The mediating role of C-reactive protein and handgrip strength between obesity and walking limitation

OBJECTIVES: To study the association between different obesity indicators and walking limitation and to examine the role of C‐reactive protein (CRP) and handgrip strength in that association. DESIGN: A cross‐sectional, population‐based study. SETTING: The Health 2000 Survey with a representative sample of the Finnish population. PARTICIPANTS: Subjects aged 55 and older with complete data on body composition, CRP, handgrip strength, and walking limitation (N=2,208). MEASUREMENTS: Body composition, anthropometrics, CRP, medical conditions, handgrip strength, and maximal walking speed were measured in the health examination. Walking limitation was defined as maximal walking speed less than 1.2 m/s or difficulty walking half a kilometer. RESULTS: The two highest quartiles of body fat percentage and CRP and the two lowest quartiles of handgrip strength were all significantly associated with greater risk of walking limitation when chronic diseases and other covariates were taken into account. In addition, high CRP and low handgrip strength partially explained the association between high body fat percentage and walking limitation, but the risk of walking limitation remained significantly greater in persons in the two highest quartiles than in those in the lowest quartile of body fat percentage (odds ratio (OR)=1.75, 95% confidence interval (CI)=1.19–2.57 and OR=2.80, 95% CI 1.89–4.16). The prevalence of walking limitation was much higher in persons who simultaneously had high body fat percentage and low handgrip strength (61%) than in those with a combination of low body fat percentage and high handgrip strength (7%). Using body mass index and waist circumference as indicators of obesity yielded similar results as body fat percentage. CONCLUSION: Low‐grade inflammation and muscle strength may partially mediate the association between obesity and walking limitation. Longitudinal studies and intervention trials are needed to verify this pathway.     

Development of large numbers of mast cells at sites of idiopathic chronic dermatitis in genetically mast cell-deficient WBB6F1-W/Wv mice

The normal skin and other tissues of adult mast cell-deficient WBB6F1- W/Wv or WCB6F1-Sl/Sld mice contain less than 1.0% the number of mast cells present in the corresponding tissues of the congenic normal (+/+) mice. As a result, genetically mast cell-deficient WBB6F1-W/Wv or WCB6F1-Sl/Sld mice are widely used for studies of mast cell differentiation and function. We found that mast cells developed at sites of idiopathic chronic dermatitis in WBB6F1-W/Wv mice and that the number of mast cells present in the skin of WBB6F1-W/Wv mice was proportional to the severity of the dermatitis (in ear skin, there were 33 +/- 4 mast cells/mm2 of dermis at sites of severe dermatitis v 9 +/- 3 at sites of mild dermatitis, 0.8 +/- 0.3 in skin without dermatitis, and 100 +/- 7 in the normal skin of congenic WBB6F1-+/+ mice; in back skin, the corresponding values were 2.0 +/- 0.6, 1.1 +/- 0.9, 0.025 +/- 0.025, and 26.2 +/- 3.2). The development of mast cells was a local, not systemic, consequence of the dermatitis. Thus, WBB6F1-W/Wv mice with severe dermatitis lacked mast cells in skin not showing signs of dermatitis and also in the peritoneal cavity, stomach, cecum, and tongue. Idiopathic chronic dermatitis was not associated with the local development of mast cells in WCB6F1-Sl/Sld mice, a mutant whose mast cell deficiency is due to a mechanism distinct from that of WBB6F1-W/Wv mice. These findings may have implications for understanding the nature of the mast cell deficiency in WBB6F1-W/Wv and WCB6F1-Sl/Sld mice and for the use of these mutants to analyze mast cell differentiation and function.