Gene polymorphisms and increased DNA damage in morbidly obese women

Luperini, Bruno Cesar Ottoboni; Almeida, Daniela Volcan; Porto, Mariana Alves; Marcondes, João Paulo de Castro; Prado, Renato Paschoal; Rasera, Irineu; Oliveira, Maria Rita Marques de; Salvadori, Daisy Maria Fávero

doi:10.1016/j.mrfmmm.2015.01.004

Cited by 19 publications

(9 citation statements)

References 59 publications

(62 reference statements)

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“…Different African populations showed dramatically different frequencies, such as 4% in one African study compared with 98.7% for Nigerians. A different Euro-Brazilian population, studied by Luperini et al (2015), showed a frequency (41.1%) consistent with that observed in our study.…”

Section: Discussionsupporting

confidence: 91%

Leptin (rs7799039) and solute carrier family 30 zinc transporter (rs13266634) polymorphisms in Euro-Brazilian pregnant women with gestational diabetes

et al. 2017

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ABSTRACT. Leptin (LEP), a protein that plays a fundamental role in the metabolism of energy reserves, and the solute carrier family 30 A8 zinc transporter (SLC30A8) have been consistently associated with diabetes. Women with gestational diabetes are at moderate risk of developing diabetes type 1 and 2 after pregnancy, in addition to complications to the fetus. We investigated the association of the polymorphisms rs7799039 (LEP) and rs13266634 (SLC30A8) in a case-control study in Euro-Brazilians with gestational diabetes (GDM, N = 180). Realtime PCR with fluorescent probes (TaqMan system) was applied to genotyping. All polymorphisms were in Hardy-Weinberg equilibrium. The minor allele frequencies, for healthy and GDM, respectively, for the A-allele (LEP gene rs7799039) were 40.3% (95%CI = 35-45%) vs 36.6% (95%CI = 31-42%), P = 0.345; and for the T-allele (SLC30A8 gene rs13266634) were 27.8% (95%CI = 23-32%) vs 23.5% (95%CI = 18-29%), P = 0.227. Genotype comparisons for both polymorphisms showed no significant difference (P > 0.05). The polymorphisms rs7799039 and rs13266634 were not associated with GDM in the population studied (P > 0.05). The minor allele frequencies for both polymorphisms were similar to those of other Caucasian populations.

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Section: Discussionsupporting

confidence: 91%

Leptin (rs7799039) and solute carrier family 30 zinc transporter (rs13266634) polymorphisms in Euro-Brazilian pregnant women with gestational diabetes

et al. 2017

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“…Taken together, the results of the present research indicate that obesity reduction, due to exercise, alleviates DNA damage. Our results are supported by Luperini et al, who reported obesity as a cause of DNA damage, based on significantly high levels of DNA strand breaks and oxidized purines and pyrimidines in morbidly obese females compared with that in eutrophic females 17 ) . Additionally, Karaman et al, suggested that comet-tail length had positive correlations with waist circumference and BMI 18 ) .…”

Section: Discussionsupporting

confidence: 90%

Effects of aerobic exercise intervention on serum cartilage oligomeric matrix protein levels and lymphocyte DNA damage in obese elderly females

Cho

Roh

2016

J Phys Ther Sci

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[Purpose] The aim of the reported research was to investigate the effects of regular aerobic exercise on cartilage oligomeric matrix protein and oxidative DNA damage in obese, elderly females. [Subjects and Methods] Sixteen class I obese, elderly females, according to World Health Organization criteria, were randomly and equally assigned to a control group (n=8) or an exercise group (n=8). The exercise group participated in exercise sessions of 60 minutes per day, 3 days per week, for a period of 8 weeks. [Results] After aerobic exercise intervention, weight, body mass index, body fat, waist circumference, and DNA damage (Tail moment) were significantly decreased, compared with baseline values. In contrast, serum cartilage oligomeric matrix protein levels were not significantly different among any groups or time-points. [Conclusion] Regular aerobic exercise may be effective for reducing obesity-induced high DNA damage levels in obese females, without causing the deformation or degradation of lower extremity articular cartilage.

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“…Mutations are known to result from oxidative stress which produces reactive oxygen and nitrogen species (ROS/RNS) and other types of metabolites that cause DNA double strand breaks and other lesions [35]. Obesity leads to increased DNA damage and reduced DNA repair in both animal model systems and humans [36, 37]. In obesity-associated inflammation, activated myeloid cells appear to be a major source of ROS [38].…”

Section: Adipose Tissue Inflammation and Cancer Initiationmentioning

confidence: 99%

Cancer as a Matter of Fat: The Crosstalk between Adipose Tissue and Tumors

et al. 2018

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Obesity has been linked to the increased risk and aggressiveness of many types of carcinoma. A state of chronic inflammation in adipose tissue (AT), resulting in genotoxic stress, may contribute to carcinogenesis and cancer initiation. Evidence that AT plays a role in cancer aggressiveness is solid and mounting. During cancer progression, tumor cells engage in a metabolic symbiosis with adjacent AT. Mature adipocytes provide adipokines and lipids to cancer cells, while stromal and immune cells from AT infiltrate carcinomas and locally secrete paracrine factors within the tumor microenvironment. This review focuses on the crosstalk between AT and tumor cells that promotes tumor growth and increases cellular lipid metabolism, metastasis, and chemoresistance.

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Gene polymorphisms and increased DNA damage in morbidly obese women

Cited by 19 publications

References 59 publications

Leptin (rs7799039) and solute carrier family 30 zinc transporter (rs13266634) polymorphisms in Euro-Brazilian pregnant women with gestational diabetes

Leptin (rs7799039) and solute carrier family 30 zinc transporter (rs13266634) polymorphisms in Euro-Brazilian pregnant women with gestational diabetes

Effects of aerobic exercise intervention on serum cartilage oligomeric matrix protein levels and lymphocyte DNA damage in obese elderly females

Cancer as a Matter of Fat: The Crosstalk between Adipose Tissue and Tumors

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