Showing papers by "Claude Bouchard published in 2008"

The Association Between Sleep Duration and Weight Gain in Adults: A 6-Year Prospective Study from the Quebec Family Study

Abstract: OBESITY IS ONE OF THE MOST IMPORTANT PUBLIC HEALTH PROBLEMS TODAY, AND, ALTHOUGH MUCH HAS BEEN LEARNED REGARDING THE REGULATION of body weight, the prevalence of obesity continues to rise. Individual and environmental factors that have an influence on energy balance are not fully understood. Current treatments for obesity have been largely unsuccessful in maintaining long-term weight loss, suggesting the need for new insight into the mechanisms that result in altered metabolism and behavior and may lead to obesity. Parallel to an increase in body weight, one has also observed a reduction in sleep times. Indeed, over the past 40 years, daily sleep duration in the United States population has decreased by 1.5 to 2 hours, and the proportion of young adults sleeping less than 7 hours per night has more than doubled between 1960 and 2001–2002 (from 15.6% to 37.1%).1–4 Thus, lack of sleep has become a widespread habit driven by the demands and opportunities of our modern “24-hour” lifestyle. Nearly one third of adults report sleeping less than 6 hours per night, leading some to suggest that we live in a sleep-deprived society.5 Not surprisingly, reports of fatigue and tiredness are more frequent today than a few decades ago.6 Cross-sectional studies in adults have repeatedly found an association between reduced sleep and increased weight.7–9 Similar findings have been observed in cross-sectional studies of children, suggesting that short sleep duration correlates with an increased risk of being overweight or obese.10–12 The most plausible explanation to date of the sleep duration–body weight relationship is an alteration of the neuroendocrine control of appetite characterized by a decrease in the levels of the anorexigenic hormone leptin and an increase in the levels of the orexigenic factor ghrelin.7,9,13 Thus, these neuroendocrine changes have the potential to favor a positive caloric balance and weight gain over time.13 However, these studies cannot differentiate cause from effect. It may, therefore, be argued that the association between short sleep duration with higher body weight is bidirectional and results from other factors that impact on body weight regulation. To our knowledge, only 3 studies have examined associations between sleep duration and obesity in a longitudinal design in adults. The first study from Hasler et al (2004) reported a relationship between sleep time and future weight.14 However, the generalizability of the results is uncertain, as the study was based on subjects with a high risk of psychiatric disorders. The second study from Gangwisch et al (2005) showed that sleep duration is associated with obesity in a large longitudinally monitored United States sample.8 However, the study lacked repeated measures of sleep duration and used self-reported weights. Finally, the third study from Patel et al (2006) found that short sleep duration predicted higher weight gain independent of baseline weight.15 However, sleep duration was assessed at only 1 time point, body weight was assessed from a questionnaire, and the study was limited to middle-aged women in the nursing profession. The present study examines longitudinal associations between sleep duration and adiposity indices in the Quebec Family Study. We hypothesize that short sleep duration predisposes to increased body weight and fat gain due to a combination of increased caloric intake and reduced physical activity.

FTO: the first gene contributing to common forms of human obesity.

Abstract: Genome-wide association, the latest gene-finding strategy, has led to the first major success in the field of obesity genetics with the discovery of FTO (fat mass and obesity associated gene) as an obesity-susceptibility gene. A cluster of variants in the first intron of FTO showed a strong and highly significant association with obesity-related traits in three independent genome-wide association studies, a finding that has been replicated in several other studies including adults and children of European descent. Homozygotes for the risk allele weigh on average 3-4 kg more and have a 1.67-fold increased risk of obesity compared with those who did not inherit a risk allele. We are still at an early stage in our understanding of the pathways through which FTO confers to increased obesity risk. Studies in humans and rodents have suggested a central role for FTO through regulation of food intake, whereas others have proposed a peripheral role through an effect on lipolytic activity in adipose tissue. There is no doubt that many more obesity-susceptibility loci remain to be discovered. Progress on this front will therefore require major collaborative efforts and pooling of compatible datasets. We stand to learn a lot about the genetic architecture of human obesity in the coming years. The expectations are high but many challenges remain. Among the latter, translating new advances into useful guidelines for prevention and treatment of obesity will be the most demanding.

Genetic variants of FTO influence adiposity, insulin sensitivity, leptin levels, and resting metabolic rate in the Quebec Family Study.

