Adipsin deficiency does not impact atherosclerosis development in Ldlr^-/- mice

Area of Science:

• Cardiovascular Biology
• Immunology
• Metabolic Disorders

Background:

• Obesity is a major risk factor for atherosclerosis, with adipokines from adipose tissue implicated in its development.
• Adipsin, an abundant adipokine downregulated in obesity, catalyzes a key step in alternative complement activation, a pathway involved in atherosclerosis.
• Adipsin is a novel biomarker for coronary artery disease, but its direct role in atherogenesis is unknown.

Purpose of the Study:

• To investigate the role of adipsin in the development of atherosclerosis.
• To determine if adipsin deficiency influences diet-induced atherogenesis in a mouse model.

Main Methods:

• Generated adipsin-deficient (adipsin-/-) Ldlr-/- double-knockout (DKO) mice.
• Induced atherosclerosis via high-fat, high-cholesterol diet.
• Assessed metabolic profiles, atherosclerotic lesion size (aortic root and arch), and complement activity.

Main Results:

• DKO mice showed similar atherosclerotic lesion sizes compared to Ldlr-/- controls.
• Metabolic parameters (body weight, insulin sensitivity, lipid profiles) were comparable between groups.
• Complement activity was compensated in adipsin-deficient mice.

Conclusions:

• Adipsin deficiency does not impact atherosclerosis development in Ldlr-/- mice.
• Despite its role in alternative complement activation, adipsin is unlikely to be a major mediator of atherosclerotic complications in obesity.