No abstract

Objective. To determine the effects of rheumatoid arthritis (RA) on whole-body protein metabolism.Methods. We examined protein metabolism and its hormonal and cytokine mediators before and 12 weeks after progressive resistance muscle strength training in 8 healthy young (mean k SD age 25 2 2 years) and 8 healthy elderly (70 rt 5 years) men and women, and in 8 adults with RA (42 2 13 years). An additional 6 healthy elderly subjects (69 k 3 years) served as a swimming-only control group.Results. Subjects with RA had higher rates of protein breakdown than did young or elderly healthy subjects (79.9 f 17.2 versus 60.3 f 5.8 and 63.7 2 12.4 pmoles/gm total body potassium/hour, respectively, P < 0.05), while there was no effect of age per se. Patients treated with methotrexate had normal rates of protein breakdown (P < 0.01 versus RA without methotrexate; P not significant versus healthy young subjects). Increased protein catabolism in RA was no longer evident after strength training. In multiple regression analysis, levels of tumor necrosis factor a (TNFa) (r = 0.47, P = 0.01) and growth hormone (r = -0.51, P = 0.006) were associated with protein breakdown, and plasma glucagon levels were inversely correlated with protein synthesis (r = -0.45, P =0.02). Growth hormone (r = -0.56, P = 0.002) and glucagon (r = 0.45, P = 0.04, levels were associated with protein oxidation.Conclusion. Adults with RA have increased whole-body protein breakdown, which correlates with growth hormone, glucagon, and TNFa production.Despite the many advances in our understanding of the disordered immune response that occurs in rheumatoid arthritis (RA), little information has been available about the effect of inflammation on metabolism and body composition in RA. Previous work from our laboratory has shown that body cell mass and physical activity are significantly reduced, and resting energy expenditure (REE) significantly increased, in patients with RA compared with healthy age-, sex-, race-, and weight-matched controls (1-3). This hypermetabolism of RA (defined as an increase in REE by >lo% above predicted levels) was directly associated with the production of tumor necrosis factor a (TNFa) and interleukin-lp (IL-1p) by peripheral blood mononuclear cells (PBMC) from these patients, which was approximately 2-fold higher than that in the control subjects. We have termed the cytokine-associated loss of lean body mass in RA rheumatoid cachexia, and have proposed that this cachexia is an important contributor to morbidity and mortality in RA, and offers insights into inflammatory mediators of cachexia (4).Understanding the mediators of the decline in body cell and protein mass is important because loss of more than -40% of baseline body cell mass is fatal, as shown in starvation, aging, and in acute illness (5). In

Supplementation with a multivitamin formulated at about 100% Daily Value can decrease the prevalence of suboptimal vitamin status in older adults and improve their micronutrient status to levels associated with reduced risk for several chronic diseases.

Ornithine and citrulline have different arginine-sparing capabilities when provided in an arginine-deficient diet. Rats were fed arginine-deficient diets containing ornithine or citrulline to see the effect on net fluxes of free arginine, ornithine and citrulline across the portal-drained viscera (PDV) and liver. The diets contained either 10 g arginine/kg diet (+Arg) or no arginine: the -Arg/+Ala diet contained additional alanine and the -Arg/+Orn and -Arg/+Cit diets contained ornithine and citrulline, respectively, in amounts isomolar to the amount of arginine in the control (+Arg) diet. Blood arginine concentrations were 50% lower than control values (P < 0.001) in rats fed the -Arg/+Ala or the -Arg/+Orn diet. However, addition of citrulline to the arginine-deficient diet restored blood arginine concentrations. The source of the circulating arginine in the rats fed the -Arg/+Cit diet was neither the PDV nor the liver; net splanchnic uptake of arginine was 0.3 mumol/min. Net citrulline release was substantial from the PDV (0.65 mumol/min) as well as from the splanchnic bed (0.67 mumol/min) of rats fed the -Arg/+Cit diet, such that blood citrulline concentrations were more than double (P < 0.001) those in rats fed the +Arg or -Arg/+Orn diet. Splanchnic release of citrulline in rats fed the -Arg/+Cit diet but not in rats fed the -Arg/+Orn diet supported the production of arginine in non-splanchnic organs such as, presumably, the kidney.