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C Bouchard

Publications and source records attributed to C Bouchard.

At least 37 records · Page 2Linked to original sources
PubMed2002

Allelic variants in the GABA(A)alpha6 receptor subunit gene (GABRA6) is associated with abdominal obesity and cortisol secretion.

INTRODUCTION: Cortisol is involved in the regulation of adipose-tissue differentiation, function and distribution, and in excess causes abdominal obesity. At the level of the brain, cortisol secretion is partly controlled by gamma-aminobutyric acid (GABA), which is the major inhibitory neurotransmitter in the vertebrate brain, and acts by binding to GABA(A) receptors. METHOD: We examined the potential impact of a 1519T>C polymorphism in the GABA(A)alpha6 receptor subunit (GABRA6) gene on obesity and obesity-related phenotypes as well as circulating hormones, including salivary cortisol in 284 unrelated Swedish men born in 1944. The subjects were genotyped by using PCR amplification of the 3' non-coding region of the GABRA6 gene followed by digestion with the restriction enzyme AlwNI. RESULTS: The frequency of allele T was 0.54 and 0.46 for allele C. Carriers for the T allele (n=211) had borderline significantly higher waist-to-hip ratio (P=0.094) and abdominal sagittal diameter (P=0.084) compared to homozygotes for the C allele (n=56). The homozygotes for the T allele had, in comparison to heterozygotes, significantly (P=0.004-0.024) higher mean cortisol levels at 11:45 am, and 30, 45 and 60 min after a standardized lunch and, finally, at 5:00 pm. In addition, T/T subjects had significantly (P=0.031) higher diurnal cortisol secretion compared to T/C subjects. Other hormones, glucose and serum lipids were not different across the genotype groups. CONCLUSION: These findings suggest a role of the 1519T>C polymorphism in GABRA6 in the predisposition to hypercortisolism and perhaps abdominal obesity. The pathophysiology may involve various environmental factors, particularly stress, that destabilize the GABA-hypothalamic-pituitary-adrenal systems in those with genetic vulnerability.

Abdomen↗
PubMed2002

Adiposity, adipose tissue distribution and mortality rates in the Canada Fitness Survey follow-up study.

OBJECTIVE: To compare mortality rates across indicators of adiposity and relative adipose tissue distribution in the Canadian population. SUBJECTS: The sample included 10,323 adult participants 20-69 y of age from the Canada Fitness Survey who were monitored for all-cause mortality over 13 y. METHODS: BMI, waist circumference (WC) and the sum of five skinfolds (SF5) were indicators of adiposity, and the first principal component of skinfold residuals (PC1) represented subcutaneous adipose tissue distribution. Proportional hazards regression was used to estimate relative mortality risk from mortality rates across levels of adiposity and adipose tissue distribution, controlling for the confounding effects of age, smoking status and alcohol consumption. RESULTS: :Significant curvilinear (J-shaped) relationships in men and linear relationships in women were observed between BMI, WC and SF5 and all-cause mortality rates. PC1 was not related to mortality rates in either men or women. In women, the inclusion of the other indicators of adiposity and adipose tissue distribution did not significantly add to the prediction of mortality rates beyond BMI; however, combinations of BMI and both WC and SF5 produced significant models in men. CONCLUSION: The results support the hypothesis that overall level of adiposity is an important predictor of all-cause mortality, more so than the relative distribution of subcutaneous body fat, once overall level of body fatness has been accounted for.

Adipose Tissue↗
PubMed2002

A C-1291G polymorphism in the alpha2A-adrenergic receptor gene (ADRA2A) promoter is associated with cortisol escape from dexamethasone and elevated glucose levels.

