Possible adaptive mechanisms that may defend against weight gain during periods of excessive energy intake were investigated by overfeeding six lean and three overweight young men by 50% above baseline requirements with a mixed diet for 42 d [6.2 +/- 1.9 MJ/d (mean +/- SD), or a total of 265 +/- 45 MJ]. Mean weight gain was 7.6 +/- 1.6 kg (58 +/- 18% fat). The energy cost of tissue deposition (28.7 +/- 4.4 MJ/kg) matched the theoretical cost (26.0 MJ/kg). Basal metabolic rate (BMR) increased by 0.9 +/- 0.4 MJ/d and daily energy expenditure assessed by whole-body calorimetry (CAL EE) increased by 1.8 +/- 0.5 MJ/d. Total free-living energy expenditure (TEE) measured by doubly labeled water increased by 1.4 +/- 2.0 MJ/d. Activity and thermogenesis (computed as CAL EE--BMR and TEE--BMR) increased by only 0.9 +/- 0.4 and 0.9 +/- 2.1 MJ/d, respectively. All outcomes were consistent with theoretical changes due to the increased fat-free mass, body weight, and energy intake. There was no evidence of any active energy-dissipating mechanisms.

The doubly-labelled water (2H180) method was used to measure total energy expenditure (TEE) in ten uon-pregnant, non-lactating (NPNL), six pregnant (P) and fourteen lactating (L) women in a rural Gambian community. Measurements were made on free-living subjects at a period of peak energetic stress when high agricultural work loads coincided with a hungry season to induce moderately severe negative energy balance. TEE averaged 10.42 (SD 2.08) MJ/d, equivalent to 1.95 (SD 0.38) times resting metabolic rate (RMR). The energy cost of physical activity plus thermogenesis, derived as TEE -RMR,

Recent evidence shows that specific fatty acids affect cell metabolism, modifying the balance between fatty acid oxidation and lipogenesis. These effects may have important implications in addressing the present epidemic of nutrition-related chronic disease. Intake of dietary saturated and n-6 PUFA have increased while n-3 fatty acid intake has decreased. Obesity, type 2 diabetes and insulin resistance are highly prevalent, and both are strongly related to disorders of lipid metabolism characterized by an increased plasma and intracellular fatty acid availability. Thus, it has been hypothesized that change in the quality of dietary fat supply is able to modify the degree of insulin sensitivity. Animal studies provide support for this notion. However, there is limited human data either from normal or diabetic subjects. This review aims to analyse human studies that address this question. To this purpose, the experimental design, dietary compliance, insulin-sensitivity method used and confounding variables are discussed in order to identify the role of dietary fat quality as a risk factor for insulin resistance. Most studies (twelve of fifteen) found no effect relating to fat quality on insulin sensitivity. However, multiple study design flaws limit the validity of this conclusion. In contrast, one of the better designed studies found that consumption of a high-saturated-fat diet decreased insulin sensitivity in comparison to a high-monounsaturated-fat diet. We conclude that the role of dietary fat quality on insulin sensitivity in human subjects should be further studied, using experimental designs that address the limitations of existing data sets.Insulin sensitivity: Fat quality: Lipid metabolism

No abstract

Free-living energy expenditure (EE) was assessed in 37 young pregnant Gambian women at the 12th (n = 11, 53.5 +/- 1.7 kg), 24th (n = 14, 54.7 +/- 2.1 kg), and 36th (n = 12, 65.0 +/- 2.6 kg) wk of pregnancy and was compared with nonpregnant nonlactating (NPNL) control women (n = 12, 50.3 +/- 1.6 kg). The following two methods were used to assess EE: 1) the heart rate (HR) method using individual regression lines (HR vs EE) established at different activity levels in a respiration chamber and 2) the doubly labeled water (2H2(18)O) method in a subgroup of 25 pregnant and 7 control women. With the HR method the EE during the agricultural rainy season was found to be 2,408 +/- 87, 2,293 +/- 122, and 2,782 +/- 130 kcal/day at 12, 24, and 36 wk of gestation and were not significantly different from the control group (2,502 +/- 133 kcal/day). These findings were confirmed by the 2H2(18)O measurements, which failed to show any effect of pregnancy on EE. Expressed per unit body weight, the free-living EE was found to be lower (P less than 0.01 with 2H2(18)O method) at 36 wk of gestation than in the NPNL group. It is concluded that, in these Gambian women, energy-sparing mechanisms that contribute to meet the additional energy stress of gestation are operating during pregnancy (e.g., diminished spontaneous physical activity).