Despite the prevalence of chronic inflammatory diseases in developed countries, few studies have considered the metabolic alterations observed in these disorders. To determine which perturbations in protein metabolism occur during chronic inflammation, and the consequences they have on nutritional requirements, a model of ulcerative colitis was adapted for use in adult rats. Adult Sprague-Dawley male rats (9 mo old) received dextran sulfate sodium (DSS) in their drinking water at 50 g/L for 9 d, then at 20 g/L for 18 d. A group of control rats, matched for age and weight, was pair-fed to the treated rats. DSS induced body weight loss and chronic inflammation characterized by an increase of spleen, liver, ileum and colon weights, of blood leukocytes and acute-phase protein levels. The main inflammatory site was the colon, which presented characteristic histological alterations and increased myeloperoxydase activity. Inflammation was accompanied by oxidative stress, characterized by increased plasma protein carbonyl content and increased liver glutathione concentration, but decreased glutathione concentration in muscle. This DSS-induced colitis led to a stimulation of protein synthesis in spleen (+223%), ileum (+40%) and colon (+63%). By contrast, protein synthesis in muscle slowed down (-23%). In conclusion, like acute inflammation, chronic inflammation induced a stimulation of protein metabolism in several splanchnic organs. In muscle, both protein synthesis and degradation were reduced. Taken together, these data are consistent with inadequate amino acid supply to meet the increased requirement resulting from chronic inflammation.

Moderate-severe lipodystrophy affected one third of West African patients on long-term HAART and was associated with a less favorable metabolic profile.