OBJECTIVES: The objective of the current study was to examine the potential impact of a C right arrow G substitution at position -1291 of the alpha2A-adrenergic receptor gene (ADRA2A) promoter on obesity and estimates of insulin, glucose, and lipid metabolism as well as circulating hormones, including salivary cortisol in 284 unrelated Swedish men born in 1944. MAIN OUTCOME MEASURES: The subjects were genotyped by using PCR amplification of the promoter region of the ADRA2A gene followed by digestion with the restriction enzyme MspI. RESULTS: The frequencies were 0.23 for allele C and 0.77 for allele G. The observed genotype frequencies were 45.8 and 54.2% for C/G and G/G, respectively. Heterozygotes (n=121) had significantly (P=0.009) higher salivary cortisol levels after 0.5 mg dexamethasone compared with G/G homozygotes (n=143). Fasting glucose was found to be significantly (P=0.017) higher in heterozygotes than in G/G homozygotes. The latter group had also a borderline significantly (P=0.080) higher mean diastolic blood pressure. 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, total testosterone, insulin-like growth factor I, serum leptin, fasting insulin and serum lipids were not different across the ADRA2A genotype groups. CONCLUSIONS: In conclusion, we have shown that an C --> G polymorphism at position -1291 of the ADRA2A gene is associated with a subnormal cortisol response to dexamethasone, elevated glucose levels and perhaps increased diastolic blood pressure. The pathophysiology could involve an altered density of the alpha2A-AR that destabilizes the sympathetic-hypothalamic-pituitary-adrenal systems in those with genetic vulnerability in the alpha2A-adrenergic receptor gene promoter.

Blood Glucose↗
PubMed2002

Lipoprotein lipase polymorphisms and responses to long-term overfeeding.

OBJECTIVES: The role of the lipoprotein lipase (LPL) gene Hind III, S447X, Bam HI and Pvu II polymorphisms on body composition and lipid and lipoprotein changes in response to long-term overfeeding was studied. SUBJECTS: Twelve pairs of male monozygotic twins ate a 4.2 MJ day-1 energy surplus, 6 days a week, during a period of 100 days. RESULTS: Overfeeding induced a decrease in high-density lipoprotein 2 cholesterol (HDL2-C) and HDL2-C to HDL3-C ratio in the H2H2 (n = 12) subjects of the LPL Hind III polymorphism. In contrast, the H1H1/H1H2 (n = 12) subjects experienced increases both in the HDL2-C and HDL2-C to HDL3-C ratio (P = 0.009 and 0.007, respectively, for differences in percentage changes between H2H2 and H1H1/H1H2). In addition, the H2H2 genotype was associated with higher levels of very-low-density lipoprotein triglyceride (VLDL-TG) (P < 0.03) and VLDL-C (P < 0.05) before and after overfeeding and higher HDL-TG levels (P < 0.003) after overfeeding. Postheparin lipoprotein lipase (PH-LPL) activity tended to increase in H1H1/H1H2 and decrease in H2H2 subjects. The H2H2 subjects had lower total HDL-C than those with the genotype H1H1/H1H2 4 months and 5 years after overfeeding (P = 0.04 and 0.10, respectively). The plasma lipid differences were similar amongst subjects with the S447S (n = 4) genotype of the S447X and H2H2 genotype of the Hind III polymorphisms. Body composition changes in response to overfeeding were not different between the Hind III genotypes. LPL Pvu II and Hind III polymorphisms were associated weakly with body weight gain (P = 0.015-0.039) but strongly with adipose tissue LPL activity (P < 0.01) after the caloric surplus. CONCLUSIONS: We conclude that the H2H2 subjects of the LPL gene Hind III polymorphism experience a decrease in the concentration of antiaterogenic lipoproteins when they are exposed to long-term positive energy balance. This may have been partly caused by a diminished catabolism of TG-rich particles in H2H2 subjects. LPL Pvu II and Bam HI polymorphisms were associated with body weight gain and adipose tissue LPL activity. Genetic variation at the LPL locus could thus be one of the factors responsible for the inter-individual differences observed in plasma lipid and lipoprotein responses to chronic positive energy balance. It must be kept in mind that the sample size for this study was small. Nonetheless, it provides useful information on the genes and pathways that should be further explored.

Adult↗
PubMed2002

Variability in the response of HDL cholesterol to exercise training in the HERITAGE Family Study.

