Sylvie Normand

Physical Inactivity Differentially Alters Dietary Oleate and Palmitate Trafficking

OBJECTIVE— Obesity and diabetes are characterized by the incapacity to use fat as fuel. We hypothesized that this reduced fat oxidation is secondary to a sedentary lifestyle. RESEARCH DESIGN AND METHODS— We investigated the effect of a 2-month bed rest on the dietary oleate and palmitate trafficking in lean women (control group, n = 8) and the effect of concomitant resistance/aerobic exercise training as a countermeasure (exercise group, n = 8). Trafficking of stable isotope–labeled dietary fats was combined with muscle gene expression and magnetic resonance imaging–derived muscle fat content analyses. RESULTS— In the control group, bed rest increased the cumulative [1-13C]oleate and [d31]palmitate appearance in triglycerides (37%, P = 0.009, and 34%, P = 0.016, respectively) and nonesterified fatty acids (NEFAs) (37%, P = 0.038, and 38%, P = 0.002) and decreased muscle lipoprotein lipase (P = 0.043) and fatty acid translocase CD36 (P = 0.043) mRNA expressions. Plasma NEFA-to-triglyceride ratios for [1-13C]oleate and [d31]palmitate remained unchanged, suggesting that the same proportion of tracers enters the peripheral tissues after bed rest. Bed rest did not affect [1-13C]oleate oxidation but decreased [d31]palmitate oxidation by −8.2 ± 4.9% (P < 0.0001). Despite a decreased spontaneous energy intake and a reduction of 1.9 ± 0.3 kg (P = 0.001) in fat mass, exercise training did not mitigate these alterations but partially maintained fat-free mass, insulin sensitivity, and total lipid oxidation in fasting and fed states. In both groups, muscle fat content increased by 2.7% after bed rest and negatively correlated with the reduction in [d31]palmitate oxidation (r2 = 0.48, P = 0.003). CONCLUSIONS— While saturated and monounsaturated fats have similar plasma trafficking and clearance, physical inactivity affects the partitioning of saturated fats toward storage, likely leading to an accumulation of palmitate in muscle fat.

Beneficial effects of a 5-week low-glycaemic index regimen on weight control and cardiovascular risk factors in overweight non-diabetic subjects.

The glycaemic index (GI) has been developed in order to classify food according to the postprandial glycaemic response. This parameter is of interest, especially for people prone to glucose intolerance; however, the effects of a low-GI (LGI) diet on body weight, carbohydrate and lipid metabolism remain controversial. We studied the effects of either a LGI or high-GI (HGI) diet on weight control and cardiovascular risk factors in overweight, non-diabetic subjects. The study was a randomized 5-week intervention trial. The thirty-eight subjects (BMI 27.3 (sem 0.2) kg/m2) followed an intervention diet in which usual starch was replaced ad libitum with either LGI or HGI starch. Mean body weight decrease was significant in the LGI group ( - 1.1 (sEM 0.3) kg, P = 0.004) and was significantly greater than in the HGI group ( - 0.3 (sEM 0.2) kg, P = 0.04 between groups). Hunger sensation scales showed a trend towards a decrease in hunger sensation before lunch and dinner in the LGI group when compared with the HGI group (P = 0.09). No significant increase in insulin sensitivity was noticed. The LGI diet also decreased total cholesterol by 9.6 % (P < 0.001), LDL-cholesterol by 8.6 % (P = 0.01) and both LDL-:HDL-cholesterol ratio (10.1 %, P = 0.003) and total:HDL-cholesterol ratio (8.5 %, P = 0.001) while no significant changes were observed in the HGI group. Lowering the GI of daily meals with simple dietary recommendations results in increased weight loss and improved lipid profile and is relatively easy to implement with few constraints. These potential benefits of consuming a LGI diet can be useful to develop practical dietetic advice.

