Biomedical subjects

C Bouchard

Publications and source records attributed to C Bouchard.

At least 145 records · Page 8Linked to original sources

PubMed2000

NOS3 Glu298Asp genotype and blood pressure response to endurance training: the HERITAGE family study.

Endothelium-dependent vasodilation is a mechanism that may affect blood pressure response to endurance training. Because NO plays a central role in this process, the endothelial NO synthase gene is a good candidate for the regulation of exercise blood pressure. We investigated the associations between an endothelial NO synthase gene polymorphism (Glu298Asp) and endurance training-induced changes in resting and submaximal exercise blood pressure in 471 white subjects of the HERITAGE Family Study. Two submaximal exercise tests at 50 W were conducted both before and after a 20-week endurance training program. Steady-state exercise blood pressure was measured twice in each test with an automated unit. The Glu298Asp polymorphism was typed with a PCR-based method and digestion with BAN:II. Both systolic and diastolic blood pressure at 50 W decreased in response to the training program, whereas resting blood pressure remained unchanged. The decrease in diastolic blood pressure at 50 W was greater (P=0.0005, adjusted for age, gender, baseline body mass index, and baseline diastolic blood pressure at 50 W) in the Glu/Glu homozygotes (4.4 [SEM 0.4] mm Hg, n=187) than in the heterozygotes (3.1 [0.4] mm Hg, n=213) and the Asp/Asp homozygotes (1.3 [0.7] mm Hg, n=71). The genotype accounted for 2.3% of the variance in diastolic blood pressure at 50 W training response. Both the Glu298 homozygotes and the heterozygotes had a greater (P=0.013) training-induced reduction in rate-pressure product at 50 W than the Asp298 homozygotes. These data suggest that DNA sequence variation in the endothelial NO synthase gene locus is associated with the endurance training-induced decreases in submaximal exercise diastolic blood pressure and rate-pressure product in sedentary normotensive white subjects.

Adult↗

PubMed2000

Associations between the leptin receptor gene and adiposity in middle-aged Caucasian males from the HERITAGE family study.

Linkage and association studies between three exonic polymorphisms in the leptin receptor gene and body composition variables in the HERITAGE Family Study were undertaken. Polymorphisms K109R, Q223R, and K656N have been analyzed with body mass index (BMI), sum of height skinfolds (SF8), fat mass (FM), percent body fat (%FAT), fat free mass, and plasma leptin level. Single-point linkage analysis and covariance analysis across genotypes were performed, by race, on phenotypes adjusted for age and sex. Blacks (88 parents; 231 adult offspring) from 115 nuclear families (72-119 sibpairs) and Caucasians (192 parents; 330 adult offspring) from 99 nuclear families (319-364 sibpairs) were used for these analyses. In Caucasians, BMI and FM showed suggestive linkages with K109R (P = 0.02 and P = 0.05, respectively) and associations with Q223R (P = 0.005 and P = 0.03, respectively). In blacks, no statistically significant linkage or association was observed. In Caucasians, associations with Q223R were observed in parents, but not in offspring, for BMI, FM, and %FAT (0.04< or =P< or =0.0001). Males, not females, showed differences across genotypes for the same phenotypes plus SF8 and leptin (0.03< or = P< or =0.0002). Carriers of the R223 allele showed higher values than noncarriers for BMI (+4 U, P = 0.0001), SF8 (+30 mm, P = 0.01), FM (+7 kg, P = 0.0004), %FAT (+5%, P = 0.0002), and leptin (+4 ng/mL, P = 0.0006). These results indicate a significant effect of leptin receptor on adiposity in middle-aged Caucasian males.

Adipose Tissue↗

PubMed2000

Fasting insulin levels influence plasma leptin levels independently from the contribution of adiposity: evidence from both a cross-sectional and an intervention study.