Abstract: Objective: A genome-wide association study conducted by the Welcome Trust Case Control Consortium recently associated SNPs in the FTO (fatso/fat mass and obesity associated) gene with type 2 diabetes. These associations were shown to be mediated by obesity. Other research groups found similar results in Europeans and Hispanics, but not African Americans. The mechanism by which FTO influences obesity and type 2 diabetes is currently unknown. The present study investigated the role of two FTO SNPs (rs17817449 and rs1421085) in obesity, insulin sensitivity and body-weight regulation, including energy intake and expenditure. Research Design and Methods: We genotyped 908 individuals from the Quebec City metropolitan area that participated in the Quebec Family Study (QFS), a long-term study of extensively phenotyped individuals that was designed to investigate factors involved in adiposity. Results: We found significant associations for both SNPs with several obesity-related phenotypes. In particular, rs17817449 was associated with BMI (p=0.0014), weight (p=0.0059) and waist circumference (p=0.0021) under an additive model. In addition, this FTO SNP influenced fasting insulin (p=0.011), HOMA-IR (p=0.038) and an insulin sensitivity index derived from an oral glucose tolerance test (p=0.0091). Associations were also found with resting metabolic rate (p=0.042) and plasma leptin levels (p=0.036). Adjustment for BMI abolished the associations with insulin sensitivity, resting metabolic rate and plasma leptin levels. Conclusion: These results confirm that genetic variation at the FTO locus contributes to the etiology of obesity, and thus to insulin resistance and increased plasma leptin levels.

Gene-environment interactions in the etiology of obesity: defining the fundamentals.

Abstract: The concept of gene-environment interaction refers to a situation where the response or the adaptation to an environmental factor, a behavior, or a change in behavior is conditional on the genotype of the individual. Of particular interest for our understanding of the etiology of human obesity is the role played by genotype-nutrition and genotype-physical activity interactions. Evidence for the presence of such interaction effects affecting body mass and body composition comes from experimental studies undertaken with pairs of monozygotic twins and with nuclear families. These studies reveal that there are large individual differences in the responsiveness to well-defined energy balance manipulations. Overfeeding as well as negative energy balance protocols indicate that the response to these standardized experimental treatments is strongly influenced by one's genetic background. The genes that are responsible for the individual differences in the sensitivity to alterations in energy balance remain to be fully identified. They are likely to be numerous considering the complexity of the biological systems that are involved in body weight regulation. A number of research designs and technologies are available to identify these genes and to delineate the nature and the extent of the genetic polymorphisms involved. It was the purpose of the workshop to define the conditions under which gene-behavior interaction effects of relevance to human obesity could be reliably identified.

Genes, exercise, growth, and the sedentary, obese child

Abstract: It is still not possible to provide an evidence-based answer to the question of whether regular exercise is essential for normal growth. It is also unclear whether very low levels of exercise resul...

Gene–Physical Activity Interactions: Overview of Human Studies

Abstract: Physical activity level is an important component of the total daily energy expenditure and as such contributes to body weight regulation. A body of data indicates that the level of physical activity plays a role in the risk of excessive weight gain, in weight loss programs, and particularly in the prevention of weight regain. Most studies dealing with potential gene-physical activity interaction effects use an exercise and fitness or performance paradigm as opposed to an obesity-driven model. From these studies, it is clear that there are considerable individual differences in the response to an exercise regimen and that there is a substantial familial aggregation component to the observed heterogeneity. Few studies have focused on the role of specific genes in accounting for the highly prevalent gene-exercise interaction effects. Results for specific genes have been inconsistent with few exceptions. Progress is likely to come when studies will be designed to truly address gene-exercise or physical activity interaction issues and with sample sizes that will provide adequate statistical power.

Multivitamin and dietary supplements, body weight and appetite: Results from a cross-sectional and a randomised double-blind placebo-controlled study

