Publications

. Ukkola O, Tremblay A, Després J‐P, Chagnon YC, Campfield LA, Bouchard C (Pennington Biomedical Research Center, Baton Rouge, Louisiana, USA; University of Oulu, Oulu, Finland; Laval University, Ste‐Foy, Québec, Canada; and University of Colorado Health Sciences Center, Denver, Colorado, USA). Leptin receptor Gln223Arg variant is associated with a cluster of metabolic abnormalities in response to long‐term overfeeding. J Intern Med 2000; 248: 435–439. Objectives. The role of the leptin receptor (LEPR) gene Gln223Arg polymorphism on the metabolic and body composition changes in response to overfeeding was studied. Subjects. Twelve pairs of male monozygotic twins ate a 4.2 MJ day –1 energy surplus, 6 days week –1 , during a period of 100 days. Results. Overfeeding induced a significantly greater increase in glucose ( P = 0.001 for percentage change) and insulin ( P = 0.038) areas under the curve during oral glucose tolerance tests (OGTTs) in the GlnGln ( n = 10) than in the GlnArg/ArgArg ( n = 14) subjects. In addition, the GlnGln genotype was associated with a greater increase in plasma levels of leptin ( P = 0.037) and total triglycerides ( P = 0.003), as well as a greater decrease in high‐density lipoprotein cholesterol ( P = 0.010), than for the combined GlnArg/ArgArg genotypes. Body composition changes were not different between the genotypes. Conclusions. We conclude that the GlnGln subjects of the LEPR gene polymorphism are more susceptible to metabolic abnormalities when they are exposed to long‐term positive energy balance. These findings provide new information on the genetic basis of individual differences in response to chronically elevated food intake.

To describe the prevalence of time spent in sedentary behaviors (e.g., TV/video and computer use) among youth in the US.The National Health and Nutrition Examination Survey (2001-06) provided data to examine sedentary behavior across age groups (2-5, 6-11, and 12-15 years of age), ethnic groups (European [EA], African [AA], and Mexican American [MA]), and body mass index (BMI) categories (normal weight, overweight, obese).The sample included 8 707 (50.7% boys) children aged 2 to 15 years. Seventy percent of the sample was normal weight, 18.1% was overweight, and 11.5% was obese. The total proportion of young people engaged in TV/video viewing, computer use, and total screen time > or = 2 hours daily was 33.0%, 6.7%, and 47.3%, respectively. More boys (49.4%) than girls (45.0%); older (12-15 years: 56.0%) versus younger children (2-5 years: 35.3% and 6-11 years: 49.1%); AA (66.1%) versus EA (42.5%) and MA (46.1%); obese (58.5%) versus overweight (50.8%) versus normal weight (44.6%); and low and middle income (<$25 K: 51.4% and $25-45 K: 51.2%) versus high income (>$45 K: 42.6%) children spent > or = 2 hours daily in screen time.Nearly half (47%) of US children exceed > or = 2 hours/day of time in sedentary behavior. Further, it appears there are gender, age, ethnic, BMI-defined weight status, and income differences in exceeding > or = 2 hours/day in sedentary behavior. These results will be useful in planning targeted interventions at those populations with a higher prevalence of sedentary behavior.

Lipolytic and lipoprotein lipase (LPL) activities were studied in isolated human adipocytes obtained from two intraabdominal depots (round ligament and omental) and from the subcutaneous abdominal region of nine severely obese premenopausal women (with body mass indices ranging from 37 to 51 kg/m2), aged 36 +/- 3 yr, undergoing gastrointestinal surgery. Both fat cell weight and LPL activity were significantly greater in round ligament adipose cells than in subcutaneous abdominal or in omental adipocytes (P

No abstract is provided for this article.

The correlation between haemodynamic and oxymetric parameters, and circulating cytokines has been little studied for the early phase of extensive burns. The aim of this prospective study was to evaluate survival, looking at variations in cardiac index (CI), oxygen delivery (DO2I) and consumption (VO2I) indexed to the body surface area (BSA), and circulating interleukin-6 (IL6) levels in the acute stage of major burns. Over a 12-month period, all patients admitted within 6 h of extensive thermal injury with total burn surface area (TBSA) of over 60 per cent, necessitating standardized resuscitation and mechanical ventilation, were included. Routine intensive care monitoring, including pulmonary and femoral artery catheters, was set up. During the first 3 days post-injury haemodynamic and oxymetric profiles were recorded every 6 h. Circulating IL6 samples were taken within 6 h of admission, then daily (at 24, 48 and 72 h). A comparison of the results in survivors (S) and non-survivors (NS) at those previously determined times was made. Ten consecutive patients were studied. Six patients survived (Age = 33 + 10 years; TBSA = 76 ± 11 per cent) and four died (Age = 40 ± 14 years; TBSA = 77 ± 13 per cent). Similar initial hypovolemic profiles were found in both groups. From 24 h, a hyperdynamic status was observed which increased until 72 h. This hyperkinetic evolution was more marked in the survivors (CI: 4.6 ± 2.0 for NS and 6.9 ± 1.5 l min−1 m−2 for S; SVRI: 2125 ± 1288 for NS and 918 ± 232 dynes cm−5 m2 for S at 72 h). DO2I and VO2I were always higher in the survivors. DO2I and VO2I and VO2I increased from admission to 72 h in the survivors whereas a significant drop in DO2I and VO2I occured in the non-survivors at 48 h (DO2I: 536 ± 222 for NS and 1228 ± 268 ml min−1 m−2 for S; VO2I: 120 ± 50 for NS and 251 ± 56 ml min−1 m−2 for S (P < 0.01)). Plasma IL6 revealed abnormal values with consistent peaks at 24–48 h in the survivors (respectively 17411 ± 24542 and 10746 ± 11802 pg ml−1) and only moderate peaks in the non-survivors (865 ± 652 and 912 ± 485 pg ml−1). Finally, CI, DO2I, VO2I, and circulating IL6 were always higher, and SVRI lower, in the survivors than in the non-survivors. The ability to increase DO2 and to optimize VO2 during the ‘turning point’ of 48 h seems to improve the prognosis of critically burned patients: the role of IL6 in this systemic inflammatory response is discussed.

