Biomedical subjects

Jennifer A McKenzie

Publications and source records attributed to Jennifer A McKenzie.

3 recordsLinked to original sources

PubMed2006

C-reactive protein genotype affects exercise training-induced changes in insulin sensitivity.

An etiologic role for chronic inflammation in the development of insulin resistance has been hypothesized. We determined whether the -732A/G and +219G/A C-reactive protein (CRP) gene variants affect insulin and glucose measures and whether these variants affect training-related changes in insulin sensitivity and glucose measures. Men and women 50 to 75 years old (n = 61) underwent baseline testing that included glucose tolerance, maximal oxygen consumption, body composition, CRP levels, and genotyping assessments. Tests were repeated after 24 weeks of aerobic exercise training. In bivariate analyses, CRP -732A/G G allele carriers had significantly lower baseline postprandial plasma glucose and after-training CRP levels. After exercise training, the -732A/G G allele carriers had approximately 28% increase in insulin sensitivity index (ISI) and approximately 26% reduction in insulin area under the curve (AUC), compared with the approximately 7% increase in ISI and approximately 15% reduction in insulin AUC in the A allele homozygotes (P = .03). The significant enhancement of ISI in -732A/G G allele carriers remained evident in analyses limited to those with normal glucose tolerance. Multivariate analyses adjusted for demographic and biologic variables confirmed the significant enhancement of training-induced improvement in ISI by the CRP gene variant. In addition, the CRP -732A/G and +219G/A haplotype significantly associated with training-induced improvements in ISI and insulin AUC in separate multivariate models. In conclusion, the CRP -732A/G variant modulates exercise training-related improvements in ISI and glucose AUC, and the haplotype of the CRP -732A/G and +219G/A variants significantly affected training-induced changes in ISI and insulin AUC.

Aged↗

PubMed2004

Influence of the interleukin-6 -174 G/C gene polymorphism on exercise training-induced changes in glucose tolerance indexes.

A polymorphism in the IL-6 gene, a G-to-C substitution 176 bp upstream of the ATG translation initiation site, has been associated with diabetes prevalence and insulin resistance. Interventions including exercise training are frequently used to modify cardiovascular disease risk factors. Consequently, this project examined associations between the IL-6 -174 genotype and oral glucose tolerance test outcomes in 50- to 75-yr-old sedentary men and postmenopausal women before and after aerobic exercise training. Among the 87 individuals who started the study, 56 were retested after 6 mo of aerobic exercise training. Subject characteristics at baseline did not differ between the IL-6 genotype groups with the exception of fasting glucose, which was higher (P = 0.02, covariates age, gender, and ethnicity) in the CC genotype group. The training-induced change in glucose area under the curve during the oral glucose tolerance test varied between the IL-6 -174 genotype groups (P = 0.05, covariates age, gender, ethnicity, baseline glucose area under the curve, and percent body fat change) with a significant decrease occurring only in the GG genotype group. Insulin outcomes did not differ among the groups at baseline or after training. Training-induced changes in weight, percent body fat, maximal oxygen consumption, fasting glucose, and an insulin sensitivity index also changed similarly among the genotype groups. In conclusion, fasting glucose and the extent to which glucose tolerance changes with exercise training may be influenced by the IL-6 -174 gene polymorphism.

Age Factors↗

PubMed2004

Plasma nitrate/nitrite response to an oral glucose load and the effect of endurance training.

To assess the role of circulating nitric oxide (NO) production in glucose homeostasis, plasma nitrate/nitrite (NO(x)) was assessed during oral glucose tolerance tests (OGTTs) on 64 sedentary subjects and in a subset 40 subjects before and after 6 months of endurance exercise training. NO(x) decreased with the oral glucose load (P </=.001 for linear and quadratic effects). OGTT NO(x) response indices (NO(x) response area (NO(x) AREA), change in NO(x) from baseline to the minimum (DeltaNO(x)), and NO(x) time-to-minimum) were not associated with OGTT insulin or glucose areas under the curve (AUCs) or with insulin sensitivity index (ISI). Training did not alter NO(x) AREA, or DeltaNO(x), however, NO(x) time-to-minimum occurred later after training (P =.038). Training-induced insulin AUC and ISI changes were not associated with OGTT NO(x) index changes; however, glucose total AUC changes were associated with changes in NO(x) AREA (r =.42, P =.007) and DeltaNO(x) (r =.37, P =.019). In conclusion, these data suggest that circulating NO production is not involved in glycemic control after an oral glucose load in sedentary adults. In response to endurance training, however, it appears that the time required to reach minimum NO(x) levels after a glucose load is greater after training. Furthermore, although the magnitude of NO(x) response (as indicated by NO(x) AREA and DeltaNO(x)) to an oral glucose load does not appear to change with training for all individuals, individual training-induced changes in the NO(x) response magnitude are partly explained by training-induced changes in OGTT glucose responses.

Administration, Oral↗