The aim of the present investigation was to determine whether leptinemia is only a reflection of the status of fat stores or if insulinemia has a significant influence over leptin levels. Study 1 focused on the association between fasting plasma insulin and leptin in subjects of the Quebec Family Study who were first classified as either high- or low-insulin individuals and were then individually matched on the basis of fat mass (FM). In Study 2, 19 men and 23 women took part in a 15-week weight loss program that consisted of drug therapy (fenfluramine, 60 mg/day) or placebo coupled to an energy-restricted diet (-2930 kJ/day). Body weight, FM, and fat-free mass (assessed by underwater weighing) as well as visceral and sc abdominal and mid-thigh adipose tissue measured by computed tomography were assessed before and after weight loss. Blood samples were drawn and analyzed for fasting plasma insulin and leptin before and after weight loss. In Study 1, significant positive associations were noted between log10 transformed fasting insulin and leptin in both men (r = 0.55, P < 0.0001) and women (r = 0.48, P < 0.0001). Moreover, after having carefully matched high-insulin to low-insulin individuals on the basis of FM, significantly lower leptin levels were observed in the low-insulin groups, in men (5.5 vs. 8.1 ng/mL, P < 0.05) as well as in women (18.7 vs. 24 ng/mL, P < 0.05). Results from Study 2 showed significant reductions of body weight, FM, fat-free mass, visceral abdominal tissue, sc abdominal tissue, and mid-thigh adipose tissue levels in men and women in response to the weight loss protocol. Moreover, the decrease in fasting plasma insulin was the only significant correlate of changes in fasting plasma leptin levels during weight loss, even after corrections for changes in FM in both men (r = 0.50, P < 0.05) and women (r = 0.46, P < 0.05). These results suggest that in a population characterized by a wide range of adiposity hyperinsulinemia has the potential to modulate leptin levels beyond what can be explained by total adiposity. Moreover, this relation also seems to exist in a dynamic setting (i.e. during weight loss) because changes in insulin were independent predictors of the changes in leptinemia in both men and women after correction for changes in FM.

Adipose Tissue↗

PubMed2000

Metabolic heterogeneity underlying postprandial lipemia among men with low fasting high density lipoprotein cholesterol concentrations.

The high triglyceride (TG) and low high density lipoprotein (HDL) cholesterol dyslipidemia has been associated with increased postprandial lipemia. Although fasting TG is a powerful predictor of postprandial hyperlipidemia, the role of hypoalphalipoproteinemia in postprandial TG metabolism is uncertain. We have studied postprandial lipemia among 63 men with low fasting plasma HDL cholesterol concentrations (<0.9 mmol/L), but with either low (<2.0 mmol/L) or high (>2.0 mmol/L) fasting plasma TG levels. A significant relationship was noted between postprandial TG response and fasting HDL cholesterol concentration (r = -0.43; P: < 0.0005). We also found that men with high TG/low HDL dyslipidemia (high TG and low HDL cholesterol; n = 16) were characterized by abdominal obesity as well as increased visceral adipose tissue accumulation, whereas normolipidemic controls (low TG and high HDL cholesterol; n = 26) and men with isolated low HDL cholesterol concentrations (low TG and low HDL cholesterol; n = 17) were not characterized by features of the insulin resistance syndrome (visceral obesity, hyperinsulinemia, and hypertriglyceridemia). Although controls and men with isolated low HDL cholesterol levels had similar postprandial lipemic responses, men with the high TG/low HDL dyslipidemia had a marked increase in their postprandial TG responses to the fat load compared with the other subgroups (P: < 0. 001). Men with the high TG/low HDL dyslipidemia were also characterized by higher concentrations of apolipoprotein (apo) B-48 and B-100 particles (chylomicron remnants and very low density lipoproteins, respectively) before and during the postprandial period compared with the other subjects. These results suggest that low HDL cholesterol concentration is a heterogeneous metabolic phenotype that it is not associated with postprandial hyperlipidemia unless accompanied by other features of the insulin resistance syndrome.

Adipose Tissue↗

PubMed2000

Contribution of body fatness and adipose tissue distribution to the age variation in plasma steroid hormone concentrations in men: the HERITAGE Family Study.

