In severe acne vulgaris, TNF‐α gene variants are connected to increased TNF‐α gene expression and insulin resistance
Background Acne vulgaris (AV) is a chronic inflammatory skin condition affecting the pilosebaceous unit, commonly presenting as comedones, papules, pustules, or nodules on the face, upper limbs, torso, and back, with comedones formation being the primary pathology leading to disfiguring inflammation...
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description | Background
Acne vulgaris (AV) is a chronic inflammatory skin condition affecting the pilosebaceous unit, commonly presenting as comedones, papules, pustules, or nodules on the face, upper limbs, torso, and back, with comedones formation being the primary pathology leading to disfiguring inflammation, hyperpigmentation, scarring, and psychological impact.
Aim
The purpose of this study was to investigate the significance of two genetic variants in the promoter region of the tumor necrosis factor‐alpha (TNF‐α) gene and their association with insulin resistance (IR) in acne patients. To understand how these variants contribute to AV and its associated IR.
Subjects and methods
An analytical cross‐sectional study with a case‐control design and research evaluation was carried out on 87 AV patients and 73 healthy volunteers. The medical histories of both groups were obtained, as well as the severity and duration of inflammation among acne sufferers, as well as demographic data. Biochemical analysis was performed on both sets of participants, including fasting blood glucose levels, insulin levels while fasting, IR, and serum TNF‐α. PCR‐RFLP analysis identified −863 G > A (rs1800630) and −308 G > A (rs1800629) variations, and real‐time PCR analysis evaluated TNF‐α gene expression in both patients and healthy people.
Results
Acne patients exhibited significantly higher levels of IR, fasting glucose, fasting insulin, serum TNF‐α, and TNF‐α folding change, when compared to healthy controls. The co‐dominant model for −863 G > A and −308 G > A variants exhibited significant variations between the two groups. Severe acne patients who had the A/A genotype for −308 variants exhibited higher levels of IR, serum TNF‐α, and TNF‐α folding change. Highly significant positive linear correlation between IR, serum TNF‐α, and TNF‐α folding change in severe AV.
Conclusion
There is a correlation between AV, especially severe acne, and the −863 G > A and −308 G > A polymorphism, which influences TNF‐α gene expression and serum TNF‐α levels. |
doi_str_mv | 10.1111/srt.13811 |
format | Article |
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Acne vulgaris (AV) is a chronic inflammatory skin condition affecting the pilosebaceous unit, commonly presenting as comedones, papules, pustules, or nodules on the face, upper limbs, torso, and back, with comedones formation being the primary pathology leading to disfiguring inflammation, hyperpigmentation, scarring, and psychological impact.
Aim
The purpose of this study was to investigate the significance of two genetic variants in the promoter region of the tumor necrosis factor‐alpha (TNF‐α) gene and their association with insulin resistance (IR) in acne patients. To understand how these variants contribute to AV and its associated IR.
Subjects and methods
An analytical cross‐sectional study with a case‐control design and research evaluation was carried out on 87 AV patients and 73 healthy volunteers. The medical histories of both groups were obtained, as well as the severity and duration of inflammation among acne sufferers, as well as demographic data. Biochemical analysis was performed on both sets of participants, including fasting blood glucose levels, insulin levels while fasting, IR, and serum TNF‐α. PCR‐RFLP analysis identified −863 G > A (rs1800630) and −308 G > A (rs1800629) variations, and real‐time PCR analysis evaluated TNF‐α gene expression in both patients and healthy people.
Results
Acne patients exhibited significantly higher levels of IR, fasting glucose, fasting insulin, serum TNF‐α, and TNF‐α folding change, when compared to healthy controls. The co‐dominant model for −863 G > A and −308 G > A variants exhibited significant variations between the two groups. Severe acne patients who had the A/A genotype for −308 variants exhibited higher levels of IR, serum TNF‐α, and TNF‐α folding change. Highly significant positive linear correlation between IR, serum TNF‐α, and TNF‐α folding change in severe AV.
