Discovery of adipose-produced cytokines and gut hormones has improved the understanding obesity-related mechanisms. The developmental origins of diseases theory also helped to explain the obesity risk in adults exposed to adverse intrauterine environment. In contrast to maternal conditions, the role of paternal characteristics for outcomes has been less investigated. Whether paternal adiposity is associated with obesity biomarkers in adults prior to the development of metabolic disturbances is unknown. This cross-sectional analysis included 124 women (28±5yrs) who participated in the NutriHS baseline. Early life events questionnaire, anthropometry, DXA-determined body composition and blood sample were obtained. Associations of paternal BMI with outcomes were tested by multiple linear regression, using the minimal sufficient adjustments (pre-gestational maternal, paternal education levels and current family income) suggested by Directed Acyclic Graphs. Participants had mean BMI of 25±5 kg/m2 (49% were overweight but metabolically healthy). Blood pressure and biochemical values were within the normal range. Mean obestatin and visfatin levels were 58.9±22.2 mg/dl and 18.8±8.1 mg/dl, respectively; these values did not differ between subsets with BMI <25 and ≥25 kg/m2. Pre-gestational maternal BMI was correlated to paternal BMI (r=0.344, p=0.001) and 11.3% of mothers and 39.0% of fathers were overweight/obese. In linear regression model, offspring obestatin levels was inversely associated with paternal BMI (β=-0.22, p=0.049). No significant association was observed with visfatin levels. The inverse association of paternal BMI with offspring obestatin levels in healthy women raises a possibility of being a marker of protection against obesity-related disturbances in adulthood. Further analyses of the NutriHS cohort should investigate this hypothesis.


R.G. Freitas: None. A.J. Vasques: None. F.B. Ribeiro: None. I. Solar: None. M.G. Barbosa: None. A.S. Hanada: None. A.M. Valente: None. B. Almeida-Pititto: None. B.G. Neto: None. S.G. Ferreira-Vivolo: None.


Fundação de Amparo à Pesquisa do Estado de São Paulo (2018/11433-9); Fundação de Amparo à Pesquisa do Estado de São Paulo (2018/11401-0)

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