Adipsin deficiency does not impact atherosclerosis development in Ldlr−/− mice
| Autor: | Longhua Liu, Li Qiang, Weidong Wang, Lexiang Yu, Michelle Chan |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
Male
0301 basic medicine medicine.medical_specialty Physiology Endocrinology Diabetes and Metabolism Adipose tissue Adipokine Inflammation 030204 cardiovascular system & hematology Diet High-Fat Cholesterol Dietary Coronary artery disease Mice 03 medical and health sciences 0302 clinical medicine Adipokines Physiology (medical) Internal medicine medicine Animals Aorta Mice Knockout Rapid Report business.industry Body Weight Complement System Proteins Atherosclerosis medicine.disease Lipids Plaque Atherosclerotic Complement system Mice Inbred C57BL Blot 030104 developmental biology Endocrinology Receptors LDL LDL receptor Biomarker (medicine) Complement Factor D Insulin Resistance medicine.symptom business |
| Zdroj: | Am J Physiol Endocrinol Metab |
| ISSN: | 1522-1555 0193-1849 |
| DOI: | 10.1152/ajpendo.00440.2020 |
| Popis: | Obesity is a potent risk factor for atherosclerotic morbidity and mortality. Cytokines secreted from adipose tissue, namely, adipokines, have been suggested to be actively involved in atherosclerosis. One of the most abundant adipokines, adipsin, is downregulated in obesity. It catalyzes the rate-limiting step of alternative complement activation, which is one of the three complement pathways potentially involved in inflammation in atherosclerosis. Interestingly, adipsin has been identified as a novel biomarker in human coronary artery disease. However, its role in the development of atherosclerosis remains unexplored. We crossed adipsin(−/−) mice onto an Ldlr(−/−) background [double-knockout (DKO) mice] and induced atherogenesis by high-fat and high-cholesterol feeding. Metabolic profiles were systemically characterized, and atherosclerotic plaques were measured at both aortic root and arch regions. Western blotting was conducted to assess adipsin level and complement activity. The DKO mice exhibited similar sizes of atherosclerotic lesions as Ldlr(−/−) control mice at both the aortic root and arch regions. Accordingly, they displayed comparable metabolic parameters, including body weight, insulin sensitivity, and lipid profiles, along with compensated complement activity. Adipsin deficiency does not impact the development of atherosclerosis in Ldlr(−/−) mice despite its crucial function in alternative complement activation. Therefore, it is unlikely to play an important role in mediating the risk of atherosclerotic complications in obesity. NEW & NOTEWORTHY Adipsin deficiency does not impact the development of atherosclerosis in Ldlr(−/−) mice despite its crucial function in alternative complement activation. Therefore, it is unlikely to play an important role in mediating the risk of atherosclerotic complications in obesity. |
| Databáze: | OpenAIRE |
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