Biomedical subjects

T Rice

Publications and source records attributed to T Rice.

At least 19 recordsLinked to original sources

PubMed2006

Genome-wide scan to identify quantitative trait loci for baseline resting heart rate and its response to endurance exercise training: the HERITAGE Family Study.

Evidence of a genetic component for resting heart rate (RHR) has been found. Quantitative trait loci (QTLs) for baseline RHR have been reported, but not for RHR training response. It is of interest to identify QTLs that may harbor genes influencing RHR variation at baseline and in response to regular exercise training. Here, a multipoint variance components linkage scan using 654 markers was performed to search for QTLs that influence RHR adjusted for several covariates at baseline and in response to 20 weeks of endurance training (post-training minus baseline) in 99 White and 127 Black families in the HERITAGE Family Study. Potentially interesting linkages were revealed on 4 q and 11 p for baseline RHR, and on 1 q and 21 q for RHR training response in Whites. The QTLs on 2 q, 6 q, 7 q, 12 q, 14 q, and 15 q for baseline RHR, and on 3 p, 20 p and 21 q for RHR training response were found in Blacks. Promising linkages (lod scores >or= 1.75, p or= 135/80 mm Hg) subset of 40 White families suggesting a pleiotropic gene for BP and RHR with interactions. In conclusion, among QTLs on 1 q, 2 p, 3 p, 4 q, and 11 p that replicated across subsamples and studies, 11 p is most promising for dense mapping and association studies in HERITAGE and other cohorts.

Black People↗

PubMed2005

Genome-wide linkage scans for prediabetes phenotypes in response to 20 weeks of endurance exercise training in non-diabetic whites and blacks: the HERITAGE Family Study.

AIMS/HYPOTHESIS: Impaired insulin secretion, insulin action, insulin-independent glucose effectiveness, glucose tolerance and the associated abnormalities in insulin and glucose metabolism phenotypes are precursors of type 2 diabetes. Genome-wide multipoint variance component linkage scans were carried out using 654 markers to identify quantitative trait loci for insulin sensitivity, acute insulin response to glucose, disposition index and glucose effectiveness training responses in whites and blacks in the HERITAGE Family Study. METHODS: These phenotypes were obtained from an IVGTT with the minimal model. The distributions of insulin sensitivity, acute insulin response to glucose and disposition index training responses (post-training minus baseline) were approximately normalised using a square-root transformation. All phenotypes were adjusted for the effects of age, BMI and their respective baseline values within sex and generation by race prior to linkage scans. RESULTS: In blacks, a promising linkage with a maximum lod score of 3.1 on 19q (54-62 Mb) for glucose effectiveness training response was found. Six interesting linkages with lod scores of at least 1.0 were found for disposition index training response in whites. They included 1p (30 Mb), 3q (152 Mb), 6p (23-42 Mb), 7q (95-96 Mb), 10p (15 Mb) and 12q (119-126 Mb). CONCLUSIONS/INTERPRETATION: Quantitative trait loci for 20 weeks of endurance exercise training responses in insulin action and glucose metabolism phenotypes were found on chromosome 19q as well as 6p and 7q, with nominal (6p, 7q) but consistent (6p) linkages across the races.

Adolescent↗

PubMed2004

Quantitative trait loci for maximal exercise capacity phenotypes and their responses to training in the HERITAGE Family Study.

