Abstract
Fasting plasma leptin levels reflect fat mass, but dynamic leptin responses to secretagogues, and the influence of race/ethnicity, have not been well studied. Here, we compared basal and stimulated leptin levels in relation to cardiometabolic risk and weight trajectories in black and white subjects. We studied 254 (127 black and 127 white) normoglycemic adults enrolled in the Pathobiology of Prediabetes in a Biracial Cohort (POP-ABC) study. At baseline and annually, POP-ABC participants underwent physical examination, oral glucose tolerance test, and measurements of body fat (dual energy X-ray absorptiometry), fasting plasma leptin, insulin, cortisol, lipids, and leptin secretory response to single-dose (2 mg) dexamethasone (dex). The interactions among basal and stimulated leptin and changes in adiposity/cardiometabolic measures during the ensuing year were then analyzed. The mean (±SD) fasting leptin level (50.6 ± 47.7 vs. 39.5 ± 37.6 ng/mL, P = 0.004) and body mass index (BMI) (31.9 ± 7.14 vs. 29.0 ± 7.66 kg/m2, P = 0.0043) were higher in black women vs. white women, but similar in black men vs. white men (leptin: 12.4 ± 2.07 vs. 11.1 ± 1.40 ng/mL; BMI: 29.4 ± 7.68 vs. 28.1 ± 4.23 kg/m2). The peak leptin response to dex (~200% baseline) did not differ significantly by gender or race. Total body fat correlated positively with fasting leptin (r = 0.81, P < 0.0001) and inversely stimulated leptin levels (r = -0.26, P < 0.0001). Fasting leptin was unrelated to 1-year change in weight or fat mass, whereas stimulated leptin levels were significantly associated with 1-year trajectories in weight (P = 0.0016) and total fat mass (P = 0.0035). Stimulated leptin levels also had significant interactions with insulin sensitivity (homeostasis model of insulin resistance, P = 0.01), triglycerides (P = 0.0078), fasting glucose (P = 0.027), systolic blood pressure (P = 0.037), and high-sensitivity C-reactive protein (P = 0.027). We found no significant ethnic disparities in basal or dynamic leptin secretion in relation to adiposity. Fasting leptin levels were not associated with 1-year weight change, while stimulated levels showed weak though significant association with 1-year weight change.
Highlights
Leptin regulates body weight and influences metabolic processes in rodents [1,2,3] and human beings [4,5,6,7,8]
Excluded were persons enrolled in active weight loss programs, Abbreviations: ANOVA, analysis of variance; BMI, body mass index; BP, blood pressure; Dex, dexamethasone; DEXA, dual energy X-ray absorptiometry; FPG, fasting plasma glucose; HOMA-B, homeostasis model of beta-cell function; HOMA-IR, homeostasis model of insulin resistance; hsCRP, high-sensitivity C-reactive protein; NGT, normal glucose tolerance; OGTT, oral glucose tolerance test; POP-ABC, Pathobiology of Prediabetes in a Biracial Cohort; 2-hr plasma glucose (2hrPG), two-hour post-load plasma glucose during 75-gram standard oral glucose tolerance test; T2D, type 2 diabetes
The mean age was lower and body mass index (BMI) higher in black than white subjects, but total and trunk fat mass were similar in the two groups
Summary
Leptin regulates body weight and influences metabolic processes in rodents [1,2,3] and human beings [4,5,6,7,8]. The analysis of plasma leptin levels in relation to human metabolic pathophysiology has focused largely on specimens collected under basal (fasting) conditions [9,10,11,12,13]. The findings from such studies indicate that fasting leptin levels are directly correlated with measures of adiposity [9,10,11] in lean and obese subjects as well as in persons with diabetes [14]. We compared basal and stimulated leptin levels in relation to cardiometabolic risk and weight trajectories in black and white subjects
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