OBJECTIVE: A low-fat, high-carbohydrate diet (≤30% of total energy intake as fat) in conjunction with moderate intensity physical activity is widely recommended for weight maintenance and reduction. The aim of this study was to assess the effect of adding daily exercise to a short-term high-carbohydrate diet on fasting and postprandial leptin levels.
SUBJECTS: Eight healthy, postmenopausal women aged 60±4 y (mean±s.d.) (body mass index, BMI: 26.4±2.3 kg m−2; predicted maximal oxygen uptake: 29±2 ml kg−1 min−1).
DESIGN: Plasma responses were studied after subjects consumed the same high-fat, mixed meal on three occasions: after 3 days on a low-carbohydrate diet (35, 50 and 15% energy from carbohydrate, fat and protein, respectively) (Low-CHO); after 3 days on an isoenergetic high-carbohydrate diet (corresponding values 70, 15 and 15%) (High-CHO); and after 3 days on the same high-carbohydrate diet with 60 min of brisk walking daily (High-CHO-Ex).
MEASUREMENTS: Fasting and postprandial plasma or serum concentrations of leptin, glucose and insulin.
RESULTS: Fasting leptin was significantly higher (P<0.05) after the High-CHO (18.4±2.6 ng ml−1) (mean±s.e.m.) than after both the Low-CHO and the High-CHO-Ex interventions, which did not differ significantly from each other (16.9±2.1 and 15.5±2.0 ng ml−1, respectively; P=0.08). Overall (fasted and postprandial states), plasma leptin concentrations were significantly higher after the High-CHO than after the High-CHO-Ex intervention. There was a strong, positive, linear relation between postprandial insulin responses and postprandial leptin concentrations at 6 h. In addition, there was a strong, negative, linear relation between whole-body insulin sensitivity (based on postprandial responses of glucose and insulin) and postprandial leptin concentrations at 6 h.
CONCLUSION: Daily moderate intensity exercise, without concomitant changes in body fat mass, suppressed fasting and postprandial circulating leptin concentrations after consumption of a short-term high-carbohydrate diet. As shown in previous studies, insulin appears to be an important modulator of leptinaemia.
Leptin, the protein product of the obese gene, is primarily secreted by adipocytes and has a critical role in regulating energy balance via its actions on food intake and energy expenditure.1 It functions largely as a long-term regulator of energy balance2 rather than a short-term satiety signal.3 Circulating leptin concentrations are highly correlated with adipose tissue mass.4 Furthermore, plasma leptin decreases during short-term fasting and is restored after refeeding,5 despite a minimal change in adipose mass, indicating that recent energy balance has a major influence on plasma leptin levels.
Circulating leptin concentration is also affected by dietary macronutrient content.6 Over a 24-h period, plasma leptin concentrations in healthy women were lower when high-fat, low-carbohydrate meals were consumed than when low-fat, high-carbohydrate meals were consumed. This effect of dietary macronutrient content on 24-h plasma leptin could potentially contribute to increased energy intake while consuming high-fat diets7 and, conversely, to reduction in energy intake and body weight during consumption of high-carbohydrate diets.8,9
Exercise, with associated changes in energy expenditure, fuel flux and systemic hormone concentrations, may also contribute to leptin regulation. However, exercise-training studies have generally showed no effect on fasting plasma leptin or reductions arising from concomitant reductions in body fat mass.10 An exception to this is the study by Hickey et al,11 which reported reduction in fasting plasma leptin in exercise-trained females, despite stable fat mass. Exercise has also been shown to suppress average 24-h circulating leptin,12 an effect opposite to that of high-carbohydrate feeding.6
A low-fat, high-carbohydrate diet (≤30% of total energy intake as fat) in conjunction with moderate intensity physical activity is widely recommended for weight maintenance and reduction.13,14 As mentioned above, both high-carbohydrate diets and exercise influence circulating leptin, but there is currently no information on the effect of their combination. The present study aimed to assess the effect of adding daily exercise to a short-term high-carbohydrate diet on fasting and postprandial leptin levels. Since insulin is an important regulator of leptinaemia,15 a further aim of our study was to assess the relation between postprandial circulating leptin and insulin. Other aspects of this study have been presented elsewhere.16 Insulin data are presented here and discussed only in the context of leptin.
