Bays Harold E, González-Campoy J Michael, Bray George A, Kitabchi Abbas E, Bergman Donald A, Schorr Alan Bruce, Rodbard Helena W, Henry Robert R
L-MARC Research Center, 3288 Illinois Avenue, Louisville, KY 40213, USA.
Expert Rev Cardiovasc Ther. 2008 Mar;6(3):343-68. doi: 10.1586/14779072.6.3.343.
When caloric intake exceeds caloric expenditure, the positive caloric balance and storage of energy in adipose tissue often causes adipocyte hypertrophy and visceral adipose tissue accumulation. These pathogenic anatomic abnormalities may incite metabolic and immune responses that promote Type 2 diabetes mellitus, hypertension and dyslipidemia. These are the most common metabolic diseases managed by clinicians and are all major cardiovascular disease risk factors. 'Disease' is traditionally characterized as anatomic and physiologic abnormalities of an organ or organ system that contributes to adverse health consequences. Using this definition, pathogenic adipose tissue is no less a disease than diseases of other body organs. This review describes the consequences of pathogenic fat cell hypertrophy and visceral adiposity, emphasizing the mechanistic contributions of genetic and environmental predispositions, adipogenesis, fat storage, free fatty acid metabolism, adipocyte factors and inflammation. Appreciating the full pathogenic potential of adipose tissue requires an integrated perspective, recognizing the importance of 'cross-talk' and interactions between adipose tissue and other body systems. Thus, the adverse metabolic consequences that accompany fat cell hypertrophy and visceral adiposity are best viewed as a pathologic partnership between the pathogenic potential adipose tissue and the inherited or acquired limitations and/or impairments of other body organs. A better understanding of the physiological and pathological interplay of pathogenic adipose tissue with other organs and organ systems may assist in developing better strategies in treating metabolic disease and reducing cardiovascular disease risk.
当热量摄入超过热量消耗时,热量的正平衡以及能量在脂肪组织中的储存往往会导致脂肪细胞肥大和内脏脂肪组织蓄积。这些致病性解剖学异常可能引发促进2型糖尿病、高血压和血脂异常的代谢和免疫反应。这些是临床医生诊治的最常见代谢性疾病,并且都是主要的心血管疾病危险因素。传统上,“疾病”被定义为器官或器官系统的解剖学和生理学异常,这些异常会导致不良健康后果。按照这个定义,致病性脂肪组织与身体其他器官的疾病一样,都是一种疾病。这篇综述描述了致病性脂肪细胞肥大和内脏肥胖的后果,强调了遗传和环境易感性、脂肪生成、脂肪储存、游离脂肪酸代谢、脂肪细胞因子和炎症的机制性作用。要充分认识脂肪组织的全部致病潜力,需要一个综合的视角,认识到脂肪组织与身体其他系统之间“相互作用”和相互影响的重要性。因此,脂肪细胞肥大和内脏肥胖所伴随的不良代谢后果,最好被视为致病性脂肪组织的致病潜力与身体其他器官的遗传或后天局限性和/或损伤之间的一种病理协同关系。更好地理解致病性脂肪组织与其他器官及器官系统之间的生理和病理相互作用,可能有助于制定更好的策略来治疗代谢性疾病并降低心血管疾病风险。