Effect of Physical Inactivity on the Oxidation of Saturated and Monounsaturated Dietary Fatty Acids: Results of a Randomized Trial

Objectives: Changes in the way dietary fat is metabolized can be considered causative in obesity. The role of sedentary behavior in this defect has not been determined. We hypothesized that physical inactivity partitions dietary fats toward storage and that a resistance exercise training program mitigates storage. Design: We used bed rest, with randomization to resistance training, as a model of physical inactivity. Setting: The trial took place at the Space Clinic (Toulouse, France). Participants: A total of 18 healthy male volunteers, of mean age ± standard deviation 32.6 ± 4.0 y and body mass index 23.6 ± 0.7 kg/m2, were enrolled. Interventions: An initial 15 d of baseline data collection were followed by 3 mo of strict bed-rest alone (control group, n = 9) or with the addition of supine resistance exercise training every 3 d (exercise group, n = 9). Outcome measures: Oxidation of labeled [d31]palmitate (the main saturated fatty acid of human diet) and [1-13C]oleate (the main monounsaturated fatty acid), body composition, net substrate use, and plasma hormones and metabolites were measured. Results: Between-group comparisons showed that exercise training did not affect oxidation of both oleate (mean difference 5.6%; 95% confidence interval [95% CI], −3.3% to 14.5%; p = 0.20) and palmitate (mean difference −0.2%; 95% CI, −4.1% to 3.6%; p = 0.89). Within-group comparisons, however, showed that inactivity changed oxidation of palmitate in the control group by −11.0% (95% CI, −19.0% to −2.9%; p = 0.01) and in the exercise group by −11.3% (95% CI, −18.4% to −4.2%; p = 0.008). In contrast, bed rest did not significantly affect oleate oxidation within groups. In the control group, the mean difference in oleate oxidation was 3.2% (95% CI, −4.2% to 10.5%; p = 0.34) and 6.8% (95% CI, −1.2% to 14.7%; p = 0.08) in the exercise group. Conclusions: Independent of changes in energy balance (intake and/or output), physical inactivity decreased the oxidation of saturated but not monounsaturated dietary fat. The effect is apparently not compensated by resistance exercise training. These results suggest that Mediterranean diets should be recommended in sedentary subjects and recumbent patients.

Is advice for breakfast consumption justified? Results from a short-term dietary and metabolic experiment in young healthy men

Short-term (2 weeks) effects of the consumption of a high-energy (2920 kJ (700 kcal)) or low-energy (418 kJ (100 kcal)) breakfast on dietary patterns, blood variables and energy expenditure (indirect calorimetry) were compared in ten free-living healthy young men in a crossover study. During the high-energy breakfast, total energy intake was increased, the intake of protein and lipids was unchanged but the intake of carbohydrates was increased. Thus, 48 (sd 4)% of energy came from carbohydrates in the high-energy breakfast compared with 42 (sd 5)% in the low-energy breakfast. Excluding breakfast, the macronutrient composition of the diet remained identical in the two situations. After the high-energy breakfast, fasting serum triacylglycerol concentration was higher and HDL-cholesterol concentration was lower than after the low-energy breakfast. A high glycaemic response was observed in the morning after the high-energy breakfast period, while there was a peak of free fatty acids after the low-energy breakfast. The high-energy breakfast induced a strong inhibition of fat oxidation throughout the day. Although long-term adaptation to a high-energy breakfast cannot be excluded, the high-energy breakfast in this study did not appear to be favourable to health. Our results do not support the current advice to consume more energy at breakfast.

Influence of dietary fat on postprandial glucose metabolism (exogenous and endogenous) using intrinsically 13 C-enriched durum wheat