Abstract: Two studies were conducted to compare characteristics of consumers and non-consumers of vitamin and/or dietary supplements (study 1) and to assess the effect of a multivitamin and mineral supplementation during a weight-reducing programme (study 2). Body weight and composition, energy expenditure, and Three-Factor Eating Questionnaire scores were compared between consumers and non-consumers of micronutrients and/or dietary supplements in the Quebec Family Study (study 1). In study 2, these variables and appetite ratings (visual analogue scales) were measured in forty-five obese non-consumers of supplements randomly assigned to a double-blind 15-week energy restriction ( - 2930 kJ/d) combined with a placebo or with a multivitamin and mineral supplement. Compared with non-consumers, male consumers of vitamin and/or dietary supplements had a lower body weight (P < 0.01), fat mass (P < 0.05), BMI (P < 0.05), and a tendency for greater resting energy expenditure (P = 0.06). In women, the same differences were observed but not to a statistically significant extent. In addition, female supplements consumers had lower disinhibition and hunger scores (P < 0.05). In study 2, body weight was significantly decreased after the weight-loss intervention (P < 0.001) with no difference between treatment groups. However, fasting and postprandial appetite ratings were significantly reduced in multivitamin and mineral-supplemented women (P < 0.05). Usual vitamin and/or dietary supplements consumption and multivitamin and mineral supplementation during a weight-reducing programme seems to have an appetite-related effect in women. However, lower body weight and fat were more detectable in male than in female vitamin and/or dietary supplements consumers.

The magnitude of the energy imbalance in obesity is generally underestimated

Abstract: As the efforts to defeat the obesity epidemic amplify around the world, it is important to understand the true magnitude of the energy imbalance associated with excess weight. The energy imbalance in a weight gain situation is the difference between the number of calories ingested and the total caloric expenditure on the same day. In this regard, it would be useful to quantify the size of the energy imbalance in a number of states such as in early and late weight gain. However, there is another dimension to the topic that has begun to receive some attention, and it is an issue of the utmost importance. It has to do with the so-called ‘energy gap.’ The energy gap is defined as the difference in the amount of calories consumed or expended between normal weight individuals and persons at various levels of excess weight but when weight stability is present.

Glucose homeostasis predicts weight gain: prospective and clinical evidence.

Abstract: Background The potential long-term impact of low glycaemia on body fat accumulation has not been verified Therefore, we examined the effects of low glucose concentrations on long-term energy balance and weight gain in humans Methods Two sets of analyses were realized in order to verify this objective First, Study 1 consisted of 259 participants between 20 and 65 years of age selected from Phase 2 of the Quebec Family Study (QFS) The association between glucose concentrations at the end of an oral glucose tolerance test (OGTT) and changes in body mass was analysed prospectively (mean follow-up of 6 years) In addition, Study 2 consisted of 44 obese participants (20 men and 24 women) randomly assigned to a 15-week weight loss program in either a drug therapy group (fenfluramine) or a placebo group coupled with energy intake restriction The focus of this study was the relationship between glycaemic control at the end of the treatment and post-treatment weight regain Results In Study 1, the glucose concentrations at 120 min of the OGTT were negatively correlated with weight gain over 6 years (r = − 042, p < 001) In Study 2, the weight loss program induced a mean reduction in body weight of 10 kg in the fenfluramine and placebo groups In participants who returned for a follow-up visit (mean = 81 weeks after the intervention), the glucose area below fasting values (GABF) at the end of the OGTT increased with weight loss (p < 001) and was correlated with weight regain (r = 074, p < 001) Conclusions Lower glucose concentrations at the end of an OGTT are correlated with weight gain over time Large amounts of weight loss are associated with low glycaemia at the end of an OGTT These low glucose concentrations are strong predictors of the amount of weight regained after weight loss Copyright © 2007 John Wiley & Sons, Ltd

A major haplotype block at the rho-associated kinase 2 locus is associated with a lower risk of hypertension in a recessive manner: the HYPGENE study.

Abstract: A Major Haplotype Block at the Rho-Associated Kinase 2 Locus Is Associated with a Lower Risk of Hypertension in a Recessive Manner: The HYPGENE Study

Associations between glucose tolerance, insulin sensitivity and insulin secretion phenotypes and polymorphisms in adiponectin and adiponectin receptor genes in the Quebec Family Study

