Postprandial Leptin Response to Carbohydrate and Fat Meals in Obese Women

Romon, Monique; Lebel, P.; Fruchart, Jean‐Charles; Dallongeville, Jean

doi:10.1080/07315724.2003.10719300

Cited by 34 publications

(28 citation statements)

References 21 publications

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“…Our data were in line with a number of studies which fail to show significant correlation between leptin and insulin after consumption of HF, mixed and even high-CHO meals (Sinha et al, 1996;Pratley et al, 1997;Guerci et al, 2000;Herrmann et al, 2001;Poretsky et al, 2001). If insulin is a driving force in the control of leptin release (Havel et al, 1999;Romon et al, 1999Romon et al, , 2003Evans et al, 2001;Koutsari et al, 2003;Fogteloo et al, 2004), it is possible that this mechanism is important only when a major portion of the diet comprises CHO.…”

Section: Discussionsupporting

confidence: 73%

“…Interpretation of the postprandial response of leptin is complicated by diurnal changes in hormone release, driven in part by meal time and/or composition (Schoeller et al, 1997;Fogteloo et al, 2004), with a decline postbreakfast followed by a midnight peak (Sinha et al, 1996;Coleman and Herrmann, 1999;Havel et al, 1999). While a high-CHO breakfast may reverse the morning decline (Romon et al, 1999;Evans et al, 2001;Herrmann et al, 2001;Romon et al, 2003) irrespective of meal time (Schoeller et al, 1997), we had no evidence from our trial of a similar effect following fatty meals.…”

Section: Discussioncontrasting

confidence: 49%

“…Our study of lean men showed a decrease in leptin but not ghrelin over 6 h following a HF meal, and an increase in saturation of the fatty meal did not further alter response of either hormone. Since meals rich in SFA reduce postprandial insulin sensitivity (Robertson et al, 2002), and insulin may be an important modulator of leptin (Havel et al, 1999;Evans et al, 2001;Koutsari et al, 2003;Romon et al, 2003;Fogteloo et al, 2004) and ghrelin (Mohlig et al, 2002;Saad et al, 2002;Flanagan et al, 2003), we wanted to determine whether increasing dietary SFA may differentially alter these hormones. Interpretation of the postprandial response of leptin is complicated by diurnal changes in hormone release, driven in part by meal time and/or composition (Schoeller et al, 1997;Fogteloo et al, 2004), with a decline postbreakfast followed by a midnight peak (Sinha et al, 1996;Coleman and Herrmann, 1999;Havel et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

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Effect of high-fat meals and fatty acid saturation on postprandial levels of the hormones ghrelin and leptin in healthy men

et al. 2005

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Objective: Ghrelin and leptin play a role in control of food intake and adiposity but mechanisms regulating these hormones in man are poorly defined and evidence that dietary fats may have adverse effects is inconclusive. We investigated whether high-fat meals, which differed in saturated fatty acid (SFA) content acutely modified these hormones. Design: Randomised, double-blind, crossover trial. A high-fat (HF) test meal (5974 g fat; 71% of energy as fat) was given for breakfast on two occasions. Meals comprised either high (B70:30) or low (B55:45) saturated:unsaturated fatty acid (SFA:USFA) ratio. Fasting and postprandial measurements of serum total ghrelin (RIA), leptin (enzyme-linked immunosorbent assay (ELISA)) and insulin (RIA) were made over 6 h. Postprandial measurements were also made at 10 and 24 h following a fat-exclusion lunch, snack and dinner. Subjects: A total of 18 lean, healthy men. Results: There was no significant effect of the fatty meal (time, P40.05), nor a differential effect of SFA:USFA ratio (treatment * time, P40.05) on ghrelin over 6 h. Leptin decreased in response to both HF treatments (time, Po0.001) but increased SFA content did not further inhibit hormone secretion (treatment * time, P40.05). There was no significant correlation between ghrelin or leptin and circulating insulin (P40.05). Conclusion:We conclude that HF diets may adversely effect serum leptin, although the circadian decrease may account in part for this response. Increasing dietary SFAs had no deleterious effects on leptin or total ghrelin.

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Section: Discussionsupporting

confidence: 73%

Section: Discussioncontrasting

confidence: 49%

Section: Discussionmentioning

confidence: 99%

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Effect of high-fat meals and fatty acid saturation on postprandial levels of the hormones ghrelin and leptin in healthy men

et al. 2005

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“…There are apparently no such studies comparing meal-related endocrine patterns in rats of different body weight. However, there is some evidence in humans (21,24), albeit not consistently demonstrated (14,43,51), that levels of insulin and lipids after a fat-rich meal compared with premeal baseline show a greater increase in the obese than in the lean subjects.…”

Section: Discussionmentioning

confidence: 99%

Leptin secretion after a high-fat meal in normal-weight rats: strong predictor of long-term body fat accrual on a high-fat diet