In the HERITAGE Family Study, 675 sedentary, healthy, white and black men and women, aged 17 to 65 years, performed 20 weeks of supervised cycle ergometer exercise at the same relative intensity and weekly volume. As a group, subjects had normal mean baseline lipid levels for North Americans with the exception of below average high density lipoprotein cholesterol (HDL-C) levels. A significant mean increase in plasma HDL-C of 3.6 % was observed; however, there was marked variability in responsiveness to training, ranging from a mean 9.3 % decrease in Quartile 1 of HDL-C response to a mean 18 % increase in Quartile 4 (P < 0.0001 by ANOVA). Parallel changes in HDL(2)-C and HDL(3)-C, apolipoprotein A-I levels, and lipoprotein lipase activity were noted across quartiles. The change in HDL-C across quartiles was inversely related to baseline HDL-C (p < 0.0001) and to changes with training in plasma triglycerides (p = 0.0007). No significant differences in HDL-C response were observed across quartiles by sex, race, age, or increase in VO(2)max with training; however, weak positive associations were observed with age-adjusted education level and with reduction in abdominal fat and increase in VO(2)max at the ventilatory threshold following training. Multivariate regression analysis including baseline variables and training responses only accounted for 15.5 % of the variability in the HDL-C response to training. Thus, marked variability was found in the HDL-C response to the same endurance exercise training stimulus with only a modest amount of the response predictable by identified nongenetic factors.

Adaptation, Physiological↗
PubMed2002

Genetics and blood pressure response to exercise, and its interactions with adiposity.

Regular aerobic exercise has the potential to induce several beneficial health effects, including a decrease in blood pressure level, especially in hypertensive patients and in subjects with high-normal blood pressure. However, it is also well documented that some people show more pronounced blood pressure responses to endurance training than others, despite identical training programs and similar initial blood pressure levels. This kind of variation is an example of normal biologic diversity and most likely originates from interactions with genetic factors. Data from genetic epidemiologic studies indicate that there is a genetic component that affects both resting blood pressure and blood pressure responses to acute exercise. Evidence from molecular genetic studies is scarce, but the first reports suggest that DNA sequence variation in the hypertension candidate genes, such as angiotensinogen, also modify blood pressure responses to endurance training. The current knowledge regarding the role of genetic factors in the modification of blood pressure responses to endurance training will be summarized and discussed.

Adipose Tissue↗
PubMed2002

A +2138InsCAGACC polymorphism of the melanocortin receptor 3 gene is associated in human with fat level and partitioning in interaction with body corpulence.

BACKGROUND: The melanocortin system includes five receptors (MC1R to MC5R), and mouse and human MC4R has been shown to be involved in the regulation of feeding, and mouse MC3R in body composition. To verify a possible similar effect of MC3R in humans, we analyzed one insertion and one single nucleotide polymorphism by restriction fragment length polymorphisms (RFLP), and a microsatellite (D20S32e) in relation to body composition and glucose metabolism. METHODS: Eight hundred twelve subjects of the Québec Family Study (QFS) cohort were analyzed for body composition, food intake, and energy metabolism phenotypes. Southern Blot with the complete MC3R cDNA was used to detect a new +2138InsCAGACC variant by Pst1 restriction. PCR-RFLP with BsaJ1 was used to type amino acid polymorphism V81I arising from a G241A nucleotide change. PCR and automatic DNA sequencers were used for the analysis of the TG dinucleotide repeat D20S32e located between -1933/-1892 of MC3R. In a covariance analysis among genotypes, phenotypes were adjusted for age and sex as covariates. Food intake and energy metabolism phenotypes were also adjusted for body mass index (BMI), and leptin and abdominal fat, as assessed by a computed tomography scan, for fatness using six skinfold thicknesses. RESULTS: An association between the +2138InsCAGACC MC3R polymorphism was observed with fat mass (FM), percent body fat (%FAT), and total abdominal fat (ATF). Homozygote subjects for the +2138 insertion variant allele in normal weight (BMI < 25 kg/m(2)) and overweight (25 < or = BMI < 30 kg/m(2)) subjects showed a similar level of fatness despite the overall difference in BMI. In normal weight, homozygotes for the insertion allele showed higher mean values than heterozygotes and homozygotes for wild-type allele without insertion (%FAT: 24.0 +/- 1.1 versus 19.3 +/- 0.9 and 20.5 +/- 0.8, p = 0.0005; FM: 15.7 +/- 0.9 kg versus 11.7 +/- 0.7 kg and 12.6 +/- 0.6 kg, p = 0.0003). In contrast, overweight subjects homozygote for the variant allele showed lower mean values (%FAT: 27.0 +/- 1.2 versus 31.4 +/- 0.8 and 30.9 +/- 0.7, p = 0.002; FM: 18.3 +/- 1.0 kg versus 22.8 +/- 0.8 kg and 22.0 +/- 0.6 kg, p = 0.0001). This resulted in a similar level of body fat between both BMI groups for subjects homozygote for the insertion allele versus wild-type allele carriers (%FAT: +/-2-3% versus +/-10-12%; FM: +/-2 kg versus +/-9-11 kg). In obese subjects (BMI > or = 30 kg/m(2) ), a lower level of ATF was seen (-15%, p = 0.002). Other polymorphisms and phenotypes tested showed no association. CONCLUSION: A new 12138InsCAGACC MC3R polymorphism is associated with the level of adiposity and with body fat partitioning in interaction with corpulence in humans.