Conclusion
There is a correlation between AV, especially severe acne, and the −863 G > A and −308 G > A polymorphism, which influences TNF‐α gene expression and serum TNF‐α levels.</description><identifier>ISSN: 0909-752X</identifier><identifier>ISSN: 1600-0846</identifier><identifier>EISSN: 1600-0846</identifier><identifier>DOI: 10.1111/srt.13811</identifier><identifier>PMID: 38923681</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Acne ; acne vulgaris ; Acne Vulgaris - blood ; Acne Vulgaris - genetics ; Adolescent ; Adult ; Biochemical analysis ; Blood levels ; Case-Control Studies ; Comedones ; Cross-Sectional Studies ; Fasting ; Female ; Folding ; Gene expression ; Gene polymorphism ; Genetic diversity ; Genetic Predisposition to Disease - genetics ; Genetic variance ; Glucose ; Humans ; Hyperpigmentation ; Inflammation ; Insulin ; Insulin resistance ; Insulin Resistance - genetics ; Laboratory testing ; Male ; Nodules ; Original ; Polymorphism ; Polymorphism, Single Nucleotide ; Psychology ; serum TNF‐α ; Severity of Illness Index ; Skin diseases ; Skin resistance ; TNF‐α gene ; TNF‐α gene expression ; Torso ; Tumor necrosis factor ; Tumor Necrosis Factor-alpha - blood ; Tumor Necrosis Factor-alpha - genetics ; Tumor necrosis factor-TNF ; Young Adult</subject><ispartof>Skin research and technology, 2024-07, Vol.30 (7), p.e13811-n/a</ispartof><rights>2024 The Author(s). published by John Wiley & Sons Ltd.</rights><rights>2024 The Author(s). Skin Research and Technology published by John Wiley & Sons Ltd.</rights><rights>2024. This article is published under http://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c4041-8272752d13a299f52acf5955fa50c6d77a4446374f5759a7ff524c3019f9a07a3</cites><orcidid>0000-0001-6582-907X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11197027/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11197027/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,1411,11541,27901,27902,45550,45551,46027,46451,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38923681$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>AbdElneam, Ahmed Ibrahim</creatorcontrib><creatorcontrib>Alhajlah, Sharif</creatorcontrib><creatorcontrib>Al‐Dhubaibi, Mohammed Saleh</creatorcontrib><creatorcontrib>Bahaj, Saleh Salem</creatorcontrib><creatorcontrib>Mohammed, Ghada Farouk</creatorcontrib><creatorcontrib>Alantry, Ahmed Kaid</creatorcontrib><creatorcontrib>Atef, Lina Mohammed</creatorcontrib><title>In severe acne vulgaris, TNF‐α gene variants are connected to increased TNF‐α gene expression and insulin resistance</title><title>Skin research and technology</title><addtitle>Skin Res Technol</addtitle><description>Background
Acne vulgaris (AV) is a chronic inflammatory skin condition affecting the pilosebaceous unit, commonly presenting as comedones, papules, pustules, or nodules on the face, upper limbs, torso, and back, with comedones formation being the primary pathology leading to disfiguring inflammation, hyperpigmentation, scarring, and psychological impact.
Aim
The purpose of this study was to investigate the significance of two genetic variants in the promoter region of the tumor necrosis factor‐alpha (TNF‐α) gene and their association with insulin resistance (IR) in acne patients. To understand how these variants contribute to AV and its associated IR.
Subjects and methods
An analytical cross‐sectional study with a case‐control design and research evaluation was carried out on 87 AV patients and 73 healthy volunteers. The medical histories of both groups were obtained, as well as the severity and duration of inflammation among acne sufferers, as well as demographic data. Biochemical analysis was performed on both sets of participants, including fasting blood glucose levels, insulin levels while fasting, IR, and serum TNF‐α. PCR‐RFLP analysis identified −863 G > A (rs1800630) and −308 G > A (rs1800629) variations, and real‐time PCR analysis evaluated TNF‐α gene expression in both patients and healthy people.