Because leptin production by adipose tissue is under hormonal control, we examined the impact of epinephrine administration on plasma leptin concentrations.We measured plasma leptin, insulin, and free fatty acid (FFA) responses after a 60-minute epinephrine infusion (0.010 microg/kg fat free mass/min) followed by a 30-minute recovery period (no infusion) in a group of 11 lean (mean body mass index +/- SD: 22.6 +/- 1.1 kg/m(2)) and 15 obese (30.0 +/- 1.3 kg/m(2)) premenopausal women. Leptin, insulin, and FFA levels were measured in plasma before (-15 and 0 minutes) and at every 30 minutes over the 90-minute period.In both lean and obese individuals, plasma leptin was significantly reduced by epinephrine (p < 0.0001). Body fat mass was associated with fasting leptin levels (r = 0.64, p < 0.0005) as well as with the decrease in leptinemia (r = -0.51, p < 0.01) produced by epinephrine administration. Furthermore, we noted a large range of leptin response to epinephrine among our subjects, especially in obese women (from -12 to -570 ng/mL per 60 minutes). However, there was no association between postepinephrine leptin and FFA levels (r = -0.14, p = 0.55).Results of this study indicate that leptin levels decrease after epinephrine administration in both lean and obese premenopausal women. However, the heterogeneity in the response of leptin to catecholamines suggests potential alterations of the leptin axis that may contribute to generate a positive energy balance and, thus, may favor weight gain in some obese individuals.

To determine the efficacy of exercise training in treating the metabolic syndrome.The sample included 621 black and white participants from the HERITAGE Family Study, identified as sedentary and apparently healthy (no chronic disease or injury). The metabolic syndrome was defined as having three or more risk factors according to the guidelines of the National Cholesterol Education Program, including elevated waist circumference, blood pressure, triglycerides, blood glucose, and low HDL cholesterol. The presence of the metabolic syndrome and component risk factors were determined before and after 20 wk of supervised aerobic exercise training.The prevalence of the metabolic syndrome was 16.9% in this sample (105/621) of apparently healthy participants. Of the 105 participants with the metabolic syndrome at baseline, 30.5% (32 participants) were no longer classified as having the metabolic syndrome after the exercise training. Among the 32 participants who improved their metabolic profile, 43% decreased triglycerides, 16% improved HDL cholesterol, 38% decreased blood pressure, 9% improved fasting plasma glucose, and 28% decreased their waist circumference. There were no sex or race differences in the efficacy of exercise in treating the metabolic syndrome: 32.7% of men, 28.0% of women, 29.7% of black, and 30.9% of white participants with the metabolic syndrome were no longer classified as having the syndrome after training.Aerobic exercise training in patients with the metabolic syndrome can be useful as a treatment strategy and provides support for a role for physical activity in the prevention of chronic disease.

Journal Article Ncol RFLP in human brain creatine kinase gene (CKBB) Get access F.T. Dionne, F.T. Dionne * Physical Activity Sciences Laboratory, Laval UniversityQuébec, G1K 7P4, Canada * To whom correspondence should be addressed Search for other works by this author on: Oxford Academic PubMed Google Scholar L. Turcotte, L. Turcotte Physical Activity Sciences Laboratory, Laval UniversityQuébec, G1K 7P4, Canada Search for other works by this author on: Oxford Academic PubMed Google Scholar J. Grondin, J. Grondin Physical Activity Sciences Laboratory, Laval UniversityQuébec, G1K 7P4, Canada Search for other works by this author on: Oxford Academic PubMed Google Scholar M.C. Thibault, M.C. Thibault Physical Activity Sciences Laboratory, Laval UniversityQuébec, G1K 7P4, Canada Search for other works by this author on: Oxford Academic PubMed Google Scholar C. Bouchard C. Bouchard Physical Activity Sciences Laboratory, Laval UniversityQuébec, G1K 7P4, Canada Search for other works by this author on: Oxford Academic PubMed Google Scholar Nucleic Acids Research, Volume 19, Issue 1, 11 January 1991, Page 195, https://doi.org/10.1093/nar/19.1.195-a Published: 11 January 1991

