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      A High Glycemic Meal Suppresses the Postprandial Leptin Response in Normal Healthy Adults

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          Abstract

          Background/Aims: To evaluate the metabolic effects of meals with varying glycemic index (GI). Methods: We measured the glucose, insulin and leptin responses to two contrasting breakfast cereals in a group of 10 young healthy volunteers. Meals were provided on two separate occasions in random order after a 12-hour overnight fast, and consisted of 50 g of available carbohydrate from either Corn Flakes (Kellogg’s), or Fiber One® (General Mills). Blood samples were obtained at rest, and 30, 60, 90 and 120 min after eating. The GI was calculated from the glucose response to the test meal normalized against a 50 g oral glucose load. Results: The GI for Corn Flakes was 125 ± 17 units and 49 ± 8 units for Fiber One®. These meals were classified as high GI and low GI, respectively, and were significantly different from each other (p < 0.0003). The area under the insulin response curve (AUC) following the low glycemic meal was significantly attenuated compared to the high glycemic meal (14,064 ± 2,694 vs. 6,828 ± 1,182 pmol/l·min, p < 0.02). The leptin AUC revealed that circulating leptin was suppressed by the high glycemic meal compared to the low (3.1 ± 1.5 vs. 9.6 ± 3.6 ng/ml·min, p < 0.04). Conclusions: Lower insulin and higher leptin suggests that low glycemic meals promote a postprandial metabolic milieu that is favorable for reduced food consumption; this may be advantageous in the control of obesity and related disorders including insulin resistance and type 2 diabetes.

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          Most cited references17

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          A mutation in the human leptin receptor gene causes obesity and pituitary dysfunction.

          The adipocyte-specific hormone leptin, the product of the obese (ob) gene, regulates adipose-tissue mass through hypothalamic effects on satiety and energy expenditure. Leptin acts through the leptin receptor, a single-transmembrane-domain receptor of the cytokine-receptor family. In rodents, homozygous mutations in genes encoding leptin or the leptin receptor cause early-onset morbid obesity, hyperphagia and reduced energy expenditure. These rodents also show hypercortisolaemia, alterations in glucose homeostasis, dyslipidaemia, and infertility due to hypogonadotropic hypogonadisms. In humans, leptin deficiency due to a mutation in the leptin gene is associated with early-onset obesity. Here we describe a homozygous mutation in the human leptin receptor gene that results in a truncated leptin receptor lacking both the transmembrane and the intracellular domains. In addition to their early-onset morbid obesity, patients homozygous for this mutation have no pubertal development and their secretion of growth hormone and thyrotropin is reduced. These results indicate that leptin is an important physiological regulator of several endocrine functions in humans.
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            Leptin.

            The discovery of the adipose-derived hormone leptin has generated enormous interest in the interaction between peripheral signals and brain targets involved in the regulation of feeding and energy balance. Plasma leptin levels correlate with fat stores and respond to changes in energy balance. It was initially proposed that leptin serves a primary role as an anti-obesity hormone, but this role is commonly thwarted by leptin resistance. Leptin also serves as a mediator of the adaptation to fasting, and this role may be the primary function for which the molecule evolved. There is increasing evidence that leptin has systemic effects apart from those related to energy homeostasis, including regulation of neuroendocrine and immune function and a role in development.
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              Effects of dietary glycaemic index on adiposity, glucose homoeostasis, and plasma lipids in animals.

              Clinical studies suggest a role for dietary glycaemic index (GI) in bodyweight regulation and diabetes risk. However, partly because manipulation of GI can produce changes in potentially confounding dietary factors such as fibre content, palatability, and energy density, its relevance to human health remains controversial. This study examined the independent effects of GI in animals. Partially pancreatectomised male Sprague-Dawley rats were given diets with identical nutrients, except for the type of starch: high-GI (n=11) or low-GI (n=10). The animals were fed in a controlled way to maintain the same mean bodyweight in the two groups for 18 weeks. Further experiments examined the effects of GI in rats in a cross-over design and C57BL/6J mice in a parallel design. Despite having similar mean bodyweight (547.9 [SE 13.4] vs 549.2 [15.2] g), rats given high-GI food had more body fat (97.8 [13.6] vs 57.3 [7.2] g; p=0.0152) and less lean body mass (450.1 [9.6] vs 491.9 [11.7] g; p=0.0120) than those given low-GI food. The high-GI group also had greater increases over time in the areas under the curve for blood glucose and plasma insulin after oral glucose, lower plasma adiponectin concentrations, higher plasma triglyceride concentrations, and severe disruption of islet-cell architecture. Mice on the high-GI diet had almost twice the body fat of those on the low-GI diet after 9 weeks. These findings provide a mechanistic basis for interpretation of studies of GI in human beings. The term GI describes how a food, meal, or diet affects blood sugar during the postprandial period. GI as an independent factor can cause obesity and increase risks of diabetes and heart disease in animals. Use of low-GI diets in prevention and treatment of human disease merits thorough examination.
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                Author and article information

                Journal
                ANM
                Ann Nutr Metab
                10.1159/issn.0250-6807
                Annals of Nutrition and Metabolism
                S. Karger AG
                0250-6807
                1421-9697
                2007
                February 2008
                10 December 2007
                : 51
                : 6
                : 512-518
                Affiliations
                aSchwartz Center for Metabolism and Nutrition; Departments of bMedicine and cNutrition, Case Western Reserve University School of Medicine and MetroHealth Medical Center, Cleveland, Ohio, and dNoll Physiological Research Center, The Pennsylvania State University, University Park, Pa., USA
                Article
                112309 Ann Nutr Metab 2007;51:512–518
                10.1159/000112309
                18073462
                ff16970a-cc9b-4b47-ba66-03929de264c4
                © 2007 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                : 30 April 2007
                : 03 October 2007
                Page count
                Figures: 3, Tables: 1, References: 41, Pages: 7
                Categories
                Original Paper

                Nutrition & Dietetics,Health & Social care,Public health
                Obesity,Insulin resistance,Diet
                Nutrition & Dietetics, Health & Social care, Public health
                Obesity, Insulin resistance, Diet

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