Article

Obesity and type 2 diabetes (T2D) significantly increase the risk of
developing an arthritic condition. METHODS: We performed a review of literature
on the pathophysiological mechanisms that underpin the relationships between
obesity, T2D and osteoarthritis (OA). RESULTS:
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. DISCUSSION: 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.
CI - Copyright (c) 2016 Elsevier Masson SAS. All rights reserved.

Langue : ANGLAIS