2007
DOI: 10.1016/j.mehy.2007.01.075
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The relationship between the metabolic syndrome and energy-utilization deficit in the pathogenesis of obesity-induced osteoarthritis

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Cited by 43 publications
(25 citation statements)
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“…Sowers et al suggested that leptin and adiponectin levels influenced OA development 29 . Another hypothesis suggests that in obese subjects, metabolic changes in the striated muscles induced by interactions between insulin resistance and systemic inflammation may lead to fatigue and muscle weakness, influencing the balance between damage and repair mechanisms and ultimately leading to OA 42,43 . Inflammatory factors are suggested to be associated with both obesity and KOA 44,45 .…”
Section: Discussionmentioning
confidence: 99%
“…Sowers et al suggested that leptin and adiponectin levels influenced OA development 29 . Another hypothesis suggests that in obese subjects, metabolic changes in the striated muscles induced by interactions between insulin resistance and systemic inflammation may lead to fatigue and muscle weakness, influencing the balance between damage and repair mechanisms and ultimately leading to OA 42,43 . Inflammatory factors are suggested to be associated with both obesity and KOA 44,45 .…”
Section: Discussionmentioning
confidence: 99%
“…This may constitute a pathogenic mechanism by which conditions such as DM could promote degenerative changes that facilitate the progression of OA [24]. Rojas-Rodríguez et al reported that pathogenesis of obesity-induced OA may be explained by the metabolic changes in the striated muscle induced by the interaction of insulin resistance and systemic inflammation in obese individuals [25]. It is also known that pro-inflammatory molecules are among critical mediators of the disturbed processes implicated in OA pathophysiology [26].…”
Section: Discussionmentioning
confidence: 99%
“…Adipose tissue is known as a source of proinflammatory and anti-inflammatory adipokines, which have been suggested to play a role in OA pathogenesis 4–7. Furthermore, hyperglycaemia and diabetes have been related to OA,8–12 possibly via insulin-like growth factor I resistance of chondrocytes,13 via changes in striated muscles due to insulin resistance,14 or via formation of advanced glycation end products 15 16. The association of OA with measures of atherosclerosis suggests another systemic link with OA,17 18 possibly via systemic inflammation or pathology of subchondral bone vasculature 19…”
Section: Introductionmentioning
confidence: 99%