Adipose Tissue↗
PubMed2001

Regulation of cyclin D2 gene expression by the Myc/Max/Mad network: Myc-dependent TRRAP recruitment and histone acetylation at the cyclin D2 promoter.

Myc oncoproteins promote cell cycle progression in part through the transcriptional up-regulation of the cyclin D2 gene. We now show that Myc is bound to the cyclin D2 promoter in vivo. Binding of Myc induces cyclin D2 expression and histone acetylation at a single nucleosome in a MycBoxII/TRRAP-dependent manner. Down-regulation of cyclin D2 mRNA expression in differentiating HL60 cells is preceded by a switch of promoter occupancy from Myc/Max to Mad/Max complexes, loss of TRRAP binding, increased HDAC1 binding, and histone deacetylation. Thus, recruitment of TRRAP and regulation of histone acetylation are critical for transcriptional activation by Myc.

Acetylation↗
PubMed2001

Insulin-like growth factor 2 (IGF2 ) and IGF-binding protein 1 (IGFBP1) gene variants are associated with overfeeding-induced metabolic changes.

AIMS/HYPOTHESIS: The aim of this study was to investigate the role of insulin-like growth factor 1 (IGF1), IGF2, IGF binding protein 1 (IGFBP1) and IGFBP3 gene variants on the metabolic changes observed in response to a 100-day overfeeding protocol conducted with 12 pairs of monozygotic twins. METHODS: Genotyping was done by PCR-RFLP and DNA sequencer methods. Body fat measurements included hydrodensitometry and abdominal fat from computed tomography. Plasma glucose and insulin during fasting and in response to an OGTT were assayed. Plasma lipids were measured enzymatically. RESULTS: In response to caloric surplus, fasting plasma insulin (p < 0.05) and OGTT insulin (p = 0.004) but not glucose area, increased more among the subjects with IGF2 Apa I GG (n = 12) than those with AA + AG (n = 12). The changes were independent of changes in total fatness. The subjects with IGFBP1 Bgl II AA (n = 8) showed greater increases in abdominal visceral fat (p < 0.01), OGTT insulin area (p = 0.05) and total cholesterol (p < 0.03) with overfeeding than the subjects with AG + GG (n = 16). IGFBP3 Nde I and the IGF1 (CT)n markers were not associated with responsiveness to overfeeding. CONCLUSION/INTERPRETATION: Insulin sensitivity decreased in the subjects with IGF2 Apa I GG and the subjects with IGFBP1 Bgl II AA showed an accumulation of abdominal visceral fat and the early symptoms of the metabolic syndrome after long-term caloric surplus. Genetic variation at the IGF2 and IGFBP1 loci could be among the factors responsible for the inter-individual differences observed in the response to long-term alterations in energy balance and should be further investigated in larger cohorts.

Abdomen↗
PubMed2001

A missense mutation in the human melanocortin-4 receptor gene in relation to abdominal obesity and salivary cortisol.

