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补铁不会加重葡萄糖耐量受损和糖超负荷诱导的大鼠遗传毒性。

Iron supplementation does not aggravate impaired glucose tolerance and sugar overload-induced genotoxicity in rats.

机构信息

Laboratory of Experimental Nutrition, University of Santa Cruz do Sul, Santa Cruz do Sul, Brazil.

Graduate Program in Health Promotion, University of Santa Cruz do Sul, Santa Cruz do Sul, RS, Brazil.

出版信息

Mol Cell Biochem. 2023 Aug;478(8):1719-1725. doi: 10.1007/s11010-022-04625-8. Epub 2022 Dec 23.

Abstract

High sugar intake is a major risk factor for metabolic disorders. Genotoxicity is an important factor in diabetes onset, and iron (Fe) may be an aggravating element. However, this relationship is still poorly established. Thus, this study evaluated whether Fe supplementation could aggravate obesity, impaired glucose tolerance, and sugar overload-induced genotoxicity in rats. A total of 24 rats were treated with different diets: standard diet (SD, n = 8), invert sugar overload (320 g/L, HSD, n = 8), or Fe plus invert sugar overload (2.56 mg/L of Fe, Fe-HSD, n = 8) for four months. After treatment, the Fe-HSD group showed no excessive weight gain or impaired glucose tolerance. DNA damage in blood, as assessed by comet assay, gradually increased in HSD during treatment (p < 0.001), whereas Fe-HSD showed a nonlinear increase in DNA damage. Moreover, Fe-HSD presented 0.6-fold more DNA damage compared with SD (p = 0.0055) in the 1st month of treatment. At months 2 and 3, results show a ≥ 1.4-fold increase in HSD and Fe-HSD DNA damage, respectively, compared with SD (p < 0.01). At the end of the experiment, only HSD DNA damage differed from SD (1.5-fold more, p = 0.0196). Fe supplementation did not aggravate the invert sugar-induced DNA damage (p > 0.05). In the pancreas, results showed no differences in DNA damage. Mutagenicity, evaluated by micronucleus testing, was not observed regardless of treatment (p = 0.428). Fe supplementation, in the evaluated concentration, did not aggravate weight gain, impaired glucose tolerance, and sugar overload-induced genotoxicity in rats.

摘要

高糖摄入是代谢紊乱的一个主要危险因素。遗传毒性是糖尿病发病的一个重要因素,而铁(Fe)可能是一个加重因素。然而,这种关系仍未得到充分证实。因此,本研究评估了铁补充是否会加重肥胖、葡萄糖耐量受损和糖超负荷诱导的大鼠遗传毒性。总共 24 只大鼠接受了不同的饮食治疗:标准饮食(SD,n=8)、转化糖超负荷(320 g/L,HSD,n=8)或铁加转化糖超负荷(2.56 mg/L 的 Fe,Fe-HSD,n=8)治疗四个月。治疗后,Fe-HSD 组体重无明显增加,葡萄糖耐量受损。彗星试验评估的血液 DNA 损伤在 HSD 治疗期间逐渐增加(p<0.001),而 Fe-HSD 呈非线性增加。此外,Fe-HSD 在治疗的第一个月与 SD 相比表现出 0.6 倍的 DNA 损伤增加(p=0.0055)。在第 2 个月和第 3 个月,HSD 和 Fe-HSD 的 DNA 损伤分别比 SD 增加了 1.4 倍以上(p<0.01)。在实验结束时,只有 HSD 的 DNA 损伤与 SD 不同(增加了 1.5 倍,p=0.0196)。铁补充并没有加重转化糖诱导的 DNA 损伤(p>0.05)。在胰腺中,DNA 损伤没有差异。无论治疗如何,微核试验评估的致突变性都没有观察到(p=0.428)。在评估的浓度下,铁补充不会加重肥胖、葡萄糖耐量受损和糖超负荷诱导的大鼠遗传毒性。

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