risk patients, including those with heterozygous familial hypercholesterolemia and established atherosclerotic cardiovascular disease. In a one-year follow-up, daily 10 mg Obicetrapib significantly reduced atherogenic lipids, including LDL-C, non–HDL-C, apoB, and lipoprotein(a) while increasing HDL-C [52]. The magnitude of lipid lowering correlated strongly with cardiovascular outcomes, supporting the therapeutic potential of Obicetrapib as an adjunctive strategy to reduce residual cardiovascular risk in patients with high lipid burdens [52].

3.4. Gene Editing for Improvement in Atherogenic Profile

Gene editing represents a promising frontier in cardiovascular medicine, offering the potential for one-time, durable interventions that can permanently lower atherogenic lipids and reduce the lifetime risk of cardiovascular disease. Early clinical trials have begun to explore different gene-editing strategies for lipid lowering, with the CTX310 CRISPR-Cas9 therapy targeting ANGPTL3 and Verve Therapeutics’ VERVE-102 base-editing therapy targeting PCSK9, demonstrating that multiple approaches may achieve substantial and sustained reductions in LDL cholesterol and triglycerides [53,54]. A recent study published in the New England Journal of Medicine reported the first-in-human trial of an in vivo CRISPR-Cas9 gene-editing therapy, CTX310, targeting the liver gene ANGPTL3 to lower atherogenic lipids. ANGPTL3 regulates lipid metabolism, and loss-of-function variants are associated with naturally low LDL cholesterol and triglycerides [54]. In this phase 1, dose-escalation study, 15 adults with difficult-to-treat lipid disorders received a single infusion of CTX310. At higher doses, participants experienced substantial reductions in LDL cholesterol (~48–50%) and triglycerides (~50–60%) within two weeks, with other lipid markers also improving [54]. The Heart-2 Phase 1b trial of VERVE-102, an in vivo base-editing therapy designed to permanently inactivate the PCSK9 gene in the liver, treated adults with heterozygous familial hypercholesterolemia and/or premature coronary artery disease. The treatment produced dose-dependent reductions in both PCSK9 protein levels and LDL-C. On average, LDL-C dropped 53% in the 0.6 mg/kg cohort (with a maximum individual reduction of 69%) compared with 21% in the lowest dose cohort. Together, these pioneering studies suggest that gene-editing therapies could transform the management of dyslipidemia, potentially offering single-dose alternatives to chronic medication. However, these therapies remain investigational, and their clinical applicability will depend on further evaluation of long-term safety and durability, potential off-target effects.
Importantly, improvements in lipid biomarkers with these emerging therapies should not be equated with reductions in cardiovascular events. Although reductions in LDL-C, triglycerides, apoB, remnant cholesterol, and other atherogenic lipoproteins provide a strong biological rationale for potential cardiovascular benefit, definitive cardiovascular outcomes data are not yet available for many of these newer therapeutic approaches. In contrast to therapies such as semaglutide, for which cardiovascular event reduction has been demonstrated in a dedicated outcomes trial, the clinical evidence for newer triglyceride-lowering agents, CETP inhibition, and gene-editing strategies remains largely based on changes in lipid parameters and other surrogate endpoints. Larger and longer-term studies will therefore be necessary to determine whether these favorable biomarker changes translate into reductions in cardiovascular morbidity and mortality.