AIMS/HYPOTHESIS: The melanocortin-4 receptor (MC4-R) regulates food intake and possibly energy expenditure, and the inactivation of the MC4-R by gene targeting results in obesity, a phenotype strongly associated with Type II (non-insulin-dependent) diabetes mellitus. In our study, we addressed the hypothesis that a G-->A substitution at codon 103 (Val-103Ile) of the MC4R gene influences abdominal obesity, insulin, glucose, and lipid metabolism as well as circulating hormones, including salivary cortisol. METHODS: We genotyped the missense variant at codon 103 of the MC4R gene in 284 unrelated Swedish men born in 1944 by using polymerase chain reaction amplification followed by digestion with the restriction enzyme HincII. RESULTS: The frequency of allele G was 0.97 and 0.03 for allele A. The observed genotype frequencies were 95 % and 5 % for G/G and G/A, respectively. The heterozygotes had lower waist-to-hip ratio (p = 0.023) and trends for lower body mass index (p = 0.054) and abdominal sagittal diameter (p = 0.095) compared to G/G homozygotes. Moreover, G/A subjects had borderline lower serum leptin concentrations (p = 0.087) and total cholesterol (p = 0.082). The heterozygotes had also, in comparison to G/G subjects, significantly (p < 0.01) higher mean cortisol concentrations in the morning (21.4 vs 14.6 nmol/l), at ll:45 h (11.6 vs 7.0 nmol/l), 30 min after a standardized lunch (15.3 vs 8.0 nmol/l) and finally, 60 min after lunch (10.8 vs 6.7 nmol/l). CONCLUSION/INTERPRETATION: These findings suggest that the missense mutation in the MC4R gene could contribute to the variability in body mass, abdominal fat distribution and leptin concentrations in the general population. Moreover, the G/A mutation exhibits evidence of associations with diurnal cortisol levels.

Abdomen↗
PubMed2001

Comparison of a novel norgestimate/ethinyl estradiol oral contraceptive (Ortho Tri-Cyclen Lo) with the oral contraceptive Loestrin Fe 1/20.

This multicenter study compared the contraceptive efficacy, cycle control, and safety of a new triphasic norgestimate (180/215/250 microg)/ethinyl estradiol 25 microg regimen (Ortho Tri-Cyclen Lo) (n = 1,723) with that of norethindrone acetate 1 mg/ethinyl estradiol 20 microg (Loestrin Fe 1/20) (n = 1,171). Healthy women were treated for up to 13 cycles. Demographics were similar between regimens. Contraceptive efficacy was comparable for Ortho Tri-Cyclen Lo and Loestrin Fe 1/20. The overall and method failure probabilities of pregnancy through 13 cycles were 1.9% and 1.5%, respectively, with Ortho Tri-Cyclen Lo and 2.6% and 2.4%, respectively, with Loestrin Fe 1/20. Breakthrough bleeding and spotting was reported by a significantly lower percentage of participants in the Ortho Tri-Cyclen Lo group compared with the Loestrin Fe 1/20 group. At representative Cycles 1, 3, 6, 9, and 13, breakthrough bleeding and spotting rates were 16.3, 11.5, 10.3, 7.9, and 7.7%, respectively, in the Ortho Tri-Cyclen Lo group and 34.9, 22.9, 22.2, 15.9, and 13.1%, respectively, in the Loestrin Fe 1/20 group. Compliance and safety data were similar for the two regimens.

Administration, Oral↗
PubMed2001

Glucocorticoid receptor Bcl I variant is associated with an increased atherogenic profile in response to long-term overfeeding.

