Plasma Leptin Association with Body Composition and Energy Expenditure in Sickle Cell Disease

Abstract

Objective: To examine the association between fasting plasma leptin concentrations and the hypercatabolic state observed in sickle cell disease (SCD).

Methods: Plasma leptin concentration and resting energy expenditure (REE) were measured in 37 SCD patients (10 men, 12 boys 14 to 18 years-old, seven women, and eight girls 14 to 18 year-old) and in 37 age, gender and fat mass (FM) matched controls. Body composition was measured hydrostatically, REE by whole room-indirect calorimeter, and plasma leptin using an RIA kit.

Results: Plasma leptin concentration and leptin normalized for body fat (ng/dL*kg FM⁻¹) were significantly lower in SCD patients than in non-SCD controls (4.00±3.23 vs. 9.94±14.69, p=0.021 and 0.406±0.260 vs. 0.643±0.561, p=0.024, respectively). A positive linear association between log plasma leptin and FM was observed in both males and females, adjusting for age and SCD status. The strength of this association was greater in females compared with males (slope=0.699 and 0.382 log ng/mL per 10 kg FM, respectively; p=0.013). SCD patients on average demonstrated a higher REE, adjusting for FFM (p<0.0001). Log plasma leptin and FM were not statistically significant predictors of REE after adjustment for FFM and SCD.

Conclusions: Once corrected for body composition, mean plasma leptin concentration was significantly lower among female SCD patients than among non-SCD matched controls. Although REE was higher in SCD patients, there is no simple association between leptin and REE in SCD.

• leptin
• sickle cell disease
• resting metabolic rate
• body composition

This work was supported by grants from the National Institutes of Health HL-03530 (to M.S.B.), HL-56867 (to P.J.F.), General Clinical Research Center Grant RR-00095 (to Vanderbilt University) and RR-1179204 (to Meharry Medical College), Clinical Nutrition Research Unit Grant DK-26657 (to Vanderbilt University), and Meharry COE grant (to M.S.B. and L.A.S.). We thank staff of the General Clinical Research Center (GCRC) at Vanderbilt University for help with this project. We also thank Wanda Snead for her technical help and Karen Townsend for her technical help and assistance in preparing this manuscript. Finally, we acknowledge our subjects for their enthusiasm and participation in this study.

Notes

Presented in part at the Experimental Biology ’99 Meeting, Washington DC, April 17–21, 1999.