3.5. Bariatric Surgery for Dyslipidemia

Multiple studies and meta-analyses have demonstrated that bariatric surgery produces substantial and sustained improvements in lipid metabolism and inflammatory profiles. A landmark meta-analysis published in JAMA in 2004, and referenced above, by Buchwald used pooled data from 136 studies encompassing more than 22,000 patients and demonstrated that surgical weight loss was consistently accompanied by major improvements in atherogenic lipid profiles [39]. Across procedures, mean reductions were approximately −28 mg/dL in total cholesterol, −22 mg/dL in LDL cholesterol, and −63 mg/dL in triglycerides, with a concurrent increase of +7 mg/dL in HDL cholesterol at one year post-surgery [39]. Roux-en-Y gastric bypass and biliopancreatic diversion produced the largest lipid changes, while gastric banding yielded more modest effects. In one longitudinal study, investigators followed 68 adults with severe obesity (mean BMI ~42.8 kg/m2) undergoing either Roux-en-Y gastric bypass (n = 29) or sleeve gastrectomy (n = 39) for 12 months post-surgery [55]. At baseline, 36 of the 92 plasma inflammatory markers measured were significantly elevated compared to non-obese controls, confirming a substantial low-grade inflammatory burden in the obese cohort. By 12 months post-surgery, 27 cytokines had significantly decreased, among which were IL-6, MCP-1, and TNF-related activation-induced cytokine (TRANCE) [55]. Importantly, the similarity of change across the two procedures suggests that the reduction in low-grade inflammation is largely independent of surgical type and more likely tied to the weight loss and metabolic improvements induced by the surgery. These findings strengthen the argument that bariatric surgery exerts broad anti-inflammatory benefits, which may contribute to reductions in cardiometabolic risk.
A recently published prospective cohort study in the April 2025 issue of Journal of Metabolic & Bariatric Surgery evaluated 23 patients with grade II/III obesity undergoing the Roux-en-Y gastric bypass procedure and assessed changes in BMI, full lipid profile, CRP, reactive-oxygen-species (ROS) production, and antioxidant enzyme activity at baseline and three months post-surgery [56]. The authors documented significant improvements at three months post-surgery in body weight (mean decrease from ~112 kg to ~80 kg) and BMI (from ~40.4 kg/m2 to ~28.9 kg/m2), accompanied by favorable changes in both lipid and inflammatory/oxidative stress profiles. They found statistically significant reductions in total cholesterol, triglycerides, and LDL-cholesterol, as well as CRP and ROS, accompanied by increased superoxide dismutase activity [56]. The concurrent improvements in lipid levels and reductions in inflammation and oxidative stress indicate that the beneficial effects of bariatric surgery on lipids may extend beyond mere weight loss, potentially reflecting a broader normalization of the dysregulated metabolic and inflammatory environment associated with obesity.
Cholesteryl ester transfer protein (CETP) facilitates the exchange of lipids between lipoproteins in plasma. Specifically, it transfers cholesteryl esters (CE) from high-density lipoprotein (HDL) particles to triglyceride-rich lipoproteins such as very-low-density lipoprotein (VLDL) or low-density lipoprotein (LDL) in exchange for triglycerides (TG) [57]. This CETP-mediated lipid exchange reduces HDL cholesterol content, potentially impairing reverse cholesterol transport, while enriching LDL/VLDL particles with cholesterol, increasing their atherogenicity. In obesity, elevated CETP activity contributes to a pro-atherogenic lipoprotein profile, with smaller, triglyceride-enriched HDL particles and cholesterol-dense LDL, providing a mechanistic rationale for why reductions in CETP activity after bariatric surgery may improve both HDL functionality and overall cardiovascular risk [57].

4. Conclusions

Obesity-associated dyslipidemia represents a central mechanistic link between excess adiposity and heightened cardiovascular risk. Visceral obesity drives a characteristic atherogenic lipid pattern: elevated triglycerides; apoB; non–HDL cholesterol; and small, dense LDL, with reduced HDL-C. These abnormalities arise from decreased adiponectin, increased CETP activity, insulin resistance with excess free-fatty-acid flux to the liver, and a chronic pro-inflammatory, pro-oxidative milieu. Together, these changes promote endothelial dysfunction, macrophage activation, and accelerated atherogenesis. Weight loss, regardless of modality (lifestyle, pharmacologic, or surgical), partially reverses this profile. Even 5–10% weight reduction improves insulin sensitivity, lowers triglycerides, modestly reduces LDL-C, raises HDL-C, and shifts LDL toward larger, less atherogenic particles. Bariatric surgery produces the most pronounced and durable effects on lipids and systemic inflammation, with sustained improvements in TG, LDL-C, HDL-C, cytokines, and oxidative stress markers, suggesting a broad normalization of adipose and vascular biology beyond weight loss alone.
Pharmacologic advances—including GLP-1 and dual GIP/GLP-1 receptor agonists, potent triglyceride-lowering agents (e.g., apoC-III antisense, multi-receptor agonists), CETP inhibition, and emerging in vivo gene-editing therapies targeting ANGPTL3 and PCSK9—foreshadow the possibility of durable, mechanism-based correction of atherogenic dyslipidemia. Collectively, current evidence supports obesity-associated dyslipidemia as a modifiable, partly reversible driver of cardiovascular disease (Table 2). For clinicians at the bedside and in the clinic, it is important to use validated risk factor assessments for atherosclerotic coronary artery disease, such as the PREVENT score, for patients in the primary prevention category. If weight loss is pursued in parallel with pharmacotherapies, a synergistic effect of risk reduction is expected. For patients with established ASCVD or a coronary artery calcium score > 300, lowering atherogenic particles to the lowest possible concentration is reasonable for secondary prevention. Pharmacotherapy and weight loss are not a fork in the road but rather complimentary mechanisms to achieve the best possible patient outcomes. Integrating weight loss strategies with targeted lipid and inflammation-directed therapies offers a path not only to improve lipid numbers but to fundamentally reshape lipoprotein quality, vascular inflammation, and long-term atherosclerotic risk.
Table 2. Effects of Weight Loss Interventions on Lipid Profile and Cardiovascular Risk.

Author Contributions

Conceptualization, D.S. and M.W.F.; methodology, D.S. and M.W.F.; validation, D.S. and M.W.F.; resources, and data curation, M.W.F., N.S. and M.B.; writing—original draft preparation, M.W.F., M.B. and N.S.; writing—review and editing, D.S., M.W.F., N.S. and M.B.; supervision, D.S. and M.W.F.; project administration, D.S.; All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Institutional Review Board Statement

Not applicable.

Data Availability Statement

All data obtained for this review is contained within the cited references below.

Acknowledgments

During the preparation of this manuscript/study, the author(s) used openevidence.com AI tool for the purposes of table and citation generation. The authors have reviewed and edited the output and take full responsibility for the content of this publication.

Conflicts of Interest

The authors declare no conflicts of interest.

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