The purpose of this study was to identify regions of the human genome linked to maximal oxygen uptake (VO2max) and maximal power output (MPO), and their response to a standardized 20-wk endurance-training program in sedentary black and white subjects. A total of 509 polymorphic markers covering the 22 autosomes were used in the genome-wide linkage scan. Baseline phenotypes were adjusted for age, sex, and body mass, whereas the training responses were adjusted for age, sex, and the baseline values. Regression-based single- and multipoint linkage analyses were used. In the sedentary state, a total of 351 and 102 sibling pairs were available for whites and blacks, respectively, and 329 and 90 sibling pairs, respectively, for the training response phenotypes. Baseline VO2max showed promising linkage (P < 0.0023) with 11p15.1 (whites), and suggestive evidence of linkage (0.01 > P > 0.0023) was found on 1p31, 7q32, and 7q36 (blacks). Baseline MPO exhibited promising linkage on 10q23 and suggestive evidence of linkage on 13q33 and 18q11-q12 (whites). VO2max training response yielded promising linkages with markers on 1p31 (blacks) and suggestive on 4q27, 7q34, and 13q12 (whites) and on 16q22 and 20q13.1 (blacks). Training-induced changes in MPO showed promising linkages on 5q23 (whites) and suggestive on 1q21, 4p15.1, and 4p13 (whites) and on 1q22 and 13q11 (blacks). In conclusion, the strongest evidence of linkage was found on chromosomal regions 11p15 and 10q23 for VO2 max and MPO in the sedentary state and on chromosomes 1p31 and 5q23 for their responsiveness to training. These chromosomal regions harbor several candidate genes that deserve further investigation.

Adult↗

PubMed2003

Genome-wide linkage scan reveals multiple susceptibility loci influencing lipid and lipoprotein levels in the Quebec Family Study.

A genome-wide linkage study was performed to identify chromosomal regions harboring genes influencing lipid and lipoprotein levels. Linkage analyses were conducted for four quantitative lipoprotein/lipid traits, i.e., total cholesterol, triglyceride, HDL-cholesterol (HDL-C), and LDL-C concentrations, in 930 subjects enrolled in the Québec Family Study. A maximum of 534 pairs of siblings from 292 nuclear families were available. Linkage was tested using both allele-sharing and variance-component linkage methods. The strongest evidence of linkage was found on chromosome 12q14.1 at marker D12S334 for HDL-C, with a logarithm of the odds (LOD) score of 4.06. Chromosomal regions harboring quantitative trait loci (QTLs) for LDL-C included 1q43 (LOD = 2.50), 11q23.2 (LOD = 3.22), 15q26.1 (LOD = 3.11), and 19q13.32 (LOD = 3.59). In the case of triglycerides, three markers located on 2p14, 11p13, and 11q24.1 provided suggestive evidence of linkage (LOD > 1.75). Tests for total cholesterol levels yielded significant evidence of linkage at 15q26.1 and 18q22.3 with the allele-sharing linkage method, but the results were nonsignificant with the variance-component method. In conclusion, this genome scan provides evidence for several QTLs influencing lipid and lipoprotein levels. Promising candidate genes were located in the vicinity of the genomic regions showing evidence of linkage.

Adult↗

PubMed2003

Interactions among the beta2- and beta3- adrenergic receptor genes and total body fat and abdominal fat level in the HERITAGE Family Study.

OBJECTIVE AND SUBJECTS: Interactions between markers in the beta2- and beta3-adrenergic receptor (ADR) genes and total body fat and computerized tomography-measured abdominal fat phenotypes were studied in the HERITAGE Family Study cohort of Black (n=205; 81 males and 124 females) and White (n=415; 198 males and 217 females) subjects before and after an endurance training program. RESULTS: In Black subjects, beta2- and beta3-ADR gene variants showed evidence of interactions on changes in total body fat mass and abdominal fat area (P<0.005 and =0.010, respectively). Black subjects who were carriers of both beta2-ADR Arg16 and beta3-ADR Arg64 alleles had a greater decrease in total fat mass as well as abdominal total and subcutaneous, but not visceral fat areas in response to endurance training than subjects with other genotype combinations (P from 0.011 to 0.047). After correction for multiple tests, the findings remained essentially unchanged for total body fat mass and abdominal fat area, but became nonsignificant for subcutaneous fat area. The changes in abdominal fat correlated positively with the changes in fat mass (P<0.0001). The interactions between beta2 and beta3-ADR gene markers accounted for a maximum of 3% of the variances in the response of total fat mass and abdominal fat area to endurance training in Black subjects but it was not significant in White subjects. CONCLUSION: Interactions between sequence variants in the beta2-beta3-ADR gene contributed to the changes in fat mass and abdominal adiposity in response to endurance training in Black subjects.

Abdomen↗

PubMed2003

The agouti-related protein and body fatness in humans.

