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Does cardiorespiratory fitness modify the association between birth weight and insulin resistance in adult life?

ABSTRACT: OBJECTIVE: Lower birth weight is associated with higher insulin resistance in later life. The aim of this study was to determine whether cardiorespiratory fitness modifies the association of birth weight with insulin resistance in adults. METHODS: The subjects were 379 Japanese individuals (137 males, 242 females) aged 20-64 years born after 1943. Insulin resistance was assessed using a homeostasis model assessment of insulin resistance (HOMA-IR), which is calculated from fasting blood glucose and insulin levels. Cardiorespiratory fitness (maximal oxygen uptake, VO2max) was assessed by a maximal graded exercise test on a cycle ergometer. Birth weight was reported according to the Maternal and Child Health Handbook records or the subject's or his/her mother's memory. RESULTS: The multiple linear regression analysis revealed that birth weight was inversely associated with HOMA-IR (β = -0.141, p = 0.003), even after adjustment for gender, age, current body mass index, mean blood pressure, triglycerides, HDL cholesterol, and smoking status. Further adjustments for VO2max made little difference in the relationship between birth weight and HOMA-IR (β = -0.148, p = 0.001), although VO2max (β = -0.376, p<0.001) was a stronger predictor of HOMA-IR than birth weight. CONCLUSIONS: The results showed that the association of lower birth weight with higher insulin resistance was little modified by cardiorespiratory fitness in adult life. However, cardiorespiratory fitness was found to be a stronger predictor of insulin resistance than was birth weight, suggesting that increasing cardiorespiratory fitness may have a much more important role in preventing insulin resistance than an individual's low birth weight.

SUBMITTER: Aoyama T

PROVIDER: S-EPMC3775791 | biostudies-other | 2013

REPOSITORIES: biostudies-other

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Project description:BackgroundExercise-induced improvements in cardiorespiratory fitness (CRF) often coincide with improvements in insulin sensitivity and reductions in liver fat content. However, there are limited data concerning the relationship between CRF and liver fat content in adults with varying degrees of metabolic dysfunction.MethodsThe aim of this study was to examine the association between CRF, liver fat content, and insulin resistance in inactive adults with obesity and with or without type 2 diabetes (T2D), via cross-sectional analysis. CRF was determined via a graded exercise test. Liver fat content was assessed via proton magnetic resonance spectroscopy and insulin resistance was assessed via homeostatic model of insulin resistance (HOMA-IR). A partial correlation analysis, controlling for age and gender, was performed to determine the association between CRF, demographic, cardiometabolic, and anthropometric variables. Independent t tests were performed to compare cardiometabolic outcomes between participants with T2D and participants without T2D.ResultsSeventy-two adults (46% male) with a mean age of 49.28 ± 10.8 years, BMI of 34.69 ± 4.87 kg/m2, liver fat content of 8.37 ± 6.90%, HOMA-IR of 3.07 ± 2.33 and CRF of 21.52 ± 3.77 mL/kg/min participated in this study. CRF was inversely associated with liver fat content (r = - 0.28, p = 0.019) and HOMA-IR (r = - 0.40, p < 0.001). Participants with T2D had significantly higher liver fat content (+ 3.66%, p = 0.024) and HOMA-IR (+ 2.44, p < 0.001) than participants without T2D. Participants with T2D tended to have lower CRF than participants without T2D (- 1.5 ml/kg/min, p = 0.094).ConclusionCRF was inversely associated with liver fat content and insulin resistance. Participants with T2D had lower CRF than those without T2D, however, the difference was not statistically significant. Further longitudinal studies are required to elucidate the relationship between CRF and the progression of obesity-related diseases such as T2D. Registration: ACTRN12614001220651 (retrospectively registered on the 19th November 2014) and ACTRN12614000723684 (prospectively registered on the 8th July 2014).

Project description:ObjectivePrior studies have shown that there is an inverse association between birth weight and stroke in adulthood; however, whether such association is causal remains yet known and those studies cannot distinguish between the direct fetal effect and the indirect maternal effect. The aim of the study is to untangle such relationship using novel statistical genetic approaches.MethodsWe first utilized linkage disequilibrium score regression (LDSC) and Genetic analysis incorporating Pleiotropy and Annotation (GPA) to estimate the overall genetic correlation between birth weight and stroke. Then, with a set of valid birth-weight instruments which had adjusted fetal and maternal effects, we performed a two-sample Mendelian randomization (MR) to evaluate its causal effect on stroke based summary statistics from large scale genome-wide association study (GWAS) (n = 264,498 for birth weight and 446,696 for stroke). We further validated the MR results with extensive sensitivity analyses.ResultsBoth LDSC and GPA demonstrated significant evidence of shared maternal genetic foundation between birth weight and stroke, with the genetic correlation estimated to -0.176. However, no fetal genetic correlation between birth weight and stroke was detected. Furthermore, the inverse variance weighted MR demonstrated the maternally causal effect of birth weight on stroke was 1.12 (95% confidence interval [CI] 1.00-1.27). The maternal ORs of birth weight on three subtypes of stroke including cardioembolic stroke (CES), large artery stroke (LAS) and small vessel stroke (SVS) were 1.16 (95% CI 0.93-1.43), 1.50 (95% CI 1.14-1.96) and 1.47 (95% CI 1.15-1.87), respectively. In contrast, no fetal causal associations were found between birth weight and stroke or the subtypes. Those results were robust against extensive sensitivity analyses, with Egger regression ruling out the possibility of pleiotropy and multivariable MR excluding the likelihood of confounding or mediation effects of other risk factors of stroke.ConclusionThis study provides empirically supportive evidence on the fetal developmental origins of stroke and its subtypes. However, further investigation is warranted to understand the pathophysiological role of low birth weight in developing stroke.