Iron supplementation does not aggravate impaired glucose tolerance and sugar overload-induced genotoxicity in rats
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,...
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| Veröffentlicht in: | Molecular and cellular biochemistry 2023-08, Vol.478 (8), p.1719-1725 |
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| creator | Molz, Patrícia Dallemole, Danieli Rosane Molz, Walter Augusto Priebe Steffens, Juliana Wildner Maluf, Sharbel Baroni Cruz, Dennis Rieger, Alexandre Salvador, Mirian Prá, Daniel Rech Franke, Silvia Isabel |
| description | 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
2+
, 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
|
| doi_str_mv | 10.1007/s11010-022-04625-8 |
| format | Article |
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n
= 8), invert sugar overload (320 g/L, HSD,
n
= 8), or Fe plus invert sugar overload (2.56 mg/L of Fe
2+
, 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.</description><identifier>ISSN: 0300-8177</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1007/s11010-022-04625-8</identifier><identifier>PMID: 36564575</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Bioassays ; Biochemistry ; Biomedical and Life Sciences ; Body weight gain ; Cancer Research ; Cardiology ; Chromium ; Comet assay ; Damage assessment ; Damage detection ; Damage tolerance ; Deoxyribonucleic acid ; Diabetes mellitus ; Diet ; DNA ; DNA damage ; Genotoxicity ; Glucose ; Glucose tolerance ; Iron ; Life Sciences ; Medical Biochemistry ; Metabolic disorders ; Mutagenicity ; Overloading ; Risk factors ; Sugar</subject><ispartof>Molecular and cellular biochemistry, 2023-08, Vol.478 (8), p.1719-1725</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2022. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-7d37add8678e6737cc7f4c44f7de0dd6921cc8db974eb4ad31f04cb7a6d7d3a03</citedby><cites>FETCH-LOGICAL-c375t-7d37add8678e6737cc7f4c44f7de0dd6921cc8db974eb4ad31f04cb7a6d7d3a03</cites><orcidid>0000-0002-3860-7487 ; 0000-0001-8940-7023 ; 0000-0001-5337-3490 ; 0000-0002-5247-1571 ; 0000-0003-2818-0173 ; 0000-0002-1935-3231 ; 0000-0003-2289-7739 ; 0000-0001-9404-0262 ; 0000-0001-5992-6498 ; 0000-0001-7523-7211</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11010-022-04625-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11010-022-04625-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,777,781,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36564575$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Molz, Patrícia</creatorcontrib><creatorcontrib>Dallemole, Danieli Rosane</creatorcontrib><creatorcontrib>Molz, Walter Augusto</creatorcontrib><creatorcontrib>Priebe Steffens, Juliana</creatorcontrib><creatorcontrib>Wildner Maluf, Sharbel</creatorcontrib><creatorcontrib>Baroni Cruz, Dennis</creatorcontrib><creatorcontrib>Rieger, Alexandre</creatorcontrib><creatorcontrib>Salvador, Mirian</creatorcontrib><creatorcontrib>Prá, Daniel</creatorcontrib><creatorcontrib>Rech Franke, Silvia Isabel</creatorcontrib><title>Iron supplementation does not aggravate impaired glucose tolerance and sugar overload-induced genotoxicity in rats</title><title>Molecular and cellular biochemistry</title><addtitle>Mol Cell Biochem</addtitle><addtitle>Mol Cell Biochem</addtitle><description>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
2+
, 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.</description><subject>Bioassays</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Body weight gain</subject><subject>Cancer Research</subject><subject>Cardiology</subject><subject>Chromium</subject><subject>Comet assay</subject><subject>Damage assessment</subject><subject>Damage detection</subject><subject>Damage tolerance</subject><subject>Deoxyribonucleic acid</subject><subject>Diabetes mellitus</subject><subject>Diet</subject><subject>DNA</subject><subject>DNA damage</subject><subject>Genotoxicity</subject><subject>Glucose</subject><subject>Glucose tolerance</subject><subject>Iron</subject><subject>Life Sciences</subject><subject>Medical Biochemistry</subject><subject>Metabolic disorders</subject><subject>Mutagenicity</subject><subject>Overloading</subject><subject>Risk 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supplementation does not aggravate impaired glucose tolerance and sugar overload-induced genotoxicity in rats</title><author>Molz, Patrícia ; Dallemole, Danieli Rosane ; Molz, Walter Augusto ; Priebe Steffens, Juliana ; Wildner Maluf, Sharbel ; Baroni Cruz, Dennis ; Rieger, Alexandre ; Salvador, Mirian ; Prá, Daniel ; Rech Franke, Silvia Isabel</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-7d37add8678e6737cc7f4c44f7de0dd6921cc8db974eb4ad31f04cb7a6d7d3a03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Bioassays</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Body weight gain</topic><topic>Cancer Research</topic><topic>Cardiology</topic><topic>Chromium</topic><topic>Comet assay</topic><topic>Damage assessment</topic><topic>Damage detection</topic><topic>Damage tolerance</topic><topic>Deoxyribonucleic acid</topic><topic>Diabetes 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biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Molz, Patrícia</au><au>Dallemole, Danieli Rosane</au><au>Molz, Walter Augusto</au><au>Priebe Steffens, Juliana</au><au>Wildner Maluf, Sharbel</au><au>Baroni Cruz, Dennis</au><au>Rieger, Alexandre</au><au>Salvador, Mirian</au><au>Prá, Daniel</au><au>Rech Franke, Silvia Isabel</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Iron supplementation does not aggravate impaired glucose tolerance and sugar overload-induced genotoxicity in rats</atitle><jtitle>Molecular and cellular biochemistry</jtitle><stitle>Mol Cell Biochem</stitle><addtitle>Mol Cell Biochem</addtitle><date>2023-08-01</date><risdate>2023</risdate><volume>478</volume><issue>8</issue><spage>1719</spage><epage>1725</epage><pages>1719-1725</pages><issn>0300-8177</issn><eissn>1573-4919</eissn><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
2+
, 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.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>36564575</pmid><doi>10.1007/s11010-022-04625-8</doi><tpages>7</tpages><orcidid>https://orcid.org/0000-0002-3860-7487</orcidid><orcidid>https://orcid.org/0000-0001-8940-7023</orcidid><orcidid>https://orcid.org/0000-0001-5337-3490</orcidid><orcidid>https://orcid.org/0000-0002-5247-1571</orcidid><orcidid>https://orcid.org/0000-0003-2818-0173</orcidid><orcidid>https://orcid.org/0000-0002-1935-3231</orcidid><orcidid>https://orcid.org/0000-0003-2289-7739</orcidid><orcidid>https://orcid.org/0000-0001-9404-0262</orcidid><orcidid>https://orcid.org/0000-0001-5992-6498</orcidid><orcidid>https://orcid.org/0000-0001-7523-7211</orcidid></addata></record> |
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| ispartof | Molecular and cellular biochemistry, 2023-08, Vol.478 (8), p.1719-1725 |
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| source | Springer Nature - Complete Springer Journals |
| subjects | Bioassays Biochemistry Biomedical and Life Sciences Body weight gain Cancer Research Cardiology Chromium Comet assay Damage assessment Damage detection Damage tolerance Deoxyribonucleic acid Diabetes mellitus Diet DNA DNA damage Genotoxicity Glucose Glucose tolerance Iron Life Sciences Medical Biochemistry Metabolic disorders Mutagenicity Overloading Risk factors Sugar |
| title | Iron supplementation does not aggravate impaired glucose tolerance and sugar overload-induced genotoxicity in rats |
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