DNA damage and cytotoxicity in adult subjects with prediabetes

Pereira, Camila Schreiner; Molz, Patrí­cia; Palazzo, Roberta Passos; Freitas, Thiago Aley Brites de; Maluf, Sharbel Weidner; Horta, Jorge André; Prá, Daniel; Franke, Silvia Isabel Rech

doi:10.1016/j.mrgentox.2013.02.002

Cited by 31 publications

(23 citation statements)

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“…It has been reported that diabetes is associated with an increased production of reactive oxygen species and greater oxidative damage to DNA [32,33]. Recently, it has also been reported that the overall frequency of DNA damage and cytotoxicity correlates with the level of HbA 1c in people with prediabetes [34].…”

Section: Discussionmentioning

confidence: 99%

Prediabetes and the risk of cancer: a meta-analysis

et al. 2014

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Aims/hypothesis The results from prospective cohort studies of prediabetes (impaired fasting glucose and/or impaired glucose tolerance) and risk of cancer are controversial. We conducted a meta-analysis to evaluate the risk of cancer in association with impaired fasting glucose and impaired glucose tolerance. Methods The PubMed, EMBASE and Cochrane Library databases were searched for prospective cohort studies with data on prediabetes and cancer. Two independent reviewers assessed the reports and extracted the data. Prospective studies were included if they reported adjusted RRs with 95% CIs for the association between cancer and prediabetes. Subgroup analyses were conducted according to endpoint, age, sex, ethnicity, duration of follow-up and study characteristics. Results Data from 891,426 participants were derived from 16 prospective cohort studies. Prediabetes was associated with an increased risk of cancer overall (RR 1.15; 95% CI 1.06, 1.23).The results were consistent across cancer endpoint, age, duration of follow-up and ethnicity. There was no significant difference for the risk of cancer with different definitions of prediabetes. In a site-specific cancer analysis, prediabetes was significantly associated with increased risks of cancer of the stomach/colorectum, liver, pancreas, breast and endometrium (all p<0.05), but not associated with cancer of the bronchus/ lung, prostate, ovary, kidney or bladder. The risks of sitespecific cancer were significantly different (p=0.01) and were highest for liver, endometrial and stomach/colorectal cancer. Conclusions/interpretation Overall, prediabetes was associated with an increased risk of cancer, especially liver, endometrial and stomach/colorectal cancer.

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Section: Discussionmentioning

confidence: 99%

Prediabetes and the risk of cancer: a meta-analysis

et al. 2014

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“…Several studies have shown that there is no increase in DNA damage in DM2 [21, 22]. Other studies have indicated that an increase in micronuclei will not likely occur in early DM2 [23], but only in uncompensated DM2 (i.e., A1C > 8%) [24]. In our study, only 4 (approximately 6%) out of the 70 subjects had uncompensated DM2 (A1C > 8.0%); therefore, it was not likely that the sample would present an increase in chromosomal DNA damage.…”

Section: Discussionmentioning

confidence: 99%

Vitamin C Intake Reduces the Cytotoxicity Associated with Hyperglycemia in Prediabetes and Type 2 Diabetes

Franke

Müller

Santos

et al. 2013

BioMed Research International

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Hyperglycemia leads to the formation of free radicals and advanced glycation end-products (AGEs). Antioxidants can reduce the level of protein glycation and DNA damage. In this study, we compared the levels of vitamin C intake, which is among the most abundant antioxidants obtained from diet, with the levels of fasting plasma glucose (FPG), glycated hemoglobin (A1C), DNA damage, and cytotoxicity in prediabetic subjects and type 2 diabetic subjects. Our results indicated that there was no significant correlation between FPG or A1C and DNA damage parameters (micronuclei, nucleoplasmic bridges, and nuclear buds). FPG and A1C correlated with necrosis (r = 0.294; P = 0.013 and r = 0.401; P = 0.001, resp.). Vitamin C intake correlated negatively with necrosis and apoptosis (r = −0.246; P = 0.040, and r = −0.276; P = 0.021, resp.). The lack of a correlation between the FPG and A1C and DNA damage could be explained, at least in part, by the elimination of cells with DNA damage by either necrosis or apoptosis (cytotoxicity). Vitamin C appeared to improve cell survival by reducing cytotoxicity. Therefore, the present results indicate the need for clinical studies to evaluate the effect of low-dose vitamin C supplementation in type 2 diabetes.

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“…However, other parameters that could affect the frequency of MN and NAs, such as prediabetes, metabolic syndrome, or obesity, which are also related to inflammatory processes and DNA damage, were not considered [4,15,37,[45][46][47][48][49][50][51].…”

Section: Effects Of Dmmentioning

confidence: 99%