Abstract
We studied the effect of food restriction, overfeeding, and normofeeding on cachexia, inflammatory and metabolic parameters, and insulin sensitivity in chronic adjuvant arthritis (AA) in rats. Food restriction during AA increased circulating ghrelin, corticosterone, decreased leptin, and ameliorated arthrogram score and systemic inflammation compared to normofeeding. Overfeeding worsened arthrogram score and systemic inflammation, and led to lipid accumulation in the liver, but not to alterations of adipokine and ghrelin plasma levels relative to normofeeding. Independently of feeding status, AA induced cachexia, in which modulation of mRNA expressions for appetite-regulating neuropeptides (NPY, AgRP, POMC, CART) in the arcuate nucleus (ARC) does not play a primary role. The overexpression of IL-1β mRNA in the ARC suggests its role in the mechanisms of impaired energy balance during AA under all feeding conditions. Normal HOMA index in all arthritic groups does not indicate the development of insulin resistance by feeding interventions in these rats.
Highlights
The world wide growing incidence of obesity has triggered increased research into the adverse health consequences of this condition
This study shows that feeding status modulates the disease severity, mRNA levels of IL-1β and of the key neuropeptides regulating appetite in the arcuate nucleus (ARC), as well as metabolic responses in chronic adjuvant arthritis
We have recently demonstrated an enhanced mRNA expression of IL-1β in the ARC of normally fed arthritic rats suggesting its role in arthritis-induced cachexia [19]
Summary
The world wide growing incidence of obesity has triggered increased research into the adverse health consequences of this condition. There is a large body of evidence that chronic subclinical inflammation associated with changes in endocrine functions of adipose tissue leads to metabolic disturbances including development of insulin resistance, diabetes, and cardiovascular disease [1]. Whether increased levels of systemic inflammation during obesity can predispose susceptible individuals to the development of autoimmune inflammatory diseases such as rheumatoid arthritis (RA). It has to be noted that severe rheumatoid disease is associated with inflammatory cachexia characterized by the loss of lean body tissue that is often compensated for by gain in body fat. It has been described that higher BMI was associated with increased leptin levels and a less severe radiographic joint damage of small joints in patients with RA [4, 5]. In rodent models of RA, chronic arthritis was less severe in food restricted rats [7], or in ob/ob mice with leptin deficiency [8]
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