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Plasma leptin is influenced by diet composition and exercise

Abstract

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.

Introduction

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.

Methods

Subjects

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.

Design

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.

Analytical methods

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.

Results

Leptin

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.

Figure 1
figure1

Plasma leptin concentrations in the fasted state (0 h) and for 6 h following consumption of a high-fat mixed meal after 3 days on a low-carbohydrate diet (Low-CHO), after 3 days on a high-carbohydrate diet (High-CHO) and after 3 days on the same high-carbohydrate diet with 60 min daily of moderate intensity exercise (High-CHO-Ex). Mean±s.e.m. for eight women. Results from statistical analyses based on repeated measures ANOVA are given in the text.

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.

Figure 2
figure2

Serum insulin concentrations in the fasted state (0 h) and for 6 h following consumption of a high-fat, mixed meal after 3 days on a low-carbohydrate diet (Low-CHO), after 3 days on a high-carbohydrate diet (High-CHO) and after 3 days on the same high-carbohydrate diet with 60 min daily of moderate intensity exercise (High-CHO-Ex). Mean±s.e.m. for eight women. Results from statistical analyses based on total AUCs are given in the text.

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.

Figure 3
figure3

(a) Relation between insulin response to the test meal (expressed as 6-h AUC) and plasma leptin concentrations at 6 h following consumption of a high-fat, mixed meal after 3 days on a low-carbohydrate diet (Low-CHO, r=0.84, P=0.009), after 3 days on a high-carbohydrate diet (High-CHO, r=0.77, P=0.02) and after 3 days on the same high-carbohydrate diet with 60 min daily of moderate intensity exercise (High-CHO-Ex, r=0.89, P=0.003). (b) Relation between whole-body insulin sensitivity (ISI(gly)) (calculated from postprandial insulin and glucose responses17) and plasma leptin concentrations at 6 h following consumption of a high-fat, mixed meal after 3 days on a low-carbohydrate diet (Low-CHO, r=−0.80, P=0.01), after 3 days on a high-carbohydrate diet (High-CHO, r=−0.75, P=0.03) and after 3 days on the same high-carbohydrate diet with 60 min daily of moderate intensity exercise (High-CHO-Ex, r=−0.78, P=0.02).

Discussion

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.

References

  1. 1

    Friedman JM, Halaas JL . Leptin and the regulation of body weight in mammals. Nature 1998; 395: 763–770.

    CAS  Article  Google Scholar 

  2. 2

    Havel PJ . Control of energy homeostasis and insulin action by adipocyte hormones: leptin, acylation stimulating protein, and adiponectin. Curr Opin Lipidol 2002; 13: 51–59.

    CAS  Article  Google Scholar 

  3. 3

    Romon M, Lebel P, Velly C, Marecaux N, Fruchart JC, Dallongeville J . Leptin response to carbohydrate or fat meal and association with subsequent satiety and energy intake. Am J Physiol 1999; 277: E855–E861.

    CAS  Google Scholar 

  4. 4

    Considine RV, Sinha MK, Heiman ML, Kriauciunas A, Stephens TW, Nyce MR, Ohannesian JP, Marco CC, McKee LJ, Bauer TL, Caro JF . Serum immunoreactive-leptin concentrations in normal-weight and obese humans. N Engl J Med 1996; 334: 292–295.

    CAS  Article  Google Scholar 

  5. 5

    Weigle DS, Duell PB, Connor WE, Steiner RA, Soules MR, Kuijper JL . Effect of fasting, refeeding, and dietary fat restriction on plasma leptin levels. J Clin Endocrinol Metab 1997; 82: 561–565.

    CAS  Google Scholar 

  6. 6

    Havel PJ, Townsend R, Chaump L, Teff K . High-fat meals reduce 24-h circulating leptin concentrations in women. Diabetes 1999; 48: 334–341.

    CAS  Article  Google Scholar 

  7. 7

    Lissner L, Levitsky DA, Strupp BJ, Kalkwarf HJ, Roe DA . Dietary fat and the regulation of energy intake in human subjects. Am J Clin Nutr 1987; 46: 886–892.