The role of heredity in the response of maximal anaerobic capacities and skeletal muscle histochemical and biochemical characteristics to a 15-week cycle ergometer training program involving both continuous and interval work patterns was investigated in 14 pairs of monozygotic twins. The training program consisted mainly of series of ergocycle supramaximal exercises lasting from 15 s to 90 s and performed 4 and 5 times a week. The subjects were submitted to 10 s and 90 s all-out ergocycle tests to estimate maximal anaerobic alactacid (AAC) and lactacid (ALC) capacities, respectively. Muscle fiber types and creatine kinase (CK), hexokinase (HK), phosphofructokinase (PFK), lactate dehydrogenase (LDH), malate dehydrogenase (MDH), 3-hydroxyacyl CoA dehydrogenase (HADH), and oxoglutarate dehydrogenase (OGDH) activities were determined in a biopsy from the vastus lateralis. Training increased AAC, ALC, fiber type I proportion, MDH, HADH, and OGDH (P less than 0.05) and decreased fiber type IIb proportion and the PFK/OGDH ratio. No significant change was observed for CK, HK, PFK, and LDH. Large interindividual differences in the response to training were observed for all variables. However, intraclass correlations indicated that the extent of the response of ALC and CK, HK, LDH, MDH, and OGDH activities and of the PFK/OGDH activity ratio to training were significantly similar within pairs of twins. Although the role of heredity appeared absent for the changes in fiber type proportions and in anaerobic alactacid capacity, the present results suggest that the response of anaerobic lactacid capacity and most enzyme activities to high-intensity intermittent training is significantly determined by the genotype.

No abstract is provided for this article.

The fat mass (FM) and obesity-associated (FTO) gene is the first obesity-susceptibility gene identified by genome-wide association scans and confirmed in several follow-up studies. Homozygotes for the risk allele (A/A) have 1.67 times greater risk of obesity than those who do not have the allele. However, it is not known whether regular exercise-induced changes in body composition are influenced by the FTO genotype. The purpose of our study was to test whether the FTO genotype is associated with exercise-induced changes in adiposity. Body composition was derived from underwater weighing before and after a 20-week endurance training program in 481 previously sedentary white subjects of the HERITAGE Family Study. FTO single-nucleotide polymorphism (SNP) rs8050136 was genotyped using Illumina GoldenGate assay. In the sedentary state, the A/A homozygotes were significantly heavier and fatter than the heterozygotes and the C/C homozygotes in men (P = 0.004) but not in women (P = 0.331; gene-by-sex interaction P = 0.0053). The FTO genotype was associated with body fat responses to regular exercise (P < 0.005; adjusted for age, sex, and baseline value of response trait): carriers of the C allele showed three times greater FM and %body fat losses than the A/A homozygotes. The FTO genotype explained 2% of the variance in adiposity changes. Our data suggest that the FTO obesity-susceptibility genotype influences the body fat responses to regular exercise. Resistance to exercise-induced reduction in total adiposity may represent one mechanism by which the FTO A allele promotes overweight and obesity.

The molecular pathways that are activated and contribute to physiological remodeling of skeletal muscle in response to endurance exercise have not been fully characterized. We previously reported that ∼800 gene transcripts are regulated following 6 wk of supervised endurance training in young sedentary males, referred to as the training-responsive transcriptome (TRT) (Timmons JA et al. J Appl Physiol 108: 1487-1496, 2010). Here we utilized this database together with data on biological variation in muscle adaptation to aerobic endurance training in both humans and a novel out-bred rodent model to study the potential regulatory molecules that coordinate this complex network of genes. We identified three DNA sequences representing RUNX1, SOX9, and PAX3 transcription factor binding sites as overrepresented in the TRT. In turn, miRNA profiling indicated that several miRNAs targeting RUNX1, SOX9, and PAX3 were downregulated by endurance training. The TRT was then examined by contrasting subjects who demonstrated the least vs. the greatest improvement in aerobic capacity (low vs. high responders), and at least 100 of the 800 TRT genes were differentially regulated, thus suggesting regulation of these genes may be important for improving aerobic capacity. In high responders, proangiogenic and tissue developmental networks emerged as key candidates for coordinating tissue aerobic adaptation. Beyond RNA-level validation there were several DNA variants that associated with maximal aerobic capacity (Vo(₂max)) trainability in the HERITAGE Family Study but these did not pass conservative Bonferroni adjustment. In addition, in a rat model selected across 10 generations for high aerobic training responsiveness, we found that both the TRT and a homologous subset of the human high responder genes were regulated to a greater degree in high responder rodent skeletal muscle. This analysis provides a comprehensive map of the transcriptomic features important for aerobic exercise-induced improvements in maximal oxygen consumption.