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Transforming growth factor beta 1 (TGFβ1) plasmatic levels and haplotype structures in obesity: a role for TGFβ1 in steatosis development

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Abstract

Background

Obesity is considered a chronic inflammatory disease and transforming growth factor beta 1 (TGFβ1) might exert important roles in disease pathogenesis regulating adipocyte differentiation and immune-inflammatory environment. However, the role of this cytokine as a biomarker in obesity is poorly addressed. Therefore, the present study aimed to evaluate the impact of TGFB1 polymorphisms and TGFβ1 plasmatic levels in obesity

Methods and results

TGFB1 promoter region polymorphisms (rs1800468, G-800A and rs1800469, C-509 T) were evaluated in 75 obese patients and 45 eutrophic patients through PCR–RFLP and plasmatic TGFβ1 was quantified through ELISA from 37 of the obese patients, and correlations with clinical and biochemical parameters were tested. Despite no association was found between TGFB1 polymorphisms and obesity susceptibility, several correlations with clinical data were noted. Among others, AC haplotype negatively correlated with plasmatic TGFβ1, while plasmatic TGFβ1 negatively correlated with C-reactive protein and positively correlated with liver abnormalities on ultrasound and, specifically, with steatosis presence and degree. Conversely, GT haplotype, which associates with higher TGFβ1 production, was also positively correlated with the same parameters of liver abnormalities. Further, plasmatic vitamin D negatively correlated with TGFβ1, while positively correlated with AC haplotype.

Conclusion

Overall, the results indicate that TGFβ1 might exert important roles in obesity pathophysiology and correlate with biochemical and clinical parameters both at systemic protein as well as at genetic level. Importantly, the consistent positive correlation at both levels with steatosis might suggest this cytokine as a biomarker for this hepatic abnormality in obese patients.

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Data availability

Data are available from the corresponding author upon reasonable request.

Code availability

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Acknowledgements

The authors acknowledge all the volunteer donors involved in this study from Blood Center of the Hospital das Clínicas/UNESP—School of Medicine in Botucatu, State University of São Paulo (São Paulo, Brazil) and staff from Hospital Santa Casa de Misericórdia in Curitiba (Paraná, Brazil) for the support during sample collection. This study was supported by CNPq (Proc. n° 152170/2019-7 and n° 306386/2017-8), CAPES, and FINEP.

Funding

This study was supported by the Brazilian National Council for Scientific and Technological Development (CNPq, Processes n° 152170/2019-7 and n° 306386/2017-8), the Coordination of Superior Level Staff Improvement (CAPES), and the Brazilian Innovation Agency (FINEP).

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IF: conceptualization, methodology, investigation, formal analysis, data curation, writing—original draft. MB: methodology, investigation, formal analysis, writing—original draft. MRZR: conceptualization, data curation, supervision, project administration, writing—original draft. LOC: data curation, formal analysis. NRFW: data curation, formal analysis. ACLC: resources, supervision. LRR: supervision, funding acquisition, resources, project administration. MSM: supervision, funding acquisition, resources, project administration. MAEW: supervision, resources, project administration, writing—review & editing. GAFV: conceptualization, methodology, formal analysis, visualization, data curation, supervision, writing—original draft, writing—review & editing.

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Correspondence to Glauco Akelinghton Freire Vitiello.

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The study protocol was submitted and approved (Protocol No. 3799/2011 and CAAE 79894217.9.0000.0020) by the Human Research Ethics Committee of the UNESP School of Medicine (Botucatu, São Paulo, Brazil) and by the Pontifical Catholic University of Paraná (PUCPR—Curitiba, Paraná, Brazil), respectively, according to Resolution No. 466/12 of the Brazilian National Health Council.

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Felicidade, I., Bocchi, M., Ramos, M.R.Z. et al. Transforming growth factor beta 1 (TGFβ1) plasmatic levels and haplotype structures in obesity: a role for TGFβ1 in steatosis development. Mol Biol Rep 48, 6401–6411 (2021). https://doi.org/10.1007/s11033-021-06640-2

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