The effect of the glucocorticoid receptor (GRL) gene Bcl I polymorphism on body composition and metabolic changes in response to overfeeding was studied. Twenty-four men (mean age 21+/-2 years) who constituted 12 pairs of identical twins ate a 4.2 MJ/day energy surplus, 6 days a week, during a period of 100 days. The GRL Bcl I marker was identified by Southern Blot technique. Total body fat was assessed by hydrodensitometry and abdominal fat areas were measured by computed tomography. Fasting plasma glucose and insulin during an oral glucose tolerance test (OGTT) were assayed. The insulin and glucose areas were computed using the trapezoidal method. Triglyceride and cholesterol concentrations in plasma and lipoprotein fractions were determined enzymatically. The results showed that overfeeding induced a greater increase in body weight (p=0.002) in the 2.3/2.3 kb (n=12) than in the 4.5/2.3 kb (n=12) subjects. In addition, plasma levels of total (p=0.007) and low-density lipoprotein (LDL) cholesterol (p=0.003), as well as systolic blood pressure (p=0.036) increased more in the 2.3/2.3 kb than in the 4.5/2.3 kb subjects. The 2.3/2.3 kb genotype was also associated with a greater increase in abdominal visceral fat (p=0.040) compared to the 4.5/2.3 kb genotype. In conclusion, 2.3/2.3 kb subjects of the GRL Bcl I polymorphism experience greater increases in body weight, blood pressure and cholesterol levels as well as visceral fat than 4.5/2.3 kb subjects in response to overfeeding. These data suggest that overfeeding induces an atherogenic profile in subjects who are homozygotes for the 2.3 kb allele.

Adult↗
PubMed2001

Genetic variation at the lipoprotein lipase locus and plasma lipoprotein and insulin levels in the Québec Family Study.

The associations between the S447X, BamHI, HindIII and PvuII DNA variants of the lipoprotein lipase (LPL) gene and indicators of body fat, fat distribution and plasma lipids and insulin were studied in the Québec Family Study cohort. Strong linkage disequilibrium among all the markers was observed. For the S447X polymorphism, plasma very low density lipoprotein (VLDL)-cholesterol (chol) (P<0.001), total triglyceride (TG) (P=0.033) and VLDL-TG (P<0.001) levels were lower and high density lipoprotein (HDL)-chol level higher (P<0.001) in the subjects homozygous or heterozygous for X447 (X447+, n=160) compared to the homozygotes for the S447 allele (X447-, n=576). The BamHI, PvuII and HindIII polymorphisms were not associated with the plasma lipid values when all X447 allele carriers were removed. In addition, the HindIII polymorphism as well as the HindIII and S447X markers combination influenced the insulin area under the curve during an oral glucose tolerance test. We conclude that DNA sequence variation in the LPL gene contributes significantly to the variability in the levels of VLDL-chol, total- and VLDL-TG as well as HDL-chol. The effects of the other polymorphisms considered here are most likely mediated by their linkage disequilibrium with the S447X mutation. In addition, genetic variation at the LPL locus may, by an unknown mechanism, influence insulin metabolism but not body fat variability.

Adult↗
PubMed2001

Race differences in the response of postheparin plasma lipoprotein lipase and hepatic lipase activities to endurance exercise training in men: results from the HERITAGE Family Study.

Endurance exercise training is known to produce favorable changes in the metabolic profile including reduced plasma triglyceride (TG) and increased high-density lipoprotein (HDL) cholesterol concentrations. These metabolic improvements are likely to contribute to the reduced coronary heart disease (CHD) risk often observed in physically active individuals. However, the physiological mechanisms responsible for such improvements in TG and HDL cholesterol concentrations with endurance exercise are not fully understood. The effect of a 20-week endurance exercise training program on plasma lipoproteins as well as on post-heparin plasma lipoprotein lipase (PH-LPL) and hepatic lipase (PH-HL) activities were therefore examined in a sample of 200 White and 69 Black men who were part of the HERITAGE Family Study. As expected, there were decreases in adiposity and in abdominal fat accumulation following training in both White and Black men. We also found that exercise training was associated with decreases in plasma cholesterol, TG and apolipoprotein B levels, as well as with an increase in HDL cholesterol concentrations in White men. In contrast, Black men showed an increase only in HDL(2) cholesterol over the 20-week period. Higher PH-LPL and lower PH-HL activities were noted in both ethnic groups at follow-up. Whereas in White men improvement of the lipoprotein-lipid profile was related to increased PH-LPL activity, no association between PH-LPL (or PH-HL) and lipoprotein-lipid variables was observed in Black men. Results of the present study suggest that in Whites, the increase in PH-LPL activity in response to endurance exercise training is associated with a better lipoprotein-lipid profile, therefore reducing CHD risk. However, the generally better metabolic profile of Black individuals may minimize further improvement of lipoprotein-lipid concentrations by exercise training.