Obesity has been associated with alterations in plasma steroid hormone concentrations in men. Older men present an altered steroid hormone profile compared to younger individuals, and an increase in body fatness and changes in adipose tissue (AT) distribution are noted with advancing age. Thus, there is a need to examine the relative importance of increased body fatness and changes in AT distribution with advancing age to plasma steroid hormone and sex hormone-binding globulin levels in men. We, therefore, investigated the relationships among age, body fatness, AT distribution, and the plasma steroid hormone profile in a group of 217 Caucasian men (mean age +/- SD, 36.2 +/- 14.9 yr) who covered a wide age range (17-64 yr). Compared to young adult men, older men were characterized by increased adiposity (P < 0.0001) expressed either as body mass index or total body fat mass assessed by underwater weighing. Differences in AT distribution were also noted with a preferential accumulation of abdominal fat as indicated by a larger waist girth (P < 0.0001) and higher visceral AT accumulation (P < 0.0001), measured by computed tomography, in older subjects. Age was associated with decreases (P < 0.0001) in C19 adrenal steroid levels, namely reduced dehydroepiandrosterone (DHEA), DHEA fatty acid ester, DHEA sulfate, as well as androstenedione levels. Androgens, i.e. dihydrotestosterone and testosterone, were also affected by age, with lower levels of both steroids being found in older individuals (P < 0.0005). When statistical adjustment for body fatness and AT distribution was performed, differences in C19 adrenal steroids between the age groups remained significant, whereas differences in androgens and sex hormone-binding globulin concentrations were no longer significant. The present study suggests that age-related differences in plasma steroid hormone levels, especially androgens, are partly mediated by concomitant variation in adiposity in men.

Adipose Tissue↗

PubMed2000

Hypertension in obesity and the leptin receptor gene locus.

Recent animal studies indicate that leptin is involved in the regulation of blood pressure through the leptin receptor. Therefore, 51-yr-old men (N = 284) were selected; and anthropometric, endocrine, metabolic, and hemodynamic variables were examined in relation to polymorphisms of the leptin receptor gene (LEPR), by restriction fragment length polymorphism technique. Three polymorphisms were examined: Lys109Arg in exon 4, Gln223Arg in exon 6, and Lys656Asn in exon 14. In comparison with Lys109 homozygotes, Arg109 homozygotes (9%) showed lower body mass index (BMI) and abdominal sagittal diameter, as well as lower systolic (10.0 mm Hg) and diastolic (7.8 mm Hg) blood pressure. Additionally, Arg223 homozygotes (26.8%) showed lower blood pressure (7.6/5.7 mm Hg) than Gln223 homozygotes. These lower blood pressure levels were independent of other variables. No differences were found with the Lys656Asn polymorphism. Measurements of body fat mass correlated with leptin concentration in Lys109 homozygotes and in Lys109 heterozygotes but not in Arg109 homozygotes. Blood pressure correlated with leptin only in men carrying the wild-type allele Lys109. With both elevated BMI and leptin, Lys109 homozygotes had higher blood pressure than the Arg109 homozygous men (12.4/6.9 mm Hg). Men with blood pressure > or = 140/90 mm Hg had, in comparison with normotensive men, increased BMI and leptin levels, and Lys109 homozygotes were significantly more prevalent. These results suggest that leptin is associated with blood pressure regulation in men through the leptin receptor. When BMI and leptin are elevated, increased blood pressure is found only with the most prevalent LEPR genotype at codons 109 and 223, whereas variants of this receptor seem to protect from hypertension. This might explain why not all obese men are hypertensive.

Adult↗

PubMed2000

How obesity develops: insights from the new biology.

Molecular and genetic studies of animal models have identified numerous genes that may cause or contribute to the development of obesity. They have also provided significant insight into the peripheral and central pathways that control energy intake and expenditure. Genetic studies of families and populations have generated useful information on genes and mutations associated with or linked to obesity, body fat distribution, and other relevant phenotypes. This information, combined with knowledge of the chromosomal location of genes identified from animal studies, has made it possible to identify specific mutations that contribute to the development of obesity in humans.

Adolescent↗

PubMed2000

Tracking of familial resemblance for resting blood pressure over time in the Québec Family Study.

