医学
脂肪组织
脂肪因子
内科学
2型糖尿病
肥胖
腰围
内分泌学
瘦素
骨关节炎
糖尿病
胰岛素抵抗
腹部肥胖
代谢综合征
减肥
病理
替代医学
出处
期刊:Annals of Physical and Rehabilitation Medicine
日期:2016-05-20
卷期号:59 (3): 157-160
被引量:96
标识
DOI:10.1016/j.rehab.2016.04.002
摘要
Obesity and type 2 diabetes (T2D) significantly increase the risk of developing an arthritic condition.We performed a review of literature on the pathophysiological mechanisms that underpin the relationships between obesity, T2D and osteoarthritis (OA).The pathophysiology of the link between obesity and OA is related to both the direct effect of excess mechanical loads being placed on the cartilage and to an adipose tissue effect. Adipocytes produce and release adipokines (e.g. leptin). They are also the seat of a local inflammatory reaction when the adipose tissue is ectopic (visceral vs. subcutaneous adipose tissue), and then systemic effects that add even more to a micro-inflammatory mechanism. In diabetics, insulin resistance can add to these mechanisms, which can damage cartilage, bone and synovial tissue. These all act together to reduce mobility in obese subjects and contribute to a vicious cycle centered on OA, especially when the obesity is predominantly abdominal and/or associated with T2D.Prevention of obesity-related OA must be the focus in high-risk subjects, such as those who are obese with metabolic syndrome>"metabolically healthy" obese, have T2D, and normal weight subjects with abdominal obesity (defined as waist circumference>102cm for men and 88cm for women). The primary component of this prevention effort is weight loss combined with a balanced diet and regular physical activity.
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