Key result
Parental obesity and diabetes are linked to adverse serum adipokine profiles in nonobese, nondiabetic offspring.
Why the study?
Adipokines are implicated in obesity-related traits, but the association of parental obesity or diabetes with adipokine profiles in nonobese nondiabetic offspring is unclear.
Does parental history of obesity or diabetes mellitus alter circulating adipokine profiles in nonobese, nondiabetic offspring?
Cohort (n=2,034)
Does parental history of obesity or diabetes mellitus alter circulating adipokine profiles in nonobese, nondiabetic offspring?
Answers are grounded in this paper and cite their sources.
Parental history of diabetes or obesity is associated with an altered adipokine profile in nonobese, nondiabetic offspring, suggesting early preclinical biomarker alterations.
Background Adipokines are implicated in the development of obesity‐related traits. We hypothesized that nonobese participants without diabetes mellitus (DM) whose parents were obese or hadDMwould have altered circulating adipokines compared with those without parental history of these conditions. Methods and Results Participants in the community‐based Framingham Third Generation cohort who were not obese (body mass index <30) and not diabetic with both parents in the Framingham Offspring cohort were included in this analysis (n=2034, mean age 40 years, 54% women). Circulating concentrations of fetuin A, RBP4 (retinol binding protein 4), FABP4 (fatty acid binding protein 4), leptin, LEP‐R (leptin receptor), and adiponectin were assayed. ParentalDMwas defined as occurring before age 60 years, and obesity was defined as body mass index ≥30 before age 60 years. General estimating equations were used to compare concentrations of adipokines among participants with 0, 1, or 2 parents affected by obesity orDM(separate analyses for each), adjusting for known correlates of adipokines. Overall, 44% had at least 1 parent who was obese and 15% had parents withDM. Parental obesity was associated with higher serum levels ofFABP4 andLEP‐R in their offspring (P=0.02 for both). ParentalDMwas associated with lower adiponectin but higherRBP4 concentrations in offspring (P≤0.02 for both). Conclusions In our community‐based sample, a parental history ofDMor obesity was associated with an altered adipokine profile in nonobese nondiabetic offspring. Additional studies are warranted to evaluate whether such preclinical biomarker alterations presage future risk of disease.
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Zachariah et al. (2017) conducted a cohort in Nonobese nondiabetic offspring (n=2,034). Parental obesity and diabetes mellitus vs. No parental history of obesity or diabetes mellitus was evaluated on Circulating concentrations of adipokines (fetuin A, RBP4, FABP4, leptin, LEP-R, and adiponectin) (p=≤0.02). Parental obesity was associated with higher serum FABP4 and LEP-R, and parental diabetes with lower adiponectin and higher RBP4 in nonobese, nondiabetic offspring.
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