The etiology of familial resemblance for systolic (SBP) and diastolic (DBP) blood pressure, both within a single time point as well as across time points, was assessed to determine how familial etiologies underlying a trait may change across time. SBP and DBP measurements were taken roughly 12 years apart in family members participating in the longitudinal Québec Family Study. A longitudinal (bivariate) familial correlation model yields 3 types of correlations: intraindividual cross-time (e.g., father's BP at time 1 with his own BP at time 2); interindividual within-time (e.g., father time 1 with child time 1); and interindividual cross-time (e.g., father time 1 with child time 2). In addition, the change in BP across time (i.e., time 1-time 2) is examined using a univariate family correlation model. This combined method is useful in assessing the degree to which the same familial factors are operating across time (interindividual cross-time correlations), as well as the degree to which different heritable components are involved across time (change score). Maximal heritabilities for SBP were about 70% at each time point, while for DBP the heritability was larger at time 1 (87%) than time 2 (39%). Both the change scores (48% for SBP and 54% for DBP) and the cross-time comparisons (58% to 72% for SBP and 63% to 65% for DBP) evidenced significant familial resemblance. These results illustrate how simple methodologies can be used to specify how familial etiologies underlying a trait may change across time. For BP, the model includes unique familial factors that are specific to each time measurement, and an additional familial factor which is common to both time points. The factors leading to differences in longitudinal familial resemblance for BP (i.e., the unique factors) may be primarily genetic in origin, while those leading to stability across time may include both genetic and familial environmental effects. Sex and/or age interactions with the genotypes are also suggested.

Adult↗

PubMed2000

The RsaI polymorphism in the alpha-fibrinogen gene and response of plasma fibrinogen to physical training--a controlled randomised clinical trial in men.

We have previously reported cross-sectional data on an interaction effect between physical activity and alpha-fibrinogen RsaI polymorphism on fibrinogen in postmenopausal women. In the present controlled randomised study, we investigated the role of the RsaI polymorphism in determining the response of fibrinogen to long-term regular exercise. Middle-aged men (n = 140), randomly selected from the population registry, were randomised into an exercise or a reference group for a 3-year low intensity exercise intervention. Complete data were available in 125 men. The RsaI restriction enzyme detects threonine (Thr) to alanine change in the fibrinogen alpha codon 312. Anaerobic ventilatory threshold increased by 4%, but decreased by 2% in the exercise and reference groups, respectively. Mean fibrinogen did not decrease in either study group. However, in the exercise group, individual changes in anaerobic threshold explained 48% of the variance in fibrinogen changes in the Thr homozygotes. Our data offer a new aspect of beneficial effects of regular physical exercise on risk factors for coronary heart disease.

Amino Acid Substitution↗

PubMed1999

Direct induction of cyclin D2 by Myc contributes to cell cycle progression and sequestration of p27.

Ectopic expression of Myc induces Cdk2 kinase activity in quiescent cells and antagonizes association of p27(kip1) with Cdk2. The target gene(s) by which Myc mediates this effect is largely unknown. We now show that p27 is rapidly and transiently sequestered by cyclin D2-Cdk4 complexes upon activation of Myc and that cyclin D2 is a direct target gene of Myc. The cyclin D2 promoter is repressed by Mad-Max complexes and de-repressed by Myc via a single highly conserved E-box element. Addition of trichostatin A to quiescent cells mimics activation of Myc and induces cyclin D2 expression, suggesting that cyclin D2 is repressed in a histone deacetylase-dependent manner in quiescent cells. Inhibition of cyclin D2 function in established cell lines, either by ectopic expression of p16 or by antibody injection, inhibits Myc-dependent dissociation of p27 from Cdk2 and Myc-induced cell cycle entry. Primary mouse fibroblasts that are cyclin D2-deficient undergo accelerated senescence in culture and are not immortalized by Myc; induction of apoptosis by Myc is unimpaired in such cells. Our data identify a downstream effector pathway that links Myc directly to cell cycle progression.

3T3 Cells↗

PubMed1999

Familial risk of obesity and central adipose tissue distribution in the general Canadian population.

The purpose of this study was to determine the familial risk of obesity and of an android profile of fat distribution in the general Canadian population. A sample of 15,245 participants aged 7-69 years from 6,377 households from the Canada Fitness Survey of 1981 was used. The body mass index (BMI), sum of five skinfolds (SF5), ratio of trunk-to-extremity skinfolds, adjusted for SF5, and waist circumference, adjusted for BMI were used as indicators of obesity and central fat distribution. Age- and sex-standardized risk ratios (SRRs) for spouses and first-degree relatives of obese probands indicate that there is significant familial risk for obesity and an android fat distribution in the Canadian population. SRRs for spouses and first-degree relatives of probands exceeding the 99th percentile are 3.01 and 4.96 for BMI, 7.36 and 4.15 for SF5, 1.41 and 3.18 for ratio of trunk-to-extremity skinfolds, adjusted for SF5, and 1.02 and 2.18 for waist circumference, adjusted for BMI, respectively. The SRRs are smaller for less extreme obesity (lower percentile cutoffs) than for more extreme obesity. The SRRs are greater in spouses than in first-degree relatives for SF5; however, the risk for BMI and an android fat distribution was greater among first-degree relatives than among spouses, suggesting a greater role for genetic factors.