The study was approved by Loughborough University's Ethical Advisory Committee and subjects gave their informed consent. Eight nonsmoking postmenopausal (for at least 2 y) healthy women aged 60±4 y (mean±s.d.), with body mass index (BMI) 26.4±2.3 kg m−2 participated. Their habitual diets were assessed by the weighed food inventory method as described previously.16 Subjects' habitual diets provided 7.41±1.37 MJ day−1, with 46±4% of energy as carbohydrate, 37±5% as fat and 17±3% as protein. Maximal oxygen uptake (VO2 max), predicted from the VO2/heart rate relation during uphill treadmill walking, was 29±2 ml kg−1 min−1. Two subjects were taking hormone replacement therapy and maintained this during the study. Other than this, none was taking drugs known to influence lipid or carbohydrate metabolism.
Subjects consumed a standard high-fat, mixed meal after three different interventions: (i) 3 days on a low-carbohydrate diet (Low-CHO); (ii) 3 days on a high-carbohydrate diet (High-CHO); and (iii) 3 days on the same high-carbohydrate diet with one 60-min session of brisk walking daily (High-CHO-Ex). The order of the interventions was counterbalanced, with 10-day wash-out periods during which subjects resumed their usual physical activity and dietary habits. During the day preceding each intervention, diet was standardised and subjects refrained from exercise and from alcohol consumption. No alcohol was consumed during any of the intervention periods.
Experimental diets and exercise sessions
Full details on the experimental diets and exercise sessions have been given previously.16 Briefly, the low-carbohydrate diet provided 35% of daily energy intake as carbohydrate, 50% as fat and 15% as protein. Corresponding values for the high-carbohydrate diet were 70, 15 and 15%. In the low-carbohydrate diet, the contribution of sugars and starch to total energy intake was 18 and 17%, respectively, and 47 and 23% in the high-carbohydrate diet. Saturated and monounsaturated fatty acids represented 20 and 16%, respectively, of total energy intake in the low-carbohydrate diet and 7 and 4% in the high-carbohydrate diet. Total daily energy supply was estimated to match each subject's habitual energy intake. All food items were provided for the subjects who prepared all meals, to a prescribed menu, weighing each item. Compliance, assessed by food inventories and detailed discussions with subjects, was high, that is, subjects followed the diets ‘to the gram’.
During the diet-only interventions (Low-CHO and High-CHO), no exercise other than activities of daily living were permitted. During the High-CHO-Ex intervention, subjects walked on the treadmill at 1.5±0.1 m s−1 (mean±s.d.) up a 3±1% gradient for 60 min each afternoon. VO2 and carbon dioxide production were measured as described previously.16 The average VO2 during walking was 17.7±1.1 ml kg−1 min−1, which represented 61±3% of predicted VO2 max. No subject experienced difficulty completing the walk and, on average, they rated its demands as ‘fairly hard’. Gross energy expenditure per session was 1.46±0.10 MJ.
Test meal protocol
Subjects arrived at the laboratory after a 12-h fast, at 08.00 h. Blood samples were obtained via a venous cannula in the fasted state (0 h) and 15, 30, 45, 60, 90 and 120 min after completion of the test meal, and then hourly until 6 h. The meal comprised cereal, nuts, chocolate, fruit, coconut and whipping cream (per kg body mass: 1.0 g fat, 0.9 g carbohydrate, 0.2 g protein). Subjects rested throughout the observation period, consumed only water and were always supine for at least 15 min prior to blood sampling.
Plasma leptin concentrations were determined in duplicate using a commercially available RIA (Linco Research Inc., Missouri, USA). Serum was analysed for insulin by RIA (COAT-A-COUNT; Diagnostic Products, Los Angeles, CA, USA). Plasma glucose was determined by enzymatic, colorimetric methods (Sigma Diagnostics, Poole, Dorset, UK). For all analytes, all samples from each subject were analysed in the same batch.
Calculations and statistics
Whole-body insulin sensitivity with regard to insulin effect on glycaemia (ISI(gly)) was calculated as follows: ISI(gly)=2/[(INS × GLY)+1], where INS and GLY are insulin and glucose area under the curve, respectively, over 6 h after meal ingestion expressed relative to the average values of the group of subjects.17
Two-way ANOVA for repeated measures was used to assess the effect of the interventions, postprandial time (0–6 h) and their interaction (intervention × time). In addition, summary measures of the postprandial insulin and glucose responses were calculated as the total area under serum or plasma concentration vs time curves (AUC) using the trapezoidal rule. These summary measures were compared by one-way ANOVA. The Tukey test was used for post hoc analysis. Pearson's correlation analysis was performed to test for relation between insulin concentration and leptin and between insulin sensitivity and leptin. Before statistical analyses were performed, each parameter was tested for normality using the Shapiro–Wilks' W test. Statistical analyses were performed using Statistica for Windows, version 5.0 (Tulsa, OK, USA), adopting a 5% level of significance. Data are expressed as means±s.e.m., unless otherwise stated.