The present study evaluates the influence of different amounts of fat added to starch on postprandial glucose metabolism (exogenous and endogenous). Nine women (24 (se 2) years old, BMI 20.4 (se 0.7) kg/m(2)) ingested 1 week apart 75 g glucose equivalent of (13)C-labelled starch in the form of pasta without (low fat; LF) or with 15 (medium fat; MF) or 40 (high fat; HF) g sunflower oil. During the 7 h following meal consumption, plasma glucose, non-esterified fatty acids, triacylglycerols (TG) and insulin concentrations, and endogenous (using [6,6-(2)H(2)]glucose) and exogenous glucose turnover were determined. With MF and HF meals, a lower postprandial glucose peak was observed, but with a secondary recovery. A decrease in exogenous glucose appearance explained lower glycaemia in HF. At 4 h after the HF meal the insulin, insulin:glucose and postprandial blood TG were higher than those measured after the LF and MF meals. Despite higher insulinaemia, total glucose disappearance was similar and endogenous glucose production was suppressed less than after the LF and MF meals, suggesting insulin resistance. Thus, the addition of a large amount of fat appears to be unfavourable to glucose metabolism because it leads to a feature of insulin resistance. On the contrary, the MF meal did not have these adverse effects, but it was able to decrease the initial glycaemic peak.

Physical activity-related energy expenditure with the RT3 and TriTrac accelerometers in overweight adults

Objective: The objective was to evaluate two accelerometers, the RT3 and the TriTrac‐R3D for their ability to produce estimates of physical activity‐related energy expenditure (PAEE) in overweight/obese adults.

Modulation of the postprandial phase by β-glucan in overweight subjects: effects on glucose and insulin kinetics.

Decreasing the postprandial glucose response is potentially of major importance to public health when low-glycemic index or high-fibre content foods are associated with a decreased risk of diabetes. We investigated in overweight subjects the effect of adding beta-glucan (BG) to a polenta (Pol) meal on postprandial metabolism and glucose bioavailability using stable isotopes. In this single-blind, randomized, crossover trial, 12 subjects ate two meals containing Pol with (Pol + BG) or without (Pol) 5 g BG. Concentrations of glucose, insulin, C-peptide, nonesterified fatty acids, triacylglycerol, total and exogenous glucose kinetics were assessed for 6 h postprandially. The kinetics of total and exogenous glucose importantly differed between the meals, but not the quantity of total and exogenous glucose appearing in plasma. Less total and exogenous glucose appeared during the first 120 min after the Pol + BG meal; the phenomenon was then reversed (both p < 0.0001). After 120 min, glucose and insulin responses declined, but remained higher after the Pol + BG meal (p < 0.05) in parallel to the inhibition of lipolysis. The endogenous glucose production (EGP) was significantly more inhibited after the Pol + BG meal. The addition of BG slowed the appearance of glucose in plasma, resulting in longer-lasting insulin secretion which exerted a prolonged inhibition of EGP and lipolysis.

Regulation of energy balance during long-term physical inactivity induced by bed rest with and without exercise training.

BACKGROUND Short-term physical inactivity affects energy balance and is considered conducive to weigh gain. Long-term effects are unknown. OBJECTIVE The objective of the study was to use a bed-rest model to determine the long-term effects of physical inactivity on energy balance regulation and test the effect of exercise training on energy balance adjustment to physical inactivity. DESIGN Sixteen lean women were divided into two groups (n = 8 each): a control group subjected to a strict 60-d bed rest and an exercise group subjected to a combined aerobic/resistive exercise training concomitantly to bed rest. Body composition, spontaneous energy intake, hunger, total energy expenditure (TEE), and fasting gut hormones were measured. RESULTS Based on bed-rest-induced body composition changes, the control group were in slight negative energy balance (-0.4 +/- 0.4 MJ/d; P = 0.01 vs. zero), essentially due to muscle atrophy (P < 0.001 vs. zero). The stable fat mass (P = 0.19 vs. zero), and the matching between spontaneous energy intake and TEE indicated, however, a stable energy balance. Hunger and gut hormones remained unchanged during the bed rest. In the exercise group, TEE was 24% higher than in the control group (P = 0.004). Unexpectedly, desire to consume food (P = 0.025) decreased and spontaneous energy intake (P = NS) was not stimulated, promoting a negative energy balance (-1.1 +/- 0.5 MJ/d, P = 0.0003 vs. zero). CONCLUSIONS Energy balance is regulated during 2 months of physical inactivity, contrasting with short-term experiments. Conversely, exercise-induced energy expenditure in bed-resting subjects who have no spontaneous physical activity did not induce hunger and promoted a negative energy balance, suggesting a potential role of nonexercise physical activities in energy balance regulation.