Adipose Tissue↗

PubMed1999

Effect of long-term administration of antidepressant treatments on serotonin release in brain regions involved in obsessive-compulsive disorder.

BACKGROUND: Among all antidepressant treatments, including electroconvulsive shock (ECS) therapy and monoamine oxidase inhibitors (MAOIs), only the selective serotonin (5-HT) reuptake inhibitors (SSRIs) exert a clear therapeutic effect in obsessive-compulsive disorder (OCD). An 8-week, but not a 3-week treatment with the SSRI paroxetine results in an increased electrically evoked [3H]5-HT release and a desensitization of 5-HT autoreceptors in the guinea pig orbitofrontal cortex, a brain region implicated in OCD. METHODS: In the present study, the effect of long-term treatment with the SSRI fluoxetine, ECS, and the reversible type A MAOI moclobemide was investigated on evoked [3H]5-HT release from preloaded guinea pig brain slices prepared from the hypothalamus, cingulate cortex, and orbitofrontal cortex. RESULTS: Fluoxetine treatment yielded an enhanced [3H]5-HT release in the three brain areas, but a desensitization of the 5-HT autoreceptor only in the hypothalamus and orbitofrontal cortex. ECS treatment did not result in any alteration of the electrically evoked [3H]5-HT release or of 5-HT autoreceptor sensitivity in any of the brain regions. Moclobemide increased [3H]5-HT release only in the orbitofrontal cortex without any alteration in the 5-HT autoreceptor sensitivity. CONCLUSIONS: These findings indicate that only treatments effective in OCD have the capacity to desensitize the terminal 5-HT autoreceptor in the orbitofrontal cortex.

Animals↗

PubMed1999

Familial aggregation of body mass index and subcutaneous fat measures in the longitudinal Québec family study.

Family resemblance for several measures of body fat and fat distribution was explored in the longitudinal Québec Family Study (QFS), including an overall measure of adiposity (body mass index, BMI), total subcutaneous fat (the sum of 6 skinfolds, SF6), and subcutaneous fat distribution (the trunk to extremity ratio, TER). Repeated measures were taken twice approximately 12 years apart. A longitudinal familial correlation model was used to assess familial resemblance at each of times 1, 2, and cross-time, and a univariate model was used for the change score. The change score was assumed to index the degree to which different familial factors impacted on the longitudinal resemblance, while the cross-time comparisons indexed similar familial factors across time. For BMI, the maximal heritability was 44 and 36% at times 1 and 2, respectively, 37% for the change score, and 33-43% for the cross-time comparison. While the etiology of the BMI familial effect at times 1, 2, and cross-time was assumed to be primarily polygenic, that for the change score was a function of cohort effects (environmental). For SF6, the maximal heritability (primarily genetic) was low at time 1 and for the change score (16%), but was nonsignificant at time 2 and cross-time. For TER, the maximal heritabilities were significant for each of times 1 (42%), 2 (40%), change score (59%), and cross-time comparisons (35-36%). In summary, simple univariate familial correlation analysis of the change scores and bivariate analysis of the longitudinal measures are useful in delineating the underlying factors leading to both change and stability across time.

Adipose Tissue↗

PubMed1999

The human obesity gene map: the 1998 update.

An update of the human obesity gene map incorporating published results up to the end of October 1998 is presented. Evidence from the human obesity cases caused by single gene mutations; other Mendelian disorders exhibiting obesity as a clinical feature; quantitative trait loci uncovered in human genome-wide scans and in crossbreeding experiments with mouse, rat, and pig models; association and case-control studies with candidate genes; and linkage studies with genes and other markers is reviewed. The most noticeable changes from the 1997 update is the number of obesity cases due to single gene mutations that increased from three cases due to mutations in two genes to 25 cases due to 12 mutations in seven genes. A look at the obesity gene map depicted in Figure 1 reveals that putative loci affecting obesity-related phenotypes are found on all but chromosome Y of the human chromosomes. Some chromosomes show at least three putative loci related to obesity on both arms (1, 2, 3, 6, 7, 8, 9, 11, 17, 19, 20, and X) and several on one chromosome arm only (4q, 5q, 10q, 12q, 13q, 15q, 16p, and 22q). The number of genes and other markers that have been associated or linked with human obesity phenotypes is increasing very rapidly and now approaches 200.