    CAS  Article  Google Scholar 

  8. 8

    Schaefer EJ, Lichtenstein AH, Lamon-Fava S, McNamara JR, Schaefer MM, Rasmussen H, Ordovas JM . Body weight and low-density lipoprotein cholesterol changes after consumption of a low-fat ad libitum diet. JAMA 1995; 274: 1450–1455.

    CAS  Article  Google Scholar 

  9. 9

    Kasim-Karakas SE, Almario RU, Mueller WM, Peerson J . Changes in plasma lipoproteins during low-fat, high-carbohydrate diets: effects of energy intake. Am J Clin Nutr 2000; 71: 1439–1447.

    CAS  Article  Google Scholar 

  10. 10

    Hickey MS, Israel RG . Exercise and adipose tissue production of cytokines. In: Nicklas B (ed.). Endurance exercise and adipose tissue. CRC Press LLC: Boca Raton, FL; 2002. pp 79–100.

    Google Scholar 

  11. 11

    Hickey MS, Houmard JA, Considine RV, Tyndall GL, Midgette JB, Gavigan KE, Weidner ML, McCammon MR, Israel RG, Caro JF . Gender-dependent effects of exercise training on serum leptin levels in humans. Am J Physiol 1997; 272: E562–E566.

    CAS  Google Scholar 

  12. 12

    van Aggel-Leijssen DPC, van Baak MA, Tenenbaum R, Campfield LA, Saris WHM . Regulation of average 24 h human plasma leptin level; the influence of exercise and physiological changes in energy balance. Int J Obes Relat Metab Disord 1999; 23: 151–158.

    CAS  Article  Google Scholar 

  13. 13

    NHLBI. Clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults. NIH Publication no. 98-4083; 1998. pp 1–262.

  14. 14

    Krauss RM, Eckel RH, Howard BV, Appel LJ, Daniels SR, Deckelbaum RJ, Erdman JW, Kris-Etherton P, Goldberg IJ, Kotchen T, Lichtenstein AH, Mitch WE, Mullis R, Robinson K, Wylie-Rosett J, Jeor SS, Suttie J, Tribble DL, Bazzarre TL . AHA dietary guidelines. Revision 2000: a statement for healthcare professionals from the nutrition committee of the American Heart Association. Circulation 2000; 102: 2284–2299.

    CAS  Article  Google Scholar 

  15. 15

    Saad MF, Khan A, Sharma A, Michael R, Riad-Gabriel MG, Boyadjian R, Jinagouda SD, Steil GM, Kamdar V . Physiological insulinemia acutely modulates plasma leptin. Diabetes 1998; 47: 544–549.

    CAS  Article  Google Scholar 

  16. 16

    Koutsari C, Karpe F, Humphreys SM, Frayn KN, Hardman AE . Exercise prevents the accumulation of triglyceride-rich lipoproteins and their remnants seen when changing to a high-carbohydrate diet. Arterioscl Thromb Vasc Biol 2001; 21: 1520–1525.

    CAS  Article  Google Scholar 

  17. 17

    Belfiore F, Iannello S, Camuto M, Fagone S, Cavaleri A . Insulin sensitivity of blood glucose versus insulin sensitivity of blood free fatty acids in normal, obese, and obese-diabetic subjects. Metabolism 2001; 50: 573–582.

    CAS  Article  Google Scholar 

  18. 18

    Havel PJ, Kasim-Karakas SE, Mueller W, Johnson PR, Ginsberg RL, Stern JS . Relationship of plasma leptin to plasma insulin and adiposity in normal weight women: effects of dietary fat content and sustained weight loss. J Clin Endocrinol Metab 1996; 81: 4406–4413.

    CAS  Google Scholar 

  19. 19

    Schrauwen P, van Marken WD, Westerterp KR, Saris WHM . Effect of diet composition on leptin concentration in lean subjects. Metabolism 1997; 46: 420–424.

    CAS  Article  Google Scholar 

  20. 20

    Raben A, Astrup A . Leptin is influenced both by predisposition to obesity and diet composition. Int J Obes Relat Metab Disord 2000; 24: 450–459.

    CAS  Article  Google Scholar 

  21. 21

    Kohrt WM, Landt M, Birge SJ . Serum leptin levels are reduced in response to exercise training, but not hormone replacement therapy, in older women. J Clin Endocrinol Metab 1996; 81: 3980–3985.