Leibowitz¹,

Chang²,

Dourmashkin³

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

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. Leptin secretion after a high-fat meal in normal-weight rats: strong predictor of long-term body fat accrual on a high-fat diet. Am J Physiol Endocrinol Metab 290: E258 -E267, 2006; doi:10.1152/ajpendo.00609.2004.-The objective of this study was to investigate meal-related endocrine changes that permit one to identify Sprague-Dawley rats at normal weight that are prone (OP) vs. resistant (OR) to obesity. In blood collected via chronic cardiac catheters, a 2-h high-fat meal (HFM, 50% fat, 40 kcal) at dark onset caused a significant increase in leptin, insulin, and triglycerides compared with premeal levels. Similar to patterns in already obese compared with lean rats on a high-fat diet, these meal-induced endocrine changes in normalweight rats on lab chow were almost twofold larger in OP rats that, compared with OR rats, subsequently accumulated 100% more fat mass on a chronic high-fat diet. These exaggerated endocrine changes were similarly observed in blood collected using a simpler tail vein puncture procedure. In three separate experiments, the HFM-induced rise in leptin was found to be the strongest, positive correlate (r ϭ ϩ0.58, ϩ0.62 and ϩ0.64) of long-term body fat accrual. The lowest (2-5 ng/ml) vs. highest (6 -9 ng/ml) scores for this post-HFM leptin measurement identified distinct OR and OP subgroups, respectively, when they were similar in body weight (340 -350 g), premeal leptin (2.6 -3.4 ng/ml), and meal size (40 kcal). Subsequent tests in these normal-weight OP rats revealed a distinct characteristic compared with OR rats, namely, exaggerated HFM-induced rise in expression of the orexigenic peptide galanin in the paraventricular nucleus. Thus, with this HFM-induced leptin measurement, OP rats can be identified while still at normal weight and then investigated for mechanisms that contribute to their excessive body fat accrual on a high-fat diet.insulin; triglycerides; galanin; neuropeptide Y OBESITY IS A COMPLEX DISORDER with multiple etiologies. To identify factors that cause or contribute to the development of obesity, it is essential to establish markers of susceptibility in individual subjects before the onset of this disorder. By identifying "obesity-resistant" (OR) and "obesity-prone" (OP) animals at normal body weight, studies can then be performed to characterize disturbances that precede and possibly promote the obesity. Investigations in inbred mouse or rat strains with differential propensities toward obesity have been informative (4,55,69). However, detailed studies of these populations at young ages, before they become different in their body weight, are still lacking. Reports in rats that have been selectively bred on the basis of their differential weight gain on a high-calorie diet (31, 34) hold particular promise in revealing the phenotype of OP rats at normal weight. These selectively bred animals deserve far more attention than they have received to date.

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“…Conversely, obesity is associated with high leptin concentrations and resistance to the catabolic effect of leptin to suppress appetite and heighten energy expenditure [103,106]. Although plasma leptin can be acutely increased by physiological insulinemia [107] there is no universal agreement in the literature as to whether leptin levels rise [107,108], remain unchanged [109,110], or fall [111] in the immediate postprandial phase in non-cirrhotic individuals.…”

Section: Leptinmentioning

confidence: 97%

Intestinal permeability in cirrhotic patients with and without ascites

Kalaitzakis

Johansson

Bjarnason³

et al. 2006

Scandinavian Journal of Gastroenterology

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Malnutrition is a common finding in patients with liver cirrhosis. Malnutrition has been shown to be associated with increased morbidity and mortality. Its pathogenesis remains unclear but both poor dietary intake and increased energy expenditure have been reported.Spontaneous bacterial peritonitis is an important clinical problem in cirrhotics. It may occur as a consequence of repeated access of bacteria from the intestinal lumen (translocation) to the mesenteric lymph nodes. One of the mechanisms proposed to explain bacterial translocation in cirrhosis includes increased intestinal permeability.The aims of the present study were to evaluate GI symptoms in cirrhotic patients and their possible relation to nutritional status, to assess whether gastric sensorimotor dysfunction or metabolic disturbances are associated with reduced food intake, and to investigate the role of ascites in intestinal permeability in patients with liver cirrhosis.Gastrointestinal symptoms and health-related quality of life (HRQOL) were assessed with the aid of two questionnaires. Gastric sensorimotor function was measured by means of an electronic barostat. Food intake, as assessed with a food diary, was related to fasting and postprandial glucose, insulin, leptin, and ghrelin concentrations. Intestinal permeability was evaluated by a 51 Cr-EDTA permeability test. Cirrhotics were found to have increased severity of GI symptoms compared with reference values from the general population. A relationship between GI symptoms and compromised HRQOL as well as weight loss was observed.Proximal stomach relaxation to a meal was increased in patients with liver cirrhosis as compared with healthy controls but the relation between gastric accommodation and energy intake was found to be disturbed in these patients. Gastric sensitivity to distension was shown to be related to GI symptom severity and to liver cirrhosis severity scores.Patients with liver cirrhosis exhibited higher postprandial insulin and glucose concentrations compared to controls. Cirrhotics had higher fasting leptin that fell significantly postmeal and they showed an attenuated increase of ghrelin before the next expected meal. Altered glucose and hormonal levels in patients with cirrhosis were associated with poor food intake.Only a few patients with cirrhosis had increased intestinal permeability, as assessed by a 51 Cr-EDTA test, which was not influenced to a major extent by ascites. Conclusions: In patients with liver cirrhosis GI symptom severity is high and it is associated with impaired HRQOL and weight loss. Gastric accommodation is not involved in the poor food intake observed in cirrhotics and gastric sensitivity seems to be a relevant factor for GI symptom generation in these patients. Altered postprandial glucose, leptin, and ghrelin levels are correlated to reduced energy intake in this patient group. Increased intestinal permeability is probably of limited importance in the pathophysiology of bacterial infections in patients with liver cirrhosis and ascites.

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Postprandial Leptin Response to Carbohydrate and Fat Meals in Obese Women

Abstract: These results indicate that postprandial leptin response is lower after a carbohydrate meal in obese women than in lean controls, suggesting an impairment of postprandial leptin regulation in obese women.

Cited by 34 publications

References 21 publications

Effect of high-fat meals and fatty acid saturation on postprandial levels of the hormones ghrelin and leptin in healthy men

Effect of high-fat meals and fatty acid saturation on postprandial levels of the hormones ghrelin and leptin in healthy men

Leptin secretion after a high-fat meal in normal-weight rats: strong predictor of long-term body fat accrual on a high-fat diet

Intestinal permeability in cirrhotic patients with and without ascites

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