Effect of Feeding Status on Adjuvant Arthritis Severity, Cachexia, and Insulin Sensitivity in Male Lewis Rats

• Published in: Mediators of Inflammation Vol. 2010; no. 2010; pp. 1 - 12
• Main Authors: Jurcovicova, Jana, Kiss, Alexander, Ulicna, Olga, Romzova, Marianna, Zelezna, Blanka, Stofkova, Andrea, Skurlova, Martina
• Format: Journal Article
• Language: English
• Published: Cairo, Egypt Hindawi Limiteds 01.01.2010; Hindawi Puplishing Corporation; Hindawi Publishing Corporation; Hindawi Limited; Wiley
• Subjects: Adipokines - metabolism; Adrenal Cortex Hormones - metabolism; Animal Feed; Animals; Arcuate Nucleus of Hypothalamus - metabolism; Arthritis; Arthritis - diet therapy; Arthritis - therapy; Cachexia; Cachexia - metabolism; Chemotherapy, Adjuvant - methods; Development and progression; Food habits; Genetic aspects; Ghrelin - metabolism; Health aspects; Inflammation; Insulin - metabolism; Insulin resistance; Leptin - metabolism; Male; Neuropeptides - chemistry; Rats; Rats, Inbred Lew; Czech Republic; Slovakia
• ISSN: 0962-9351; 1466-1861
• DOI: 10.1155/2010/398026

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.