Abstract: Aims Studies suggest that adiponectin (APM1) and its receptors 1 and 2 (AdipoR1 and AdipoR2) play an important role in the development of insulin resistance (IR). Our objective was to examine associations between APM1 (+45T>G, +276G>T and –3971A>G), AdipoR1 (−100G>T and −3882T>C) and AdipoR2 (−35361A>G and –1352G>A) genes single-nucleotide polymorphisms (SNPs) and adiponectin plasma levels, indicators of glucose tolerance, insulin sensitivity (IS) and insulin secretion. Methods Six hundred and twenty-two non-diabetic subjects from the Quebec Family Study (QFS) underwent a 75-g oral glucose tolerance test (OGTT), with measurement of fasting adiponectin, glucose, insulin and C-peptide levels. Indices of glucose tolerance, IS and insulin secretion were derived from fasting and OGTT measurements. Results Significant evidence of association was found between indices of IS and APM1 and AdipoR1 SNPs. The APM1 –3971G/G homozygotes exhibited a reduced area under the curve of insulin during the OGTT (P = 0.007) and higher Cederholm index (P = 0.01) compared to the A/A homozygotes. The APM1+45T>G variant was also associated with fasting (P = 0.002) and 2-h (P = 0.007) glucose values as well as with higher Cederholm index (P = 0.04) and disposition index (P = 0.02). Finally, the AdipoR1−3882T>C SNP was associated with fasting glucose (P = 0.03), the homeostasis model assessment for insulin resistance (P = 0.04) and an index of insulin secretion (P30/G30, P = 0.02). No evidence of association was found with plasma adiponectin levels. Conclusions These results provide evidence for an influence of common SNPs in the APM1 and AdipoR1 genes on different phenotypes of glucose and insulin metabolism associated with increased risk of type 2 diabetes.

Gene-Nutrition and Gene-Physical Activity Interactions in the Etiology of Obesity

Abstract: THE OBESITY EPIDEMIC Obesity is a chronic disease that leads to personal suffering for affected individuals and major costs to public health systems and societies. In the United States alone, 66% of adults meet the definition of overweight (BMI ≥25 kg/m) or obesity (BMI ≥30 kg/m). Almost one-third of US adults are frankly obese. Even more alarming is the fact that the prevalence of overweight and obese children and adolescents is now about 17%. Large disparities have been observed among specific racial/ethnic groups (1). By one estimate, obesity is currently responsible for the death of about 100,000 persons per year in the United States (2). Around the world, more than one billion people have a body weight high enough to have health implications. In countries where it is possible to quantify the costs of obesity, they have been reported to range from 2% to 7% of total health care costs (3). A recent World Cancer Research Fund report, Food, Nutrition, Physical Activity, and the Prevention of Cancer: A Global Perspective, identified body fatness as a risk factor for cancers of the esophagus, pancreas, colorectum, breast (postmenopausal), endometrium, and kidney (4).

How much progress have we made over the last few decades

Abstract: To recognize the 20th anniversary of the opening of the Pennington Biomedical Research Center in Baton Rouge, Louisiana, USA, a conference was held featuring some of the most prominent obesity researchers worldwide, addressing the most significant advances in obesity research. The Center had been founded with a gift from wealthy oilman Claude B Pennington with the mission of ‘promoting healthier lives through research and education in nutrition and preventive medicine.’ The purpose of the conference was to provide a cohesive presentation of the key events and steps that led to the major discoveries or advances in obesity science and give insight into new research directions. Only 20 of many possible topics could be adequately covered in the program of the conference. Their increasing importance is reflected in the increasing number of related publications as extracted from PubMed. The broad general areas in which these topics fall include measurement and evaluation of obesity, measurement of body composition and fat distribution, adipose tissue biology, genetics, bariatric surgery and public policy. Advances in the areas covered at the conference have had a major impact on our understanding of adipogenesis, central and peripheral regulation of body weight, health consequences of excess body weight, challenges of weight loss, magnitude of the worldwide epidemic and impact of public health policies.

Mid-Thigh Subcutaneous Adipose Tissue and Glucose Tolerance in the Quebec Family Study

Abstract: Objective: To clarify the relationship between the amount of mid-thigh subcutaneous adipose tissue (SCAT) and glucose tolerance in men and women. Methods: Midthig

Studying gene-behavior interactions: summary of recommendations.