OBJECTIVE: The objective of this study was to examine the impact of a single nucleotide polymorphism (SNP) (-38C>T) in the promoter of the human agouti-related protein (hAgRP) gene on promoter affinity for transcription factors (TFs) and its possible association with body composition phenotypes. DESIGN: Electrophoretic mobility shift assays for the functional studies and association analyses for the population studies. SUBJECTS AND METHODS: Nuclear extracts were isolated from the mouse hypothalamus cell line GT1-7 and subjected to binding assays using oligonucleotide probes corresponding to the -38C>T region and an antibody for the E12/E47 TFs. Individuals (n = 259) from the HERITAGE Family Study were genotyped for the -38C>T SNP and used in the association studies. RESULTS: Electrophoretic mobility shift and supershift assays confirmed binding of the E12/E47 TF to the -38C>T site in a genotype-dependent manner. The T allele was found exclusively in the black subjects while the genotype with the higher binding affinity, CC, was significantly associated with high BMI, fat mass, and percent body fat in the black subjects of the HERITAGE Family Study. CONCLUSIONS: The E12/E47 TF could play a role in the regulation of hAgRP expression while the population studies suggest that the TT genotype of the -38C>T SNP could play a protective role against the development of obesity in the black population of the HERITAGE Family Study.

Adipose Tissue↗

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↗

PubMed2001

Effect of slow wave and REM sleep on thyropharyngeus and stylopharyngeus activity during induced central apneas.

The pharyngeal constrictors have been hypothesized to play an important role in the regulation of upper airway (UAW) patency in patients with sleep apnea. However, little research has focused on the activation and control of muscles that determine the lateral and posterior wall of the retropalatal airway dimensions. Our aim was to investigate the effects of slow wave sleep (SWS) and rapid eye movement (REM) sleep on the activation of pharyngeal constrictor (thyropharyngeus; TP) and dilator (stylopharyngeus; SP) muscles during eupneic breathing and induced central apneas. In nine goats, we found that eupneic TP and SP activity progressively decreased from awake to SWS (57 and 56%, respectively; P<0.01) and further in REM (25.6 and 19.9%, respectively; P<0.01). In contrast, diaphragm activity decreased equally during SWS and REM (89.3 and 87.7%, respectively; P<0.01) compared to awake. Following induced apneas while SP activity was eliminated in every state, maximal TP activity was highest in awake state (318.6% of control; P<0.02), less in SWS (157.6%; P<0.02), and nearly absent in REM (117.3%; P>0.02). During the recovery from an induced apnea when diaphragm activity was at 95% of its' control, awake TP activity remained significantly elevated and SP reduced (P>0.02) while TP activity during SWS was elevated and SP had returned to control level. During REM, TP and SP activity were not different from their reduced controls (P>0.02). The data supports our hypotheses that SWS and REM sleep causes a reduction in the eupneic TP and SP activity, as well as a reduction in TP response to induced apneas. However, the relative imbalance in TP vs SP activity during the recovery from an apnea (awake and SWS) suggest that an imbalance of active neuromuscular forces may contribute to upper airway narrowing in mixed apneas, but not in central apnea during sleep.

Animals↗

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↗

PubMed2001

Race differences in the pattern of familial aggregation for dehydroepiandrosterone sulfate and its responsiveness to training in the HERITAGE Family Study.

Using a familial correlation model to assess familial influences, baseline dehydroepiandrosterone sulfate (DHEAS) and its change (post-training minus baseline) in response to a 20-week endurance exercise training program were analyzed in 85 black families who participated in the HERITAGE Family Study (HERITAGE). Baseline levels were adjusted for a polynomial in age, and the training response was adjusted for a polynomial in age, as well as the baseline values, within 4 sex-by-generation groups before genetic analysis. We found that the maximal heritability for baseline DHEAS reached 66% (with no sex and generation differences) in black families, which is slightly (but not significantly) higher than the estimate (58%) reported previously in 99 white families in HERITAGE. Whereas weak, but significant, familial effects (26%) for the training response were previously reported for whites in HERITAGE, they were undetectable in the present study. Furthermore, we found heterogeneity in the pattern of familial aggregation (primarily due to different spouse and parent-offspring correlations) for both the baseline and its training response between blacks and whites. In conclusion, baseline DHEAS levels in blacks were also determined by substantial familial factors (just as for whites), independent of the effects of age and sex. Genetic and nongenetic familial components influencing baseline DHEAS levels in both races may be different.