Adipose Tissue↗
PubMed2001

Stability of indicators of the metabolic syndrome from childhood and adolescence to young adulthood: the Québec Family Study.

The stability of indicators of the metabolic syndrome from childhood and adolescence to young adulthood was examined. The sample included 76 males and 71 females measured between the ages of 8 and 18 years and again as young adults (12 year follow-up). Indicators included the sum of three trunk skinfolds (SF3), mean blood pressure (MBP), and fasting blood glucose (GLY), high-density lipoprotein cholesterol (HDL-C), ratio of total cholesterol to HDL-C (CHOL/HDL), and triglycerides (TG). The indicators were subjected to principal components analysis to obtain a composite risk factor index (RFI). Partial interage correlations, controlling for initial age and length of follow-up, were 0.70 and 0.50 for SF3, 0.40 and 0.54 for MBP, 0.58 and 0.56 for HDL-C, 0.51 and 0.57 for CHOL/HDL, 0.37 and 0.20 (NS) for TG, 0.30 and 0.14 (NS) for GLY, and 0.51 and 0.46 for the RFI, in males and females, respectively. The results indicate that indicators of the metabolic syndrome are moderately stable from childhood and adolescence into young adulthood.

Adolescent↗
PubMed2001

Original article underweight, overweight and obesity: relationships with mortality in the 13-year follow-up of the Canada Fitness Survey.

The purpose of this study was to determine the risk of all-cause mortality in the Canadian population across the new WHO/NIH BMI categories for the classification of overweight and obesity. The sample includes 10,725 adult participants (20-69 years) in the 1981 Canada Fitness Survey. A total of 593 deaths occurred during 13 years of follow-up. Hazard ratios (HR) for mortality were estimated using Cox proportional hazards models. Compared to normal weight individuals, there is an increased risk of mortality in the underweight category (HR 1.63, 95% CI 0.93-2.85) in addition to increasing levels of risk across the overweight (HR 1.16, 95% CI 0.96-1.39), obese class I (HR 1.25, 95% CI 0.96-1.65) and obese class II and III (HR 2.96, 95% CI 1.39-6.29) categories. Similar patterns were observed in sex-specific analyses. Underweight, overweight and obese Canadians are all at increased risk of mortality compared to those who are normal weight.

Adult↗
PubMed2001

Familial resemblance for glucose and insulin metabolism indices derived from an intravenous glucose tolerance test in Blacks and Whites of the HERITAGE Family Study.

Type 2 diabetes mellitus (T2DM), characterized by hyperglycemia, is a complex disease primarily caused by impairment in insulin sensitivity (SI) and insulin secretion. While a strong genetic component for T2DM is well established, there are few reports on racial differences in the magnitude of the genetic effects of T2DM and indices of glucose and insulin metabolism. We report here on the familial resemblance for traits related to glucose metabolism at pre-exercise training levels in 492 members from 99 sedentary White families and 259 members from 108 Black families participating in the multicenter HERITAGE Family Study. All these traits were obtained from the frequently sampled intravenous glucose tolerance test (IVGTT). They include glucose disappearance index (Kg), an overall index for glucose tolerance, acute insulin response to glucose (AIR(Glucose)) which is an index for insulin secretion, and those derived from the minimal model including SI and the disposition index (DI). DI, derived as the product of SI and AIR(Glucose), is a measure of the activity of the B-cells adjusted for insulin resistance. After adjustment for age, sex, and body mass index, the maximal heritability estimates in Blacks (Whites) are 48+/-14% (25+/-8%) for Kg, 44+/-14% (46+/-8%) for AIR(Glucose), 38+/-12% (44+/-8%) for SI and 32+/-14% (24+/-8%) for DI. Interestingly, Blacks have higher heritability for overall glucose tolerance than Whites but there is no race difference in heritability estimates for insulin sensitivity or insulin secretion.

Adult↗