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Effects of Leptin Resistance on Acute Fuel Metabolism after a High Carbohydrate Load in Lean and Overweight Young Men

Department of Physiology and Nutrition, University of Navarra, Pamplona, SPAIN

Address reprint requests to: J. Alfredo Martínez, PhD, Department of Physiology and Nutrition, University of Navarra, C/ Irunlarrea s/n, Pamplona, SPAIN. E-mail: jalfmtz{at}unav.es.

Objective: Six lean (BMI = 20.8 ± 0.7) and seven overweight (BMI = 30.8 ± 1.7) young men (18–27 years old) were studied to investigate the acute effect of a high-carbohydrate meal on leptin levels and its relation to energy expenditure as well as to protein, carbohydrate and fat oxidation.

Methods: Study participants were given a high-carbohydrate meal (17% as protein, 80% as carbohydrates and 3% as lipids) covering 40% of their estimated daily energy requirements. Serum leptin, insulin, glucose, free fatty acids and triglycerides levels were measured before meal intake and during the four postprandial hours. Furthermore, energy expenditure (EE), protein, carbohydrate and lipid oxidation were measured in fasted and fed conditions.

Results: Fasting leptin was found to be positively correlated with circulating insulin concentrations (r = .748; p = 0.011) and body fat in kg (r = .827; p = 0.001). During the measured postprandial period no statistically significant changes were found in leptin levels as compared with pre-meal values in either lean or overweight men, nor differences in leptin changes between both groups. After load intake, carbohydrate oxidation was lower in overweight individuals (p < 0.05), while no significant differences were observed in protein oxidation. Cumulative lipid oxidation was found to be negatively associated with post-meal leptin values, being significantly lower in the overweight as compared with lean men (p < 0.05). This study demonstrates that the acute postprandial fuel substrate utilization is altered in overweight men with a lower carbohydrate oxidation and a strong inhibition of lipid oxidation, which could be attributed to some leptin resistance.

Conclusion: These data also suggest that short-term meal-related metabolic responses may explain the long-term body adiposity if they are sustained over long intervals.

Key words: obesity, leptin resistance, substrate oxidation

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