Abstract: The workshop was designed to review the evidence on the role of gene–nutrition and gene–physical activity interaction effects in the etiology of obesity and the growing prevalence of obesity. One important goal was to produce a set of recommendations that would be helpful to the research community and to the sponsors of the meeting. As evidenced by the papers in this publication, all contributors to the workshop made recommendations concerning future research, and these were discussed extensively during the meeting. Our goal herein is not to generate an exhaustive list of all suggestions made by the speakers at the workshop, but rather to focus on the key recommendations that can have a significant impact on the research agenda of the field. We are grouping them under five headings. However, one overarching issue needs to be raised first. The concept of gene–behavior interaction is one that is not always fully understood and appreciated. As was defined in the first paper of this supplement (1), one has to distinguish between the main effect of a gene from its potential contributions through interaction paths with behavioral or environmental factors or, perhaps more precisely, behavioral or environmental perturbations. The distinction is not always fully appreciated. For instance, some of the papers in this supplement deal with gene–behavior interaction effects only marginally. We will purposefully focus here only on recommendations that are relevant to the gene–behavior interaction research agenda. Most of the genetic studies reported to date for human obesity and related traits have reported on the main effects of genes. The genetic architecture of obesity is obviously more complex than suggested by the majority of studies published to date (2). For example, the FTO gene has been shown in a good number of studies with large sample sizes to have a significant effect on body mass index (BMI) (Loos and Bouchard, submitted). Homozygotes for the risk allele are on average about 3–4 kg heavier than homozygotes for the wild-type allele. However, it appears that there is a strong interaction between the FTO genotype and physical activity level. Indeed the carriers of the risk allele are normal weight if they are physically active (3,4). It is only the sedentary individuals who are homozygotes for the risk allele who are heavier than the other genotypes.

Genome-wide linkage analysis for circulating levels of adipokines and C-reactive protein in the Quebec family study (QFS)

Abstract: Adipose tissue synthesizes and secretes a wide range of biologically active molecules considered as inflammatory markers whose dysregulation in obesity plays a role in the development of insulin resistance and vascular disorders. Thus, finding genes that influence circulating levels of inflammatory biomarkers may provide insights into the genetic determinants of obesity-related metabolic diseases. We performed linkage analyses for fasting plasma levels of adiponectin, C-reactive protein (CRP), interleukin-6 (IL-6) and tumor-necrosis factor-alpha (TNF-α) in 764 subjects enrolled in the Quebec family study (QFS). A maximum of 393 pairs of siblings from 211 nuclear families were available for analyses. A total of 443 markers spanning the 22 autosomal chromosomes with an average inter-marker distance of 6.24 Mb were genotyped. Linkage was tested using both allele-sharing (SIBPAL) and variance component linkage methods (MERLIN). We showed suggestive evidence of linkage for plasma adiponectin levels on chromosome 15q21.1 [D15S659; logarithm of the odds (LOD) score = 2.23], 3q13.33 (D3S3023; LOD = 2.09), 20q13.2 (D20S197; LOD = 1.96) and 14q32.2 (D14S1426; LOD = 1.79). Evidence of linkage (SIBPAL) was also found for CRP on 12p11.23 (P = 0.001) and 12q15 (P = 0.0005) and for IL-6 on 14q12 (P = 0.002). None of these linkages remained significant after adjustment for body mass index. No evidence of linkage was found for TNF-α plasma levels. These results suggest that several QTLs can influence plasma levels of adiponectin and CRP, partly via their effects on adiposity.

Adiponectin concentration and insulin indicators following overfeeding in identical twins

Abstract: Low adiponectin levels have been associated with high body mass index, low insulin sensitivity, and diabetes. Objective: To assess the relationships between changes in serum adiponectin concentration and adiposity, glucose, and insulin in response to long-term overfeeding in identical twins and to calculate the twin resemblance in serum adiponectin concentrations. Subjects and design: Twenty-four sedentary young men [mean (±SD) age, 21±2 yr] who constituted 12 pairs of healthy identical twins were studied for metabolic and adiponectin changes in response to overfeeding. Intervention: Subjects were overfed by 84,000 kcal over a 100-day period. Outcome measures: The overfeeding study provides an opportunity to examine the relationships between adiponectin and changes in body weight, adiposity, plasma glucose and insulin. Results: Serum adiponectin concentration correlated positively with body weight (r= 0.41, p=0.05) at baseline but not with indicators of adiposity or with visceral fat. No relationship existed between baseline adiponectin concentration and body weight or adiposity gains with overfeeding. However, serum adiponectin decreased significantly by −2.35±0.48 μg/ml (p=0.001) in response to overfeeding. Baseline adiponectin levels correlated negatively with changes in plasma fasting glucose levels (r=−0.53, p=0.01) and homeostasis model assessment index (r=−0.41, p=0.05), independently of fat mass. The intrapair coefficient for twin resemblance (r=0.75, p=0.001) strongly suggests that baseline serum adiponectin concentration is a familial trait. Conclusions: These data provide evidence that adiponectin concentration is a familial trait in normal-weight individuals, that it decreases when challenged by positive energy balance, and that its overfeeding-induced variations are correlated with glucose and insulin levels.

Myeloperoxidase gene sequence variations are associated with low-density-lipoprotein characteristics.

