Related Experiment Video
Updated: Sep 22, 2025
Measuring the Rate of Lipolysis in Ex Vivo Murine Adipose Tissue and Primary Preadipocytes Differentiated In Vitro
Published on: March 17, 2023
Key Molecules of Triglycerides Pathway Metabolism Are Disturbed in Patients With Systemic Lupus Erythematosus
Juan Carlos Quevedo-Abeledo1, Candelaria Martín-González2,3, Carmen Ferrer-Moure4
1Division of Rheumatology, Hospital Doctor Negrín, Las Palmas de Gran Canaria, Spain.
Insights
Systemic lupus erythematosus (SLE) disrupts triglyceride metabolism, showing lower apolipoprotein C-III (ApoC3) and higher angiopoietin-like protein 4 (ANGPLT4) and lipoprotein lipase (LPL). SLE disease damage is directly linked to elevated LPL levels.
Area of Science:
- Cardiovascular Disease Research
- Lipid Metabolism Studies
- Autoimmune Disease Pathophysiology
Background:
- Systemic lupus erythematosus (SLE) patients exhibit a high incidence of premature cardiovascular disease (CVD).
- SLE is associated with dyslipidemia, indicating altered lipid profiles.
- Elevated triglycerides and triglyceride-rich lipoproteins are known contributors to CVD.
Purpose of the Study:
- To investigate differences in key triglyceride metabolism molecules—apolipoprotein C-III (ApoC3), angiopoietin-like protein 4 (ANGPLT4), and lipoprotein lipase (LPL)—between SLE patients and controls.
- To determine the relationship between these molecules and SLE disease characteristics, including accumulated disease damage.
- To elucidate the role of ApoC3, ANGPLT4, and LPL in the context of CVD risk in SLE.
Main Methods:
- A cross-sectional study involving 347 women (185 with SLE, 162 age-matched controls).
- Analysis of serum levels of ANGPTL4, ApoC3, and LPL, alongside standard lipid profiles.
- Multivariable analysis to compare molecule levels between groups and assess associations with SLE disease damage.
Main Results:
- Patients with SLE showed significantly lower ApoC3 levels (beta coef. -1.2) and significantly higher ANGPLT4 (beta coef. 63) and LPL (beta coef. 79) compared to controls, after adjusting for CV risk factors and lipid profile modifications.
- Disease damage score was independently associated with higher serum LPL levels (beta coef. 23).
- Mediation analysis indicated a direct relationship between disease damage and LPL, not mediated by ApoC3 or ANGPLT4.
Conclusions:
- The study demonstrates a disrupted axis of ApoC3, ANGPLT4, and LPL in SLE patients.
- Accumulated disease damage in SLE is a significant factor contributing to this metabolic disturbance.
- The findings highlight LPL as a potential biomarker and therapeutic target in SLE-related cardiovascular complications.
Background:
Elevated triglycerides or triglyceride-rich lipoproteins are an additional cause of cardiovascular (CV) disease. Given that patients with systemic lupus erythematosus (SLE) have a high prevalence of premature CV disease and show an altered lipid profile, our objective was to study whether three molecules that play a central role in the triglyceride metabolism: apolipoprotein C-III (ApoC3), angiopoietin-like protein 4 (ANGPLT4), and lipoprotein lipase (LPL) differ between SLE patients and controls, and how they are related to disease characteristics, including disease damage.
Methods:
Cross-sectional study that included 347 women, 185 of them diagnosed with SLE and 162 age-matched controls. ANGPTL4, ApoC3 and LPL, and standard lipid profiles were analyzed in SLE patients and controls. A multivariable analysis was performed to assess whether ANGPTL4, ApoC3 and LPL molecules differ between patients and controls and to study their relationship with SLE disease damage.
Results:
After fully multivariable analysis that included classic CV risk factors, and the modifications that the disease itself produces over the lipid profile, it was found that ApoC3 was significantly lower (beta coef. -1.2 [95%CI -1.6- -0.8) mg/dl, <0.001), and ANGPTL4 (beta coef. 63 [95%CI 35-90] ng/ml, <0.001) and LPL (beta coef. 79 [95%CI 30-128] ng/ml, p=0.002) significantly higher in patients with SLE compared to controls. Disease damage score was significantly and independently associated with higher serum levels of LPL (beta coef. 23 [95%CI 10-35] ng/ml, p=0.001). Mediation analysis suggested that the relationship between disease damage and LPL was direct and not mediated by ApoC3 or ANGPLT4.
Conclusion:
The ApoC3, ANGPLT4 and LPL axis is disrupted in patients with SLE. Disease damage explains this disturbance.
Related Concept Videos
01:24Overview of Lipid Metabolism
Lipolysis: The Breakdown of Lipids:
Lipolysis is the process of breaking down lipids, particularly triglycerides, into glycerol and fatty acids. This process typically occurs in the adipose tissue and is triggered by various hormones, including glucagon and...
01:25Blood Studies for Cardiovascular System III: Serum Lipid Profile
Serum lipids are fats and fatty substances in the blood and are crucial for various bodily functions, including energy storage, cellular structure, and hormone production. Serum lipids consist of cholesterol, triglycerides, and phospholipids.
Cholesterol is a soft, fat-like substance found in all body cells. It is crucial for producing hormones, vitamin D, and substances that aid...
01:25Lipid Catabolism
01:24Lipid Absorption
These breakdown products bind with bile salts and lecithin to form micelles, which quickly pass between microvilli to come in close contact with the apical...
01:29Cholesterol: Significance and Regulation
Considering cholesterol and...
01:06Fats as Energy Storage Molecules