Bouchard, C. FACSM; Simoneau, O. A.; Hamel, P.*; Lortie, G.; Boulay, M. R.; Marcotte, M.*; Thibault, M. C. FACSM. Author Information
No abstract is provided for this article.
No abstract is provided for this article.
In 1996, we began publishing in Obesity Research a review of the status of the human obesity gene map (1). Since then, 10 updates of the map have been published, the latest in 2006 covering the literature available as of the end of October 2005 (2). In 1999, an electronic version of the map was made available on the website of the Donald B. Brown Chair on Obesity at Université Laval in Quebec City, Canada. Later, in 2002, the web-based version of the map was migrated to the Human Genomics Laboratory web site at the Pennington Biomedical Research Center in Baton Rouge, LA, where I had moved. While the print version of the map continued to be a factual summary of the material published at a particular point in time, the web-based version (Obesity Gene Map Database or OGMDB) was enriched considerably and provided extensive linkages to other relevant resources. The printed version in Obesity (previously, Obesity Research) was well received by the scientific community, as evidenced by its relatively high rate of citation over the last 10 years (∼750 citations by the end of 2006). Similarly, the OGMDB resource enjoyed ∼15,000 hits per month in the last few years, with thousands of regular visitors. Interestingly, the most assiduous users were from the pharmaceutical industry and from biotechnology companies. Developing the yearly update of the map became progressively a major burden. For instance, the last rendition published in Obesity in 2006 reached a total of 116 journal pages. It had become an effort of a magnitude that could not be sustained without the addition of human resources dedicated solely to the project. Despite our best efforts, funds could not be raised in a timely fashion to make it possible for us to continue publishing these yearly updates. Fortunately, a joint effort by the National Institute on Aging at NIH and the Centers for Disease Control and Prevention will compensate in part for the termination of the human obesity gene map publication project and OGMDB. Indeed, these two entities have launched and are maintaining a database of human genetic association studies. The database can be accessed at http:geneticassociationdb.nih.gov. Obesity is not the main focus of the database, but it is included, along with many other diseases and conditions. While the human obesity gene map covered much more than association studies (i.e., Mendelian syndromes, human and animal model single gene defects, genomic scans performed in human cohorts and in animal models, transgenic and knockout murine data, etc.), the new NIH-CDC database focuses on one of the most critical lines of evidence to consider in assessing the role of gene polymorphisms. So it seems like a good time to move on. The field should continue to be well served by the new resource. The map project was made possible through the dedication and hard work of several colleagues at Université Laval and at the Pennington Biomedical Research Center. Even though I will not be able to thank them all here, I would like to express my gratitude to the very early collaborators, Drs. Louis Perusse and Yvon C. Chagnon, as well as John Weisnagel and Tuomo Rankinen, who joined the team soon thereafter. Thanks are also due to Drs. Eric E. Snyder, George Argyropoulos, and Aamir Zuberi, who brought additional expertise to the team in the later years. We were well supported by Diane Drolet in the early phase at Université Laval and, subsequently, by Brandon M. Walts and Nina Laidlaw at the Pennington Biomedical Research Center. I am also grateful for the contribution of the Donald B. Brown Chair on Obesity in the first few years of the project and of several units of the Pennington Biomedical Research Center in more recent times. Finally, I would like to thank the Editors of Obesity (Drs. Xavier Pi-Sunyer and, later, Barbara Corkey) and the Managing Editor, Deborah K. Moskowitz, for their encouragement and strong support for the publication of the annual update of the human obesity gene map over the last 10 years.
No abstract is provided for this article.
Skeletal age (SA) height, weight, PWC130, V̇o2 at 130 heart rate (V̇o130) and cardiorespiratory adaptation to work at 3 kgm·sec-1 were measured in 237 boys ranging in age from 8 to 18 years. Correlations for the total population for the variables of the study are generally higher with SA than with chronological age (CA), although there is no significant difference between the two sets of correlations. Analysis of linear trend indicate that significant nonlinear components are more frequent in the relationships between the variables and SA than with CA. Multiple regression analyses for each variate as dependent variable indicate that height and body weight generally contribute more to the explained variance, while SA is the next best predictor. CA is the least significant of the four independent variables. The total variance explained between any of the submaximal working capacity related measures acting as dependent variable and CA, height and weight is not significantly affected by the presence or absence of SA. The present study thus indicates that SA is not a significant factor in explaining submaximal working capacity, beyond CA, height and weight, when considered over the 8 to 18 year age span. However, when considering shorter age spans, or when considering the adolescent period (12-16 years), SA correlates better with PWC130 (.320<r<.675) and with V̇o130(.299<r<.772).
The aim of the HERITAGE Family Study (HEalth, RIsk factors, exercise Training And GEnetics) is to document the role of the genotype in the cardiovascular, metabolic and hormonal responses to aerobic exercise-training. A consortium of 5 universities in the US and Canada are involved in carrying out the study. A total of about 750 sedentary subjects (500 Caucasians and 250 Blacks) have been recruited, initially tested, exercise-trained in the laboratory with the same program for 20 weeks, and re-tested. Subjects come from 100 families of Caucasian descent and families or pairs of relatives of African-American ancestry. The study design and the aims of the project will be described. The training program, the quality control program and the reproducibility of the tests, assays and measurements will be reviewed. The effects of the training program on plasma lipids and lipoproteins will be presented. Data on familial resemblance in the sedentary state and in the response to training for selected phenotypes will be considered.
The authors declare no conflict of interest. Data sharing not applicable to this article as no datasets were generated or analysed during the current study.
