Surfactant protein d, a marker of lung innate immunity, is positively associated with insulin sensitivity
Fernández-Real JM, Valdés S, Manco M, Chico B, Botas P, Campo A, Casamitjana R, Delgado E, Salvador J, Fruhbeck G, Mingrone G, Ricart W.
Department of Diabetes, Endocrinology, and Nutrition, Institut d'Investigació Biomèdica deGirona, Girona, Spain
Data: 1/Abr/2010Endocrinologia e Nutrição [ES]
Impaired lung function and innate immunity have both attracted growing interest as a potentially novel risk factor for glucose intolerance, insulin resistance, and type 2 diabetes. We aimed to evaluate whether surfactant protein D (SP-D), a lung-derived innate immune protein, was behind these associations.
RESEARCH DESIGN AND METHODS
Serum SP-D was evaluated in four different cohorts. The cross-sectional associations between SP-D and metabolic and inflammatory parameters were evaluated in two cohorts, the cross-sectional relationship with lung function in one cohort, and the longitudinal effects of weight loss on fasting and circadian rhythm of serum SP-D and cortisol concentrations in one prospective cohort.
In the cross-sectional studies, serum SP-D concentration was significantly decreased in subjects with obesity and type 2 diabetes (P = 0.005) and was negatively associated with fasting and postload serum glucose. SP-D was also associated with A1C, serum lipids, insulin sensitivity, inflammatory parameters, and plasma insulinase activity. Smoking subjects with normal glucose tolerance, but not smoking patients with type 2 diabetes, showed significantly higher serum SP-D concentration than nonsmokers. Serum SP-D concentration correlated positively with end-tidal carbon dioxide tension (r = 0.54, P = 0.034). In the longitudinal study, fasting serum SP-D concentration decreased significantly after weight loss (P = 0.02). Moreover, the main components of cortisol and SP-D rhythms became synchronous after weight loss.
These findings suggest that lung innate immunity, as inferred from circulating SP-D concentrations, is at the cross-roads of inflammation, obesity, and insulin resistance.
CITAÇÃO DO ARTIGO Diabetes Care. 2010 Apr;33(4):847-53
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