Adolescent↗

PubMed2001

Genome-wide linkage scan to detect loci influencing levels of dehydroepiandrosterones in the HERITAGE Family Study.

A genome-wide linkage scan was performed to identify genomic regions that influence levels of dehydroepiandrosterone (DHEA), DHEA sulfate (DHEAS), and DHEA fatty acid esters (DHEA-FA) at baseline and in response to 20 weeks of endurance exercise training in sedentary white and black participants in the HERITAGE Family Study. The baseline levels were log-transformed and adjusted for the effects of age and sex prior to genetic analysis. The training responses were adjusted for the effects of age, sex, and the baseline values. A total of 509 autosomal component polymorphic markers were used for the genome scan with an average spacing of 6.0 Mb. Multipoint variance components linkage analyses were performed in nuclear families containing 360 white and 106 black sibling pairs. We found 5 genomic regions with significant linkages for baseline DHEA-FA in whites, with log odd (LOD) scores over 3.6 (P < 2 x 10(-5)). They include (1) D1S468 (LOD 4.56, 2.533 Mb, 1p36.22); (2) D2S177 (LOD 5.65, 52.663 Mb, 2p16.3); (3) D4S2397 (LOD 3.98, 32.246 Mb, 4p15.2); (4) the paraoxonase loci (LOD 3.93 approximately 3.99, 101.544 approximately 102.933 Mb, 7q21.3), and D7S821 (LOD 3.88, 104.497 Mb, 7q22.1); and (5) D12S372 (LOD 4.66, 2.129 Mb, 12q13.33). In addition, we obtained evidence of suggestive linkages (2.2 < LOD < 3.6; 2 x 10(-5) < P < 7 x 10(-4)) on chromosomes 3p, 6q, and 8q for baseline DHEAS; on chromosomes 2q, 3p, 9q, 10p, 16q, and 17p for baseline DHEA-FA in whites; and on chromosomes 9q and 11p for baseline DHEA in blacks. This is the first genome-wide linkage scan searching for genomic regions influencing human DHEA levels. Several potential candidate genes are located in these genomic regions, which warrant further studies in HERITAGE and other cohorts.

Adult↗

PubMed2001

Cardiac output and stroke volume changes with endurance training: the HERITAGE Family Study.

PURPOSE: The purpose of this study was to determine the magnitude of changes in cardiac output (Qc), stroke volume (SV), and arterial-mixed venous oxygen difference (a-vO2 diff) during submaximal exercise following a 20-wk endurance training program, with the primary focus on identifying differences in response by race, sex, and age. METHODS: The participants in this study (N = 631) were healthy and previously sedentary men (N = 277) and women (N = 354) of varying age (17-65 yr) and race (blacks, N = 217; whites, N = 414) who had completed the HERITAGE Family Study protocol. After baseline measurements, participants trained on cycle ergometers 3 d x wk(-1) for a total of 60 exercise sessions starting at the HR associated with 55% of maximal oxygen uptake (VO2max) for 30 min/session and building to the HR associated with 75% of VO2max for 50 min/session, which was maintained during the last 6 wk. HR, Qc (CO2 rebreathing), and SV (Qc/HR) were determined in duplicate at 50 W and at 60% of VO2max on two different days both before and after training. RESULTS: After training, there were significant decreases in HR and Qc, and significant increases in SV and a-vO2 diff at 50 W (except for no change in a-vO2 diff in black men). The changes in HR differed by sex and age, and the changes in SV, Qc, and a-vO2 diff differed by race. Qc decreased by 0.6 L x min(-1) at 50 W for the total sample, consistent with the decrease in VO2 at this power output. At 60% of VO2max HR decreased, and SV, Q, and a-VO2 diff increased. There were small differences in response by sex (HR and SV), race (HR), and age (HR and Qc). CONCLUSION: It is concluded that the cardiovascular systems of men and women, blacks and whites, and younger and older subjects are not limited in their ability to adapt to endurance training.