Animals↗

PubMed1999

Segregation analysis of body mass index in a large sample selected for obesity: the Swedish Obese Subjects study.

OBJECTIVE: To investigate a major gene hypothesis for body mass index (BMI) in a large sample of probands (n = 2580, ages 37-57 years) who were selected for obesity (BMI> or =34 kg/m2 for males and > or =38 kg/m2 for females), along with their spouses and first-degree relatives (n = 11,204 family members). The probands were recruited as part of an intervention trial assessing whether mortality and morbidity were improved after surgical intervention for obesity as part of the Swedish Obese Subjects (SOS) study. METHODS AND PROCEDURES: The current analyses were based on BMI measures obtained before intervention. Segregation analysis was carried out using the mixed model implementation in PAP (Pedigree Analysis Package), which allowed for ascertainment correction and for genotype-dependent effects of covariates (sex and age) in both the major gene component and the multifactorial (i.e., polygenic and familial environment) component. RESULTS: Both a major effect and a multifactorial effect were significant. The percentage of the total variance accounted for by the multifactorial effect was 17%-24% (increasing as a function of age), and by the major effect, 8%-34% (decreasing as a function of age). Although tests on the transmission probabilities (taus) were not compatible with Mendelian expectations of 1, 1/2, and 0, the equal taus model was rejected (i.e., the effect is transmitted in families) and the point estimates (0.96, 0.60, and 0.17) compared favorably to Mendelian expectations. The major effect was transmitted in a codominant fashion, consistent with a gene-environment interaction. DISCUSSION: These results suggest both multifactorial and major effect etiologies for BMI in these families of extremely obese probands. Before 20 years of age, the major effect dominates the BMI expression, but after age 20, multifactorial effects account for the most variance. Although the major effect is transmitted in these families, the pattern does not appear to be consistent with a simple Mendelian trait. The possibility of additional major loci (i.e., epistasis) and gene by environment interactions may explain these findings.

Adult↗

PubMed1999

The use of anthropometric and dual-energy X-ray absorptiometry (DXA) measures to estimate total abdominal and abdominal visceral fat in men and women.

OBJECTIVE: A single-slice computed tomography (CT) scan provides a criterion measure of total abdominal fat (TAF) and abdominal visceral fat (AVF), but this procedure is often prohibitive due to radiation exposure, cost, and accessibility. In the present study, the utility of anthropometric measures and estimates of trunk and abdominal fat mass by dual-energy X-ray absorptiometry (DXA) to predict CT measures of TAF and AVF (cross-sectional area, cm2) was assessed. RESEARCH METHODS AND PROCEDURES: CT measures of abdominal fat (at the level of the L4-L5 inter-vertebral space), DXA scans, and anthropometric measures were obtained in 76 Caucasian adults ages 20-80 years. RESULTS: Results demonstrated that abdominal sagittal diameter measured by anthropometry is an excellent predictor of sagittal diameter measured from a CT image (r=0.88 and 0.94; Total Error [TE]=4.1 and 3.1 cm, for men and women, respectively). In both men and women, waist circumference and abdominal sagittal diameter were the anthropometric measures most strongly associated with TAF (r=0.87 to 0.93; Standard Error of Estimate (SEE)=60.7 to 75.4 cm2) and AVF (r=0.84 to 0.93; SEE=0.7 to 30.0 cm2). The least predictive anthropometric measure of TAF or AVF was the commonly used waist-to-hip ratio (WHR). DXA estimates of trunk and abdominal fat mass were strongly associated with TAF (r=.94 to 0.97; SEE=36.9 to 50.9 cm2) and AVF (r=0.86 to 0.90; SEE=4.9 to 27.7 cm2). DISCUSSION: The present results suggest that waist circumference and/or abdominal sagittal diameter are better predictors of TAF and AVF than the more commonly used WHR. DXA trunk fat and abdominal fat appear to be slightly better predictors of TAF but not AVF compared to these anthropometric measures. Thus DXA does not offer a significant advantage over anthropometry for estimation of AVF.

