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Objective: Despite studies on offspring obesity and delayed parenthood, little attention has been paid to the central obesity of offspring. The purpose of this study was to test the hypothesis that maternal age at childbirth (MAC) was associated with central obesity in offspring among the adult population, and fasting insulin may play a role in this association as a mediating factor. Methods: A total of 423 adults (mean age 37.9 years, 37.1% female) were included. Information about maternal variables and other confounders was collected by face‐to‐face interview. Waist circumference and insulin were determined through physical measurements and biochemical examinations. Logistic regression model and restricted cubic spline model were used to analyze the relationship between MAC and central obesity of offspring. The mediating effect of fasting insulin levels on association between MAC and offspring waist circumference was also analyzed. Results: There was a nonlinear relationship between MAC and central obesity in offspring. Compared with subjects with MAC 27–32 years, those with MAC 21–26 years (OR = 1.814, 95% CI: 1.129–2.915) and MAC ≥33 years (OR = 3.337, 95% CI: 1.638–6.798) had higher odds to develop central obesity. Offspring fasting insulin was also higher in MAC 21–26 years and MAC ≥33 years compared with those with MAC 27–32 years. Taking the group MAC 27–32 years as reference, the mediating effect of fasting insulin levels on the waist circumference was 20.6% and 12.4% for MAC 21–26 years and ≥ 33 years, respectively. Conclusion: MAC 27–32 years has the lowest odds of central obesity in offspring. Fasting insulin levels may have a partial mediating effect on the association between MAC and central obesity. [ABSTRACT FROM AUTHOR]

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Objectives: Vitamin D deficiency was associated with obesity. However, the causal relationship remains controversial. We hypothesized that there would be family-based associations in both vitamin D deficient families and obese families for the SNPs associated with vitamin D deficiency, if vitamin D deficiency was a causal factor of obesity. We aimed to investigate the family-based association of SNPs in CYP27B1 with both vitamin D deficiency and obesity.Methods: Four hundred and nineteen pedigrees containing 1505 rural individuals aged from 18 to 79 years in Henan Province of China were included in this study. Family-based associations of rs10877012 and rs4646536 in CYP27B1 with vitamin D deficiency and obesity were investigated. Serum 25(OH)D3 concentration <20 μg/L was defined as vitamin D deficiency. BMI ≥ 28 kg/m2 was applied for obesity definition. Taqman assays were applied for SNP genotyping. Family-based associations were investigated with FBAT software.Results: It was shown that vitamin D deficiency was a risk factor of obesity (adjusted OR: 1.332, 95% CI: 1.042-1.703, P = 0.022). Furthermore, there were family-based associations for allele T of rs10877012 and allele T of rs4646536 in both vitamin D deficient families and obese families (P < 0.05). Both rs10877012 and rs4646536 were associated with serum 25(OH)D3 levels between siblings (P < 0.05), but not BMI (P > 0.05). In addition, there is linkage disequilibrium between rs10877012 and rs4646536 (D' = 1.0, r2 = 0.992).Conclusion: Vitamin D deficiency may be a causal factor of obesity. Maintaining sufficient vitamin D is beneficial to obesity prevention. [ABSTRACT FROM AUTHOR]