Adolescent↗

PubMed2001

Heart rate and blood pressure changes with endurance training: the HERITAGE Family Study.

PURPOSE: The purpose of this study was to determine the magnitude of change in resting and exercise heart rate (HR) and blood pressure (BP), by race, sex, and age, after a 20-wk endurance training program in 507 healthy and previously sedentary subjects from the HERITAGE Family Study. METHODS: After baseline measurements, subjects exercised on cycle ergometers 3 d x wk(-1) for a total of 60 exercise sessions starting at 55% of VO2max for 30 min x session(-1) and building to 75% of VO2max for 50 min x session(-1) for the last 6 wk. HR and BP at rest and during exercise (50 W, 60% of VO2max maximal exercise) were each determined in duplicate on two different days both before and after training (resting values at 24-h and 72-h posttraining). RESULTS: After the period of training, there was a small decrease in resting HR (-2.7 to -4.6 beats x min(-1) across groups at 72-h posttraining), and small changes (i.e., < 3 mm Hg) in resting systolic (SBP), diastolic (DBP), and calculated mean BP (MBP), which varied by race, sex, and age. During exercise at the same absolute work rate (50 W), HR, SBP, DBP, and MBP were all significantly reduced, with greater reductions in HR in women compared with men, and greater reductions in BP in blacks and older subjects compared with whites and younger subjects, respectively. At the same relative work rate (60% VO2max), HR, DBP, and MBP were reduced, but SBP remained unchanged. Blacks had a greater reduction in DBP, but whites had a greater reduction in HR. Finally, at maximal exercise, there was a small decrease in HR, with men and whites decreasing more than women and blacks; an 8 mm Hg increase in SBP, with men increasing more than women; a 4 mm Hg decrease in DBP, with blacks decreasing more than whites; and no change in MBP. CONCLUSION: In conclusion, the reductions in resting HR and BP with training were generally small, but the reductions during exercise were substantial and clinically important, with the older and the black populations experiencing greater reductions.

Adolescent↗

PubMed2001

Familial resemblance in ventilatory threshold: the HERITAGE Family Study.

PURPOSE: This study investigates the familial resemblance of VO2 at the ventilatory threshold (VO2vt) from 199 nuclear families (100 White and 99 Black) participating in the HERITAGE Family Study. METHODS: VO2vt (mL x min(-1)) was determined in the sedentary state and again after 20 wk of aerobic cycle ergometer exercise training in 339 individuals (131 parents and 228 of their offspring), aged between 17 and 65 yr. VO2vt was adjusted for weight, age, fat mass, and fat-free mass by using regression methods. RESULTS: There was evidence for significant familial resemblance in the sedentary state for VO2vt (maximal heritability = 58% in White and 54% in Black families) and VO2vt/VO2max (maximal heritability = 38% in White and 39% in Black families). Spouse, sibling, and parent-offspring relationships for VO2vt were significant at baseline, suggesting that both genetic and shared environmental factors may contribute to the familial resemblance in the sedentary state. There was a moderate familial component in the response of VO2vt to aerobic exercise training in Whites (22%) and a larger component in Blacks (51%). In Blacks, the familial effect for VO2vt/VO2max appeared to be accounted for by fat and fat-free mass. CONCLUSION: These results show a strong familial contribution to VO2vt in the sedentary state and to the response of VO2vt to aerobic exercise training.

Adolescent↗

PubMed2001

Individual autonomy and state involvement in health care.

This article examines the ethical basis for government involvement in health care. It first provides the case for individual autonomy, focusing on the justifications--particularly ethical ones--for allowing individuals to make their own choices in health care, and to control more of their own resources in doing so. Next, it provides the opposite case--for abridging individual autonomy, and in particular, for redistributing resources from those who are well off to those who are not. The overriding reason for favouring the latter case, which trumps the notion of individual autonomy, is to ensure that individuals who are at a disadvantage have an equal probability of attaining good health.