Plasma leptin responses to the test meal are shown in Figure 1. Two-way ANOVA for repeated measures revealed significant main effects of intervention and time. Overall, plasma leptin was higher (P=0.02) after the High-CHO than after the High-CHO-Ex intervention. Also, overall, leptin concentration decreased transiently at 4 h after the meal (P=0.04 vs fasted state) but there was a significant intervention × time effect, indicating that the pattern of change of leptin over time differed among interventions. Fasting (0 h) leptin was significantly higher after the High-CHO (18.4±2.6 ng ml−1) than after both the Low-CHO and the High-CHO-Ex interventions, which did not differ significantly from each other (16.9±2.1 and 15.5±2.0 ng ml−1, respectively; P=0.08). After the Low-CHO intervention, 4-h postprandial leptin levels were not different compared to the fasting levels but leptin was increased at 6 h (P=0.004 vs 4 h). After the High-CHO intervention, leptin levels decreased in the first 4 h (P=0.008 vs fasted state) and rose again towards the fasting levels. After the High-CHO-Ex intervention, leptin remained unchanged during the observation period.
Glucose and insulin
Fasting plasma glucose concentration was similar among interventions (5.15±0.18, 5.04±0.14 and 5.06±0.15 mmol l−1 after Low-CHO, High-CHO and High-CHO-Ex, respectively). No significant differences were observed in glucose responses to the meal (AUC) (33.3±1.3, 33.7±1.1 and 33.1±1.3 mmol l−1 h after the Low-CHO, High-CHO and High-CHO-Ex, respectively).
Insulin responses are presented in Figure 2. Serum fasting insulin was lower (P=0.03) after the High-CHO-Ex than after the High-CHO intervention. The postprandial insulin response was significantly lower after the High-CHO-Ex intervention (954±131 pmol l−1 h) than after both the Low-CHO (1163±188 pmol l−1 h, P=0.04) and the High-CHO (1212±194 pmol l−1 h, P=0.01) interventions.
Whole-body insulin sensitivity, based on postprandial glucose and insulin concentrations, was significantly higher after the High-CHO-Ex intervention (1.11±0.08) than after both the Low-CHO (1.03±0.10, P=0.02) and the High-CHO (1.00±0.10, P=0.003) interventions.
Correlations between postprandial leptin, insulin and glucose
There was a strong, positive, linear relation between postprandial insulin responses (6-h AUC) and postprandial leptin concentrations at 6 h (Figure 3a). The relation between leptin and insulin was identical irrespective of the intervention. In addition, there was a strong, negative, linear relation between ISI(gly) and 6-h postprandial leptin concentration, irrespective of the intervention (Figure 3b). No relation was found between leptin concentration at 6 h and glucose 6-h AUC.
The combination of a low-fat, high-carbohydrate diet with moderate intensity physical activity is recommended by advisory bodies for the prevention of weight gain and obesity.13,14 Leptin has a critical role in regulating energy homeostasis and is affected both by dietary macronutrient composition6 and exercise.11,12 The present study investigated the effect of combining a short-term, high-carbohydrate diet with daily moderate intensity exercise on circulating fasting and postprandial leptin levels. We found that the high-carbohydrate diet induced higher fasting leptin concentrations and a different postprandial leptin response as compared to the low-carbohydrate diet. Adding daily exercise to the high-carbohydrate diet suppressed both fasting and postprandial plasma leptin.
Previous studies that investigated the effect of altering the dietary carbohydrate:fat ratio on fasting morning plasma concentration have generally found no effect.5,18,19 There are two possible reasons why we found that plasma leptin was higher after the high-carbohydrate diet than after the low-carbohydrate diet. First, we employed more extreme dietary interventions than those used in previous studies. Second, our high-carbohydrate diet provided a large proportion of energy from sugars. Fasting leptin concentrations have been found to be higher after a high-sucrose diet than after a high-starch or a high-fat diet.20 Insulin regulates leptin production15 and thus the higher fasting leptin we observed after the high-carbohydrate, high-sugar diet may have been caused by higher insulin concentrations in response to the type of carbohydrate predominating during this diet.
