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dc.contributor.authorLieb, Wolfgangen_US
dc.contributor.authorPencina, Michael J.en_US
dc.contributor.authorLanier, Katherine J.en_US
dc.contributor.authorTofler, Geoffrey H.en_US
dc.contributor.authorLevy, Danielen_US
dc.contributor.authorFox, Caroline S.en_US
dc.contributor.authorWang, Thomas J.en_US
dc.contributor.authorD'Agostino, Ralph B.en_US
dc.contributor.authorVasan, Ramachandran S.en_US
dc.date.accessioned2011-12-29T21:03:21Z
dc.date.available2011-12-29T21:03:21Z
dc.date.issued2011-12-29
dc.identifier.citationLieb, Wolfgang, Michael J. Pencina, Katherine J. Lanier, Geoffrey H. Tofler, Daniel Levy, Caroline S. Fox, Thomas J. Wang, Ralph B. D'Agostino, Ramachandran S. Vasan. "Association of Parental Obesity With Concentrations of Select Systemic Biomarkers in Nonobese Offspring " Diabetes 58(1): 134-137. (2009)en_US
dc.identifier.issn1939-327Xen_US
dc.identifier.urihttp://hdl.handle.net/2144/2539
dc.description.abstractOBJECTIVE: Parental obesity is a risk factor for offspring obesity. It is unclear whether parental obesity also confers risk for obesity-associated conditions (e.g., a proinflammatory or prothrombotic state) in the absence of offspring obesity. RESEARCH DESIGN AND METHODS: We compared concentrations of multiple biomarkers representing distinct biological pathways (C-reactive protein [CRP], aldosterone, renin, B-type natriuretic peptide, NH2-terminal proatrial natriuretic peptide, fibrinogen, and plasminogen activator inhibitor-1) in nonobese Framingham Offspring Study participants with no parents (n = 665), one parent (n = 488), or two parents (n = 119) with obesity (BMI ≥30 kg/m2). RESULTS: Nonobese offspring with both parents with obesity had higher CRP levels (median 2.16 mg/l) than offspring with one parent (1.58 mg/l) or no parents (1.35 mg/l) with obesity. After multivariable adjustment, a nonlinear relationship with parental obesity became evident: compared with those without parental obesity, CRP levels were higher in offspring with two obese parents (P = 0.04) but not in offspring with only one obese parent (P = 0.76). Renin levels were more linearly related to parental obesity status, being significantly higher in offspring with one parent (P = 0.04) or two parents (P = 0.09) with obesity (P = 0.02 for trend). The other systemic biomarkers did not vary according to parental obesity status (all P > 0.05). CONCLUSIONS: Our findings suggest that offspring with a high risk of developing obesity have an altered biomarker profile, characterized by systemic inflammation and increased neurohormonal activity, even in the absence of obesity. This is consistent with the notion that parental obesity may confer an increased susceptibility to other adiposity-associated traits.en_US
dc.description.sponsorshipNational Institutes of Health's National Heart, Lung, and Blood Institute (N01-HC-25195, 2K24HL04334); National Institute of Diabetes and Digestive Kidney Diseases (1R01-DK-080739)en_US
dc.language.isoenen_US
dc.publisherAmerican Diabetes Associationen_US
dc.rightsCopyright 2009, American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.en_US
dc.titleAssociation of Parental Obesity With Concentrations of Select Systemic Biomarkers in Nonobese Offspringen_US
dc.typearticleen_US
dc.identifier.doi10.2337/db08-0918en_US
dc.identifier.pubmedid18931036en_US
dc.identifier.pmcid2606861en_US


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