Decision Making↗

PubMed2001

Angiogenin gene-race interaction for resting and exercise BP phenotypes: the HERITAGE Family Study.

We examined the association between an angiogenin gene polymorphism and blood pressure (BP) at rest and in response to acute exercise before and after a 20-wk endurance-training program. Subjects were 737 normotensive and borderline hypertensive subjects (257 black and 480 white). The polymorphism was detected by PCR and digestion with AvaII, yielding an allele of 253 bp or a rare allele of 194 + 59 bp. Resting and exercise [50 W; 60, 80, and 100% of maximal O2 consumption (VO2 max)] systolic (SBP) and diastolic BP were determined before and after training. Among blacks, adjusted SBP in the sedentary state was significantly lower in carriers of the rare allele at rest and exercise intensities of 60, 80, and 100% of VO2 max. In the trained state, carriers of the rare allele had a significantly (P < 0.05) lower SBP than did noncarriers at rest and at 80 and 100% of VO2 max. The genotypic effect observed among blacks was not evident among whites. Furthermore, change in BP (after--before) was not significantly associated with the genotype. In conclusion, the angiogenin gene AvaII polymorphism is associated with a lower SBP at rest and in response to acute high-intensity exercise in blacks but not in whites.

Adult↗

PubMed2001

Genomic scan for genes affecting body composition before and after training in Caucasians from HERITAGE.

An autosomal genomewide search for genes related to body composition and its changes after a 20-wk endurance-exercise training program has been completed in the HERITAGE Family Study. Phenotypes included body mass index (BMI), sum of eight skinfold thicknesses, fat mass (FM), fat-free mass, percent body fat (%Fat), and plasma leptin levels. A maximum of 364 sib-pairs from 99 Caucasian families was studied with the use of 344 markers with single-point and multipoint linkage analyses. Evidence of significant linkage was observed for changes in fat-free mass with the S100A and the insulin-like growth factor I genes (P = 0.0001). Suggestive evidence (2.0 < or = Lod < 3.0; 0.0001 < P < or = 0.001) was also observed for the changes in FM and %Fat at 1q31 and 18q21-q23, in %Fat with the uncoupling protein 2 and 3 genes, and in BMI at 5q14-q21. At baseline, suggestive evidence was observed for BMI at 8q23-q24, 10p15, and 14q11; for FM at 14q11; and for plasma leptin levels with the low-density lipoprotein receptor gene. This is the first genomic scan on genes involved in exercise-training-induced changes in body composition that could provide information on the determinants of weight loss.

Adipose Tissue↗

PubMed2001

TGF-beta(1) gene-race interactions for resting and exercise blood pressure in the HERITAGE Family Study.

We examined the possible association between a transforming growth factor (TGF)-beta(1) gene polymorphism in codon 10 and blood pressure (BP) at rest, in acute response to exercise in the pretrained (sedentary) and trained states, as well as in its training response (Delta) to 20 wk of endurance exercise. Subjects were 257 black and 480 white, healthy sedentary normotensive subjects from the HERITAGE Family Study. The polymorphism was detected by polymerase chain reaction and digestion with the Msp A1 I endonuclease yielding a wild (leucine-10) and a mutant (proline-10) allele. Resting and exercise [50 W plus 60, 80, and 100% maximal oxygen consumption (VO(2)(max))] BP were determined before and after training. Significant (P < 0.05) race-genotype interactions were found for systolic (S) BP in both the sedentary and trained states. Among whites but not in blacks, the TGF-beta(1) genotypes were significantly (P < 0.05) associated with sedentary-state SBP at rest, at 50 W, and at 60 and 100% VO(2)(max)as well as with trained-state SBP at rest and at 80 and 100% VO(2)(max). The leucine-10 homozygotes had significantly (P < 0.05) lower SBP than proline-10 homozygotes. DeltaBP was not significantly associated with genotype. These results support the hypothesis of an association between the TGF-beta(1) marker in codon 10 and SBP at rest and in response to acute exercise in whites but not in blacks.

Adult↗