Abdomen↗

PubMed1999

Body fat, resting and exercise blood pressure and the angiotensinogen M235T polymorphism: the heritage family study.

OBJECTIVE: The association of resting and exercise blood pressure (BP) and fat mass with the angiotensinogen (AGT) M235T polymorphism was investigated in 522 sedentary Caucasian subjects from 99 families. RESEARCH METHODS AND PROCEDURES: Resting BP was measured on two separate days, three times each day, and the mean of six valid measurements was used. Exercise BP was measured during a cycle ergometer test at a constant power output (50 W). Body composition was derived from under-water weighing and the AGT M235T polymorphism was typed with a polymerase chain reaction-based method. RESULTS: Neither resting nor exercise BP was associated with the AGT genotypes. In mothers, the homozygotes for the T allele showed 8.8 kg and 7.1 kg greater (p=0.017) age-adjusted body fat mass (FM) than the MM homozygotes and heterozygotes, respectively. Sixty-nine percent of all TT homozygotes were found in the highest FM tertile, whereas only 16% of the MM homozygotes fell in the same tertile (p = 0.008). Moreover, a significant interaction was seen between FM and T-allele carrier status in women with regard to resting diastolic BP (p = 0.002). Among women with a FM> or =24 kg, carriers of the T allele showed a 6.3 mmHg higher diastolic blood pressure (DBP) than non-carriers whereas no difference was found in women with a FM less than 24 kg. A similar trend toward an interaction term was evident with resting systolic blood pressure (p = 0.011) and exercise DBP (p = 0.012). Body fat was not associated with the AGT polymorphism in fathers or in offspring. DISCUSSION: These data suggest that the AGT M235T polymorphism is associated with body fatness in women, and that the relationship between DBP and AGT M235T polymorphism is dependent on FM in middle-aged sedentary normotensive women.

Adipose Tissue↗

PubMed1999

Spousal resemblance and risk of 7-year increases in obesity and central adiposity in the Canadian population.

OBJECTIVE: Spousal similarities in 7-year changes in obesity and obesity-related phenotypes were examined in a subsample of 376 pairs of spouses from a sample of 1487 participants in the 1988 Campbell's Survey follow-up of the 1981 Canada Fitness Survey. MEASURES: Indicators of body fatness included the body mass index (BMI), the sum of five skinfolds (SF5), and waist circumference (WAIST), whereas those for relative adipose tissue (AT) distribution included the ratio of two trunk to three extremity skinfolds, adjusted for SF5 (TERadj), and WAIST adjusted for BMI (WAISTadj). RESULTS: Spouse correlations were 0.17, 0.17, and 0.17 for the BMI (p<0.05) and 0.20, 0.20, and 0.21 for SF5 (p<0.05) for the initial measurement, follow-up, and 7-year change, respectively. Spouse correlations for WAIST were somewhat lower: 0.16 (p<0.05), 0.11 (p<0.05), and 0.11 (p<0.05) for the initial measurement, follow-up, and 7-year change, respectively, whereas those for TERadj and WAISTadj were low and not significant. Spouses of probands who had increases in adiposity and central AT distribution had elevated risks of also increasing in these parameters. Spousal risks (risk ratios) were 1.48 (95% CI = 1.08-2.03), 1.49 (95% CI = 1.10-2.02), and 1.68 (95% CI = 1.28-2.21) for increases in BMI, SF5, and WAIST, respectively, whereas the risks for increases in central adiposity were 1.22 (95% CI = 0.86-1-73), and 1.05 (95% CI = 0.72-1.53) for TERadj, and WAISTadj, respectively. DISCUSSION: The results indicate significant spousal resemblance and risk for increases in fatness in the general Canadian population, whereas both the spousal resemblance and risks for increases in AT distribution, adjusted for level of fatness, are non-significant. The results suggest that shared environmental factors may be important determinants of spousal similarities in changes in total body fatness over time; however, cohabitation in the short term may not lead to increases in spousal resemblance.

Adipose Tissue↗