ABSTRACT
UNASSIGNED: Excess body weight has become a global epidemic and a significant risk factor for developing chronic diseases, which are the leading causes of worldwide morbidities. Adipose tissue (AT), primarily composed of adipocytes, stores substantial amounts of energy and plays a crucial role in maintaining whole-body glucose and lipid metabolism. This helps prevent excessive body fat accumulation and lipotoxicity in peripheral tissues. In addition, AT contains endothelial cells and a substantial population of immune cells (constituting 60-70% of non-adipocyte cells), including macrophages, T and B lymphocytes, and natural killer cells. These resident immune cells engage in crosstalk with adipocytes, contributing to the maintenance of metabolic and immune homeostasis in AT. An exacerbated inflammatory response or inadequate immune resolution can lead to chronic systemic low-grade inflammation, triggering the development of metabolic alterations and the onset of chronic diseases. This review aims to elucidate the regulatory mechanisms through which immune cells influence AT function and energy homeostasis. We also focus on the interactions and functional dynamics of immune cell populations, highlighting their role in maintaining the delicate balance between metabolic health and obesity-related inflammation. Finally, understanding immunometabolism is crucial for unraveling the pathogenesis of metabolic diseases and developing targeted immunotherapeutic strategies. These strategies may offer innovative avenues in the rapidly evolving field of immunometabolism. (Rev Invest Clin. 2024;76(2):65-79).
Subject(s)
Adipose Tissue , Inflammation , Metabolic Diseases , Obesity , Humans , Adipose Tissue/metabolism , Adipose Tissue/immunology , Obesity/immunology , Obesity/metabolism , Inflammation/immunology , Inflammation/metabolism , Metabolic Diseases/immunology , Metabolic Diseases/metabolism , Metabolic Diseases/etiology , Energy Metabolism/physiology , Adipocytes/metabolism , Adipocytes/immunology , Lipid Metabolism/physiology , Animals , HomeostasisABSTRACT
BACKGROUND AND AIMS: Lipid goals have become more stringent in high risk patients. However, no studies have analyzed lipid control defined as the composite achievement of goals in low-density lipoprotein cholesterol (LDL-C), non-high-density lipoprotein cholesterol (Non-HDL-C) and apolipoproteinB-100 (ApoB-100), in patients with premature coronary artery disease (CAD). We aimed to analyze lipid control rates, and the associated factors with its poor achievement in patients with premature CAD. METHODS AND RESULTS: The study included 1196 patients with CAD diagnosed before 55 and 65 years old in men and women, respectively. The American Heart Association/American College of Cardiology (non-strict) and the American Association of Clinical Endocrinologists (strict) criteria were used to analyze lipid control rates. Sociodemographic, dietary-healthy and clinical characteristics of the patients were collected. Participants were 54 ± 8 years old, 19.7% were women, and median CAD evolution was 2.4 years. Non-strict and strict lipid control was achieved in 23.0% and 8.9% of the patients, respectively. Moreover, 46.5% and 62.8% of the patients did not achieve any lipid goal using both criteria. Sociodemographic data were not different among patients who achieved or not lipid control. Treatment adherence<85%, prescription of low- and moderate-intensity statins, and obesity were consistently associated with poor lipid control. CONCLUSIONS: Lipid control is suboptimal in patients with premature CAD. Low lipid-lowering treatment adherence, low prescription of high-intensity statins, and obesity were independently associated with poor lipid control. Novel preventive programs and more aggressive pharmacological intervention should be implemented in order to reduce the burden of premature CAD.