    CAS  Google Scholar 

  22. 22

    Perusse L, Collier G, Gagnon J, Leon AS, Rao DC, Skinner JS, Wilmore JH, Nadeau A, Zimmet PZ, Bouchard C . Acute and chronic effects of exercise on leptin levels in humans. J Appl Physiol 1997; 83: 5–10.

    CAS  Article  Google Scholar 

  23. 23

    Kraemer RR, Kraemer GR, Acevedo EO, Hebert EP, Temple E, Bates M, Etie A, Haltom R, Quinn S, Castracane VD . Effects of aerobic exercise on serum leptin levels in obese women. Eur J Appl Physiol 1999; 80: 154–158.

    CAS  Article  Google Scholar 

  24. 24

    Dirlewanger M, Di Vetta V, Giusti V, Schneiter P, Jequier E, Tappy L . Effect of moderate physical activity on plasma leptin concentration in humans. Eur J Appl Physiol 1999; 79: 331–335.

    CAS  Article  Google Scholar 

  25. 25

    Kieffer T, Habener J . The adipoinsular axis: effects of leptin on pancreatic β-cell. Am J Physiol 2000; 278: E1–E14.

    CAS  Article  Google Scholar 

  26. 26

    Coppack SW, Pinkney JH, Mohamed-Ali V . Leptin production in human adipose tissue. Proc Nutr Soc 1998; 57: 461–470.

    CAS  Article  Google Scholar 

  27. 27

    Evans K, Clark ML, Frayn KN . Carbohydrate and fat have different effects on plasma leptin concentrations and adipose tissue leptin production. Clin Sci 2001; 100: 493–498.

    CAS  Article  Google Scholar 

  28. 28

    Imbeault P, Doucet E, Mauriege P, St-Pierre S, Couillard C, Almeras N, Despres J-P, Tremblay A . Difference in leptin response to a high-fat meal between lean and obese men. Clin Sci 2001; 101: 359–365.

    CAS  Article  Google Scholar 

  29. 29

    Mueller WM, Gregoire FM, Stanhope KL, Mobbs CV, Mizuno TM, Warden CH, Stern JS, Havel PJ . Evidence that glucose metabolism regulates leptin secretion from cultured adipocytes. Endocrinology 1998; 139: 551–558.

    CAS  Article  Google Scholar 

  30. 30

    Wellhoener P, Fruehwald-Schultes B, Kern W, Dantz D, Kerner W, Born J, Fehm HL, Peters A . Glucose metabolism rather than insulin is a main determinant of leptin secretion in humans. J Clin Endocrinol Metab 2000; 85: 1267–1271.

    CAS  Article  Google Scholar 

  31. 31

    Coppack SW, Fisher RM, Gibbons GF, Humpreys SM, McDonough MJ, Potts JL, Frayn KN . Postprandial substrate disposition in human forearm and adipose tissues in vivo. Clin Sci 1990; 79: 339–348.

    CAS  Article  Google Scholar 

  32. 32

    Malkova D, Evans RD, Frayn KN, Humphreys SM, Jones PRM, Hardman AE . Prior exercise and postprandial substrate extraction across the human leg. Am J Physiol 2000; 279: E1020–E1028.

    CAS  Google Scholar 

  33. 33

    Trayhurn P, Duncan JS, Hoggard N, Rayner DV . Regulation of leptin production: a dominant role for the sympathetic nervous system? Proc Nutr Soc 1998; 57: 413–419.

    CAS  Article  Google Scholar 

  34. 34

    Couillard C, Mauriege P, Prud'homme D, Nadeau A, Tremblay A, Bouchard C, Despres J-P . Plasma leptin response to an epinephrine infusion in lean and obese women. Obes Res 2002; 10: 6–13.

    CAS  Article  Google Scholar 

  35. 35

    Keim NL, Stern JS, Havel PJ . Relation between circulating leptin concentrations and appetite during a prolonged, moderate energy deficit in women. Am J Clin Nutr 1998; 68: 794–801.

    CAS  Article  Google Scholar 

Download references

Acknowledgements

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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Keywords

  • leptin
  • insulin
  • diet
  • carbohydrate
  • exercise
  • women

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