New Findings r What is the central question of this study?We wanted to determine the effect of three high-fat meals enriched with different fatty acids [monounsaturated fatty acids (MUFAs), polyunsaturated fatty acids (PUFAs) or saturated fatty acids (SFAs)] on diet-induced thermogenesis and substrate oxidation in premenopausal women of normal weight. r What is the main finding and its importance?We found that a PUFA-rich high-fat meal led to a greater diet-induced thermogenesis in normal-weight premenopausal women compared with SFA-or MUFA-rich high-fat meals. The greater diet-induced thermogenesis for PUFA-rich meals could contribute to differences in long-term overall energy balance, and thus, weight maintenance. Substrate utilization was not different between treatments.The composition of fatty acids in a diet may differentially affect metabolism, thus playing a role in the development of obesity. Our aim was to study the effects of three high-fat (HF) meals with different degrees of saturation on diet-induced thermogenesis (DIT) and substrate oxidation in premenopausal women of normal weight. Fifteen healthy, normal-weight women, aged 18-35 years, participated in a randomized cross-over study, in which they consumed isocaloric HF meals (70% of energy from fat) rich in saturated fat (SFA; 40% of total energy), monounsaturated fat (MUFA; 42% of total energy) or polyunsaturated fat (PUFA; 42% of total energy). Indirect calorimetry was used to measure respiratory gases for a 5 h postprandial period. The data collected were used to determine respiratory exchange ratio for assessing substrate oxidation, as well as energy expenditure for the determination of DIT. The area under the curve for DIT following the PUFA-rich HF meal was greater than that of the SFA-or MUFA-rich HF meals [10.0 ± 0.7, 8.6 ± 0.8 and 8.9 ± 1.2 kcal (5 h) −1 (P = 0.02) for PUFA, MUFA and SFA, respectively]. No significant difference was found in respiratory exchange ratio (0.86 ± 0.01, 0.85 ± 0.01 and 0.85 ± 0.01 for PUFA-, MUFA-and SFA-rich HF meals, respectively) or substrate utilization following the three different HF meals (12.2 ± 1.0, 11.2 ± 0.5 and 11.6 ± 0.9 g for cumulative postprandial carbohydrate oxidation following the PUFA-, MUFA-and SFA-rich HF meals, respectively; and 3.8 ± 0.4, 4.1 ± 0.2 and 4.1 ± 0.3 g for cumulative fat oxidation of the PUFA-, MUFA-and SFA-rich HF meals, respectively). In conclusion, acute ingestion of a PUFA-rich HF meal induced a greater DIT in normal-weight women compared with SFA-or MUFA-rich HF meals. No significant differences were found for substrate utilization.

Objective: The role of lipocalin-2 (Lcn2) was determined in regulating metabolism in cell, animal, and human models. Design and Methods: Adipocytes were treated with recombinant lipocalin-2 (rLcn2) to determine the effect on lipid metabolism. rLcn2 was injected into mice to determine the effect on metabolism in vivo. To assess the relationship between Lcn2 and fat oxidation (FatOx) in humans, normal weight (NW) and obese (OB) women were given three separate high fat (HF) meals followed by indirect calorimetry. The relationship between postprandial Lcn2 with macronutrient metabolism and total energy expenditure (TEE) using Pearson correlations was determined. Results: Lcn2 increased expression of genes involved in b-oxidation including peroxisome proliferatoractivated receptor-d in adipocytes, as well as 3 H labeled oleate b-oxidation. Lcn2 injected into chow-fed mice directly increased TEE by 18% after the first dark cycle (232 6 1.4 cal vs. 341 6 1.4 cal; PBS vs. Lcn2) and remained significantly elevated by 10% after the second dark cycle (296 6 1.4 cal vs. 326 6 1.4 cal; PBS vs. Lcn2). Lcn2 was correlated with TEE in all three HF meal challenges in NW but not OB females. Conclusions: Lipocalin-2 is a novel adipokine that promotes FatOx and TEE and its function may be impaired in obesity.

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