The observation that daily exercise during the consumption of the high-carbohydrate diet suppressed fasting leptin is interesting because the majority of previous studies have showed no effect of exercise training on fasting leptin, independent of reductions in body fat mass.21,22,23 In the present study, the high-carbohydrate plus exercise intervention was too short to induce any major changes in body weight. The exercise-induced reduction in fasting leptin may be more evident during high-carbohydrate diets, which, as shown in the present study, exaggerate plasma leptin levels. In line with this reasoning, Dirlewanger et al24 found no changes in fasting leptin concentration in response to a 3-day moderate intensity exercise programme performed during the consumption of a ‘normal’ diet. However, the exercise programme used by Dirlewanger et al24 involved a somewhat lower energy expenditure than that followed by our subjects, which may have also contributed to the difference in results.
We observed an overall decrease in circulating leptin at 4 h postprandially. This decrease is not a direct response to feeding but appears to be a continuation of the natural late-night, early-morning decline in plasma leptin levels.6 Interestingly, although the pattern of the postprandial leptin response differed among interventions, leptin concentration at the late postprandial phase, that is, 6 h after the meal, was highly correlated to the postprandial insulin response (Figure 3a). This finding shows the close link between insulin and leptin25 and that exercise does not affect this relation directly. Previous reports showed that physiological increases in plasma insulin result in an increase in plasma leptin levels which is detectable approximately 4 h after the start of insulin administration.15 Similarly, increases in circulating leptin occur 4–6 h after the consumption of a carbohydrate-containing meal.6,26,27,28
The addition of daily moderate intensity exercise to the high-carbohydrate diet suppressed not only fasting but also postprandial circulating leptin. Results from in vitro29 and in vivo30 studies suggest that insulin stimulates leptin secretion by virtue of its ability to increase adipocyte glucose uptake and metabolism. In the postprandial period, adipose tissue plays a minor role in the disposal of ingested carbohydrate and skeletal muscle a major one.31 Previous work has also showed that a prolonged session of moderate intensity exercise performed 12–15 h prior to a meal facilitated enhanced postprandial glucose uptake by skeletal muscle, making this tissue even more important as a site of postprandial glucose disposal.32 Although the exercise regimen we used was not as prolonged as that employed by Malkova et al,32 we speculate that, after the High-CHO-Ex intervention, a greater proportion of the ingested carbohydrate was taken up by skeletal muscle, reducing the exposure of adipose tissue to glucose. This, in turn, may have reduced leptin secretion by adipocytes. The higher insulin sensitivity (ISI(gly)) after this intervention and the negative relation between ISI(gly) and 6-h postprandial leptin (Figure 3b) argues for such a hypothesis. Alternatively, catecholamines appear to suppress plasma leptin concentrations33,34 and so the observed exercise-induced decrease in circulating leptin may have been mediated via the effect of exercise in stimulating catecholamine secretion. However, in adrenaline infusion studies that showed decreases in plasma leptin in women, plasma adrenaline concentrations were similar to that seen during strenuous exercise.34 Thus, it is not known to what extent the exercise of moderate—rather than vigorous—intensity performed by our subjects may have reduced plasma leptin via a catecholamine-related mechanism. Whatever the mechanism is, the decrease in leptin after exercise seems a natural part of the mechanism for upregulating energy intake when expenditure increases, long before fat mass is reduced.
Decreases in circulating leptin concentrations have been related to increased sensations of hunger in dieting women, with this relation being independent of body fat loss or the degree of energy restriction.35 This suggests that low leptin levels have a role in the regulation of appetite in human subjects. Understanding leptin regulation in humans may allow the design of diets and patterns of eating that do not adversely reduce circulating leptin.
In summary, we demonstrated that, in healthy postmenopausal women, a short-term high-carbohydrate, high-sugar diet resulted in higher fasting circulating leptin concentrations than a low-carbohydrate diet. The addition of daily moderate intensity exercise to the high-carbohydrate diet suppressed both fasting and postprandial plasma leptin. We observed a strong positive relation between postprandial insulin response and leptin, confirming previous reports that insulin is an important regulator of leptinaemia. Further research on the effect of diet macronutrient composition and exercise on 24-h circulating leptin concentrations could contribute to understanding the impact of such lifestyle interventions on determinants of body weight regulation.
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This study was funded in part by British Heart Foundation Grant PG/99113. Christina Koutsari was supported by the Greek State Scholarships Foundation. We thank the subjects for their participation, and Jane Riley, Julia Wells and Professor Peter RM Jones for assistance with data collection.
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Koutsari, C., Karpe, F., Humphreys, S. et al. Plasma leptin is influenced by diet composition and exercise. Int J Obes 27, 901–906 (2003). https://doi.org/10.1038/sj.ijo.0802322
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