In order to study human fat cell morphology and metabolism in both sexes, with different levels of fatness and physical training, 53 subjects (14 women and 39 men), 25.9 ± 7.6 (mean ± SD) years of age, weighing 64.8 ± 10.8 kg and with 14.8 ± 4.7% body fat were submitted to a biopsy of subcutaneous adipose tissue in the supra-iliac region. Average fat cell diameter (ACD) was assessed measuring at least 500 cells per subject. Basal (BL), epinephrine sub-maximal (10−5 M) (ESML) and epinephrine maximal (10−4 M) (EML) stimulated lipolysis have been determined on collagenase isolated fat cells. Female subjects have larger ACD (83.4 ± 12.3 μm vs. 62.5 ± 1.9 μm) (P ≤ 0.001) and lower BL, ESML, and EML than men (P ≤ 0.05). After control over age and sex of subjects, there were significant and negative correlations between all fatness indicators (ACD, fat mass in kg, percent body fat, sum of 9 skinfolds) and BL, ESML and EML. A completely randomized factorial ANOVA design revealed a significant effect of fatness level on BL, ESML and EML, but a non-significant trend for the effect of physical training on the same variables. It is concluded that lipolytic activity is more related to body fatness than to the training status. However, training tends to accentuate lipolytic activity as shown values of BL, ESML and EML found in the lean highly trained subjects of the study.
There is growing evidence to the effect that steroid hormones are associated with a complex phenotype of metabolic abnormalities usually referred to as the metabolic syndrome. The 3β-hydroxysteroid dehydrogenases/Δ 4,5-isomerase (3β-HSD) is crucial to the biosynthesis of hormonal steroids, including aldosterone, cortisol, and testosterone. The objective of the present study was to examine the potential impact of a T→C substitution at codon Leu338 of the type I (HSD3B1) 3β-HSD gene on obesity, circulating hormones, and estimates of insulin, glucose, and lipid metabolism as well as blood pressure in 284 unrelated Swedish men born in 1944. The subjects were genotyped by using PCR amplification of exon 4 of the HSD3B1 gene followed by digestion with the restriction enzyme BglII. The frequency of allele T was 0.44 and that of allele C 0.56. Homozygotes for the C allele (n=75) had significantly (P<0.05) higher mean systolic and diastolic blood pressures compared to both heterozygotes (n=143) and homozygotes for the T allele (n=45). In addition, the C allele was significantly (P=0.018) more frequent among subjects with grade 1 hypertension (>140/90mm Hg) compared to normotensive (<130/85mm Hg) subjects. These results were all adjusted for the potential confounding effect of body mass index (BMI) and waist-to-hip ratio (WHR). Other measurements such as BMI, WHR, abdominal sagittal diameter, salivary cortisol, total testosterone, serum leptin, fasting insulin and glucose, and serum lipids were not different across the HSD3B1 genotype groups. In conclusion, a T→C polymorphism at codon Leu338 of exon 4 of the HSD3B1 gene is associated with elevated systolic and diastolic blood pressures. The pathogenic mechanism underlying this association is, however, uncertain from the present data and further studies are warranted.
The symposium will summarize the evidence concerning the dose-response relationship between physical activity and health benefits and will identify key issues for future research. It will provide an opportunity to summarize the proceedings of an evidence-based consensus meeting held at Hockley Valley Resort, Toronto, in October 2000, which examined the dose-response aspects of the relationship between physical activity and the prevention of disease, disability and premature death. The key questions of the dose-response problem will be defined (C. Bouchard). The various components of the exercise recommendations in terms of intensity, frequency, duration, fractionalization, and acute versus chronic aspects will be summarized (W. Haskell). Dose-response relationships between physical activity and common chronic diseases as well as indicators of quality of life will be reviewed (S. Blair). The implication of the dose-response components of physical activity of participation in relation to cancer and mortality rates will be discussed (I-M Lee). The symposium will conclude with a panel discussion with a view to emphasize the evidence-based conclusions reached at the consensus meeting and how they compare to the current recommendations from the Surgeon General, CDC and ACSM.
To investigate whether the relationship between short sleep duration and subsequent body weight gain is influenced by disinhibited eating behavior.Six-year longitudinal study.Community setting.Two hundred seventy-six adults aged 21 to 64 years from the Quebec Family Study.Body composition measurements, self-reported sleep duration, and disinhibition eating behavior trait (Three-Factor Eating Questionnaire) were determined at both baseline and after 6 years. For each sleep-duration group (short- [≤6 h] average, [7-8 h], and long- [≥9 h] duration sleepers), differences in weight gain and waist circumference were tested by comparing the lowest (score ≤ 3) versus the highest (score ≥ 6) disinhibition eating behavior tertiles using analysis of covariance, with adjustment for potential confounding factors. Individuals having both short sleep duration and high disinhibition eating behavior were more likely to gain weight and increase their abdominal circumference over time (P<0.05); however, short-duration sleepers having a low disinhibition eating behavior trait were not more likely to increase their adiposity indicators than were average-duration sleepers. Over the 6-year follow-up period, the incidence of overweight/obesity for short-duration sleepers with a high disinhibition eating behavior trait was 2.5 times more frequent than for short-duration sleepers with a low disinhibition eating behavior trait. Energy intake was significantly higher in short-duration sleepers with a high disinhibition eating behavior trait (P<0.05 versus all other groups).We observed that having a high disinhibition eating behavior trait significantly increased the risk of overeating and gaining weight in adults characterized by short sleep duration. This observation is novel and might explain the interindividual differences in weight gain associated with short sleep duration.
Handbook of Obesity: Clinical Applications, Third Edition is the premier reference for physicians and researchers in the field of obesity. Written by leading scientists and clinicians, this handbook offers unparalleled depth and breadth of coverage concerning this growing global and chronic disease that affects and exacerbates comorbid conditions including diabetes and heart disease. This Third Edition is full of many revisions including: The sections Etiology and Pathophysiology have been updated to reflect state-of-the-art advancements in the prevalence, etiology, and pathophysiology of obesity New chapters have been added and revisions made to the subjects of genetics, molecular biology, endocrine determinants of obesity, the metabolic syndrome, and the relationship between obesity and diabetes Written by the field's leading scientists and clinicians, Handbook of Obesity: Clinical Applications, Third Edition: has unparalleled coverage of the full range of subjects comprising the field of obesity. is packed with charts, diagrams, and tables that conveniently summarize key information and concepts elucidates state-of-the-art knowledge of the definition, prevalence, etiology, and pathophysiology of obesity
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We studied the sensitivity of cardiac structures to endurance training. To evaluate variability in adaptation, 20 sedentary subjects and ten pairs of monozygotic twins were submitted to a 20-week endurance training program. Maximal oxygen uptake increased significantly in both groups: 11 mL O2/kg/min-1 or 30% in the sedentary group and 6 mL O2/kg/min-1 or 13% in the monozygotic twins. Statistically significant increases in left ventricular diameter, posterior wall and septal thicknesses, as well as left ventricular end-diastolic volume and left ventricular mass were observed in the sedentary subjects, but not in the monozygotic twins. We could demonstrate that after training, twin pairs differed more from each other than at the start. Concomitantly, within-pair resemblance was greater after training than before. Results indicate that cardiac dimensions are amenable to significant modifications under controlled endurance training conditions and furthermore that the extent and variability of the response of cardiac structures to training are perhaps genotype dependent.