Activity energy expenditure is a major determinant of dietary fat oxidation and trafficking, but the deleterious effect of detraining is more marked than the beneficial effect of training at current recommendations

BACKGROUND Previous studies suggested that physical activity energy expenditure (AEE) is a major determinant of dietary fat oxidation, which is a central component of fat metabolism and body weight regulation. OBJECTIVE We tested this hypothesis by investigating the effect of contrasted physical activity levels on dietary saturated and monounsaturated fatty acid oxidation in relation to insulin sensitivity while controlling energy balance. DESIGN Sedentary lean men (n = 10) trained for 2 mo according to the current guidelines on physical activity, and active lean men (n = 9) detrained for 1 mo by reducing structured and spontaneous activity. Dietary [d31]palmitate and [1-¹³C]oleate oxidation and incorporation into triglyceride-rich lipoproteins and nonesterified fatty acid, AEE, and muscle markers were studied before and after interventions. RESULTS Training increased palmitate and oleate oxidation by 27% and 20%, respectively, whereas detraining reduced them by 31% and 13%, respectively (P < 0.05 for all). Changes in AEE were positively correlated with changes in oleate (R² = 0.62, P < 0.001) and palmitate (R² = 0.66, P < 0.0001) oxidation. The d31-palmitate appearance in nonesterified fatty acid and very-low-density lipoprotein pools was negatively associated with changes in fatty acid translocase CD36 (R² = 0.30), fatty acid transport protein 1 (R² = 0.24), and AcylCoA synthetase long chain family member 1 (ACSL1) (R² = 0.25) expressions and with changes in fatty acid binding protein expression (R² = 0.33). The d31-palmitate oxidation correlated with changes in ACSL1 (R² = 0.39) and carnitine palmitoyltransferase 1 (R² = 0.30) expressions (P < 0.05 for all). Similar relations were observed with oleate. Insulin response was associated with AEE (R² = 0.34, P = 0.02) and oleate (R² = 0.52, P < 0.01) and palmitate (R² = 0.62, P < 001) oxidation. CONCLUSION Training and detraining modified the oxidation of the 2 most common dietary fats, likely through a better trafficking and uptake by the muscle, which was negatively associated with whole-body insulin sensitivity.

Effect of postprandial modulation of glucose availability: short- and long-term analysis

Low glycaemic index (LGI) foods have been proposed as potential means to decrease postprandial glucose excursions and thus to improve diabetes management. We modulated glucose availability of cereal products and thus their glycaemic index to study the metabolic effect of LGI foods on daylong glucose control acutely and in the long term following a 5-week GI intervention diet in free-living subjects. In this randomised, parallel trial, two groups of nineteen overweight subjects followed an ad libitum 5-week intervention diet in which usual starch was replaced by either LGI or high GI (HGI) starch. During the exploration days (days 1 and 36), subjects ate their assigned 13C-labelled test breakfast (LGI or HGI), and total and exogenous glucose kinetics (using stable isotopes), postprandial concentrations of glucose, insulin, lipid profile and nutrient oxidation were assessed after the test breakfast and a standardised lunch. At day 1, LGI breakfast significantly decreased post-breakfast glycaemic response with a parallel decrease in exogenous and total glucose appearance (P < 0.05). Post-lunch and post-breakfast glycaemic responses were positively correlated (r 0.79, P < 0.0001). Following the 5-week diet, difference between the groups in terms of glucose kinetics and response was maintained (no significant interaction group x time) but tended to decrease over time for the post-breakfast glycaemic response. Post-lunch and post-breakfast glycaemic responses remained positively correlated (r 0.47, P = 0.004). Modulation of postprandial glucose availability at breakfast decreased plasma exogenous glucose appearance and improved glucose control at the subsequent lunch. After 5 weeks, these effects were maintained in healthy subjects but remained to be confirmed in the longer term.