Disturbances in leptin metabolism are related to energy imbalance during acute exacerbations of chronic obstructive pulmonary disease

Previously we reported an impaired energy balance in patients with chronic obstructive pulmonary disease (COPD) during an acute disease exacerbation, but limited data are available on the underlying mechanisms. Experimental a nd clinical research supports the hypothesis of involvement of the hormone leptin in body weight and energy balance homeostasis. The aim of this study was to investigate the course of the energy balance in relation to leptin and the soluble tumor necrosis factor (TNF) receptors (sTNF-R) 55 and 75, p lasma glucose, and serum insulin in patients with severe COPD during the fi rst 7 d of hospitalization for an acute exacerbation (n = 17, 11 men, age m ean [SD] 66 [10] yr, FEV1 36 [12] %pred). For reference values of the labor atory parameters, blood was collected from 23 (16 men) healthy, elderly sub jects. On admission, the dietary intake/resting energy expenditure (REE) ra tio was severely depressed (1.28 [0.57]), but gradually restored until Day 7 (1.65 [0.45], p = 0.005 versus Day 1). Glucose and insulin concentrations were elevated on admission, but on Day 7 only plasma glucose was decreased . The sTNF-Rs were not different from healthy subjects and did not change. Plasma leptin, adjusted for fat mass expressed as percentage of body weight (%FM), was elevated on Day 1 compared with healthy subjects (1.82 [3.85] v ersus 0.32 [0.72] ng%/ml, p = 0.008), but decreased significantly until Day 7 (1.46 [3.77] ng%/ml, p = 0.015 versus Day 1). On Day 7, sTNF-R55 was, in dependently of %FM, correlated with the natural logarithm (LN) of leptin (r = 0.65, p = 0.041) and with plasma glucose (r = 0.81, p = 0.015). In addit ion, the dietary intake/PEE ratio was not only inversely related with LN le ptin (-0.74, p = 0.037), but also with sTNF-R55 (r = -0.93, p = 0.001) on d ay seven. In conclusion, temporary disturbances in the energy balance were seen during an acute exacerbation of COPD, related to increased leptin conc entrations as well as to the systemic inflammatory response. Evidence was f ound that the elevated leptin concentrations were in turn under control of the systemic inflammatory response, and, presumably, the high-dose systemic glucocorticosteroid treatment.