Role of adipokines in obstructive airway disease and diabetes mellitus

Abstract

This review summarizes the state of the current literature relating to the associations of lung disease and adipokines (proteins produced by adipose tissue) in humans. The mechanistic basis for these associations in humans is not established, although a possible role for adipokines has been invoked. Leptin, a pro-inflammatory adipokine, and adiponectin, an anti-inflammatory adipokine, are causally associated with asthma in mice. Although human studies are currently inconclusive, high-serum leptin and low-serum adiponectin concentrations predict asthma, independent of obesity, in select population groups, such as premenopausal women in the United States. In contradistinction, low-serum leptin and high-serum adiponectin concentrations are associated with stable COPD, although these associations are likely confounded by fat mass. Interestingly, leptin may promote systemic and airway inflammation in stable COPD patients. On the other hand, COPD may upregulate systemic and lung adiponectin expression. The precise mechanism and significance of the associations between these adipokines and lung disease at the current stage are confusing and frankly paradoxical in places. It is now known that adipose tissue is not an inert organ simply for energy storage, but regulates systemic inflammation via a variety of secreted proteins (called adipokines). While the associations of obesity and adipokines with cardiovascular, endocrine, and rheumatological diseases are well described, the respiratory effects of obesity and adipokines are less well known. This review will focus on the effect of obesity and adipokines on asthma and chronic obstructive pulmonary disease (COPD) in humans. This area of research needs additional study that may open up novel therapeutic strategies for these lung diseases.