Abstract: The small, dense low-density-lipoprotein (LDL) phenotype is associated with an increased atherosclerosis risk. A genome-wide scan performed on 236 nuclear families of the Quebec Family Study (QFS) revealed a quantitative trait locus (QTL) for LDL peak-particle size (LDL-PPD) on the 17q21 region. This region encodes the myeloperoxidase (MPO) gene. MPO is able to oxidize LDL by its reactive intermediates. To test the associations between MPO gene polymorphisms and LDL-PPD as well as plasma lipid levels, we performed direct sequencing of the coding regions, exon-intron splicing boundaries, and the regulatory regions on 25 subjects to identify new genetic variants. Genotyping was performed either by TaqMan or direct sequencing on 680 subjects in the QFS. LDL-PPD was measured by gradient gel electrophoresis (GGE) on nondenaturing 2–16% polyacrylamide gradient gels. MPO gene sequencing revealed 16 polymorphisms. The c.-653G > A MPO polymorphism was associated with lower plasma total cholesterol, LDL cholesterol (LDL-C), and LDL apolipoprotein B (LDL-apoB) levels (P = 0.026, 0.042 and 0.014, respectively). No significant association with a gene-dosage effect were observed for LDL-PPD. The MPO gene variants are not associated with LDL-PPD and thus are unlikely to be responsible for the quantitative trait locus reported on 17q21. However, the c.-653G > A is associated with plasma LDL-C and LDL-apoB concentrations.

Comprar Handbook of Obesity: Clinical Applications, Third Edition | Claude Bouchard | 9781420051445 | Informa Healthcare

Abstract: Tienda online donde Comprar Handbook of Obesity: Clinical Applications, Third Edition al precio 200,12 € de Claude Bouchard | George A. Bray, tienda de Libros de Medicina, Libros de Endocrinologia y Nutricion - Obesidad

ASSOCIATION BETWEEN µ‐OPIOID RECEPTOR‐1 102T>C POLYMORPHISM AND INTERMEDIATE TYPE 2 DIABETES PHENOTYPES: RESULTS FROM THE QUEBEC FAMILY STUDY (QFS)

Abstract: SUMMARY 1 It has been suggested recently that molecules expressed both in the pancreas and hypothalamus, such as µ-opioid receptor 1 (OPRM1), could form an integrated brain–liver system, which may sense glucose levels and therefore contribute to the development of type 2 diabetes mellitus (T2DM). 2 In the present study, we tested associations between OPRM1 gene polymorphisms (rs1799971, 102T/C and rs0648007G/A) and indices of glucose tolerance, insulin sensitivity (IS) and insulin secretion derived from plasma measures obtained in a fasting state and following a 75 g oral glucose tolerance test (OGTT) in 749 subjects from the Quebec Family Study (QFS). Polymorphisms were tested for association with glucose tolerance (normal vs IFG and T2DM combined) by calculating a χ2 statistic and corresponding P values, whereas associations with quantitative measures of glucose tolerance, IS and insulin secretion were tested using mixed linear models implemented in the MIXED procedure of sas (SAS Institute, Cary, NC, USA). 3 Associations were found between 102T/C OPRM1 and indices of glucose tolerance and IS. Compared with T/T homozygotes, carriers of the OPRM1 C-102 variant exhibited a better glucose tolerance with a lower (P = 0.006) glucose area under the curve (AUC) following the OGTT and a better IS with a higher (P = 0.03) value of the Cederholm index, a numerical index of the curve relating glucose uptake to the log10 plasma insulin levels during the OGTT. 4 The results of the present study reveal that the 102T/C OPRM1 gene polymorphism is associated with a better glucose tolerance and improved IS, both of which suggest a potential protective effect of this variant on T2DM risk.

Effets de la chirurgie bariatrique sur la mortalité des patients suédois obèses

Abstract: et de 20/20 patients pour la douleur thoracique. Chez les 4 patients sans disparition complete de la symptomatologie, la mediane de pression du SIO etait de 18 cmH20 avec transit et endoscopie normaux. Deux patients presentaient des signes cliniques et pH-metriques de reflux. Les resultats sont restes stables sur la periode de suivi. La conclusion des auteurs est que la myotomie etendue avec fundoplicature anterieure est un traitement efficace de la MSDO severe. Les resultats fonctionnels sont ici excellents, notamment, en termes de dysphagie et de douleurs thoraciques.