Results
Acne patients exhibited significantly higher levels of IR, fasting glucose, fasting insulin, serum TNF‐α, and TNF‐α folding change, when compared to healthy controls. The co‐dominant model for −863 G > A and −308 G > A variants exhibited significant variations between the two groups. Severe acne patients who had the A/A genotype for −308 variants exhibited higher levels of IR, serum TNF‐α, and TNF‐α folding change. Highly significant positive linear correlation between IR, serum TNF‐α, and TNF‐α folding change in severe AV.
Conclusion
There is a correlation between AV, especially severe acne, and the −863 G > A and −308 G > A polymorphism, which influences TNF‐α gene expression and serum TNF‐α levels.</description><subject>Acne</subject><subject>acne vulgaris</subject><subject>Acne Vulgaris - blood</subject><subject>Acne Vulgaris - genetics</subject><subject>Adolescent</subject><subject>Adult</subject><subject>Biochemical analysis</subject><subject>Blood levels</subject><subject>Case-Control Studies</subject><subject>Comedones</subject><subject>Cross-Sectional Studies</subject><subject>Fasting</subject><subject>Female</subject><subject>Folding</subject><subject>Gene expression</subject><subject>Gene polymorphism</subject><subject>Genetic diversity</subject><subject>Genetic Predisposition to Disease - genetics</subject><subject>Genetic variance</subject><subject>Glucose</subject><subject>Humans</subject><subject>Hyperpigmentation</subject><subject>Inflammation</subject><subject>Insulin</subject><subject>Insulin resistance</subject><subject>Insulin Resistance - genetics</subject><subject>Laboratory testing</subject><subject>Male</subject><subject>Nodules</subject><subject>Original</subject><subject>Polymorphism</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Psychology</subject><subject>serum TNF‐α</subject><subject>Severity of Illness Index</subject><subject>Skin diseases</subject><subject>Skin resistance</subject><subject>TNF‐α gene</subject><subject>TNF‐α gene expression</subject><subject>Torso</subject><subject>Tumor necrosis factor</subject><subject>Tumor Necrosis Factor-alpha - blood</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><subject>Tumor necrosis factor-TNF</subject><subject>Young Adult</subject><issn>0909-752X</issn><issn>1600-0846</issn><issn>1600-0846</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>EIF</sourceid><recordid>eNp1kdFqFDEUhoNY7Fq98AUk4I2C0yaTySS5EimtLRQFXcG7cMycWVNmk20ys7Ze-Qi-ii_Sh_BJTLu1WMHchPz58p__5BDyhLNdXtZeTuMuF5rze2TGW8Yqppv2Ppkxw0ylZP1pmzzM-ZQxJg0XD8i20KYWreYz8u040IxrTEjBBaTraVhA8vklnb89_PX9x-VPusArvYgQxkyhkC6GgG7Ejo6R-uASQi6Huy_wfJUwZx8DhdAVLE-DD7RoPo8QHD4iWz0MGR_f7Dvk4-HBfP-oOnn35nj_9UnlGtbwSteqLj10XEBtTC9rcL00UvYgmWs7paBpmlaoppdKGlB9QRonGDe9AaZA7JBXG9_V9HmJncMwJhjsKvklpAsbwdu7N8F_sYu4tuVrjWK1Kg7PbxxSPJswj3bps8NhgIBxylawEtHoVuuCPvsHPY1TCqW_QmlZm8bItlAvNpRLMeeE_W0azq7KcltGaq9HWtinf8e_Jf_MsAB7G-CrH_Di_072w_v5xvI31dSu8g</recordid><startdate>202407</startdate><enddate>202407</enddate><creator>AbdElneam, Ahmed Ibrahim</creator><creator>Alhajlah, Sharif</creator><creator>Al‐Dhubaibi, Mohammed Saleh</creator><creator>Bahaj, Saleh Salem</creator><creator>Mohammed, Ghada Farouk</creator><creator>Alantry, Ahmed Kaid</creator><creator>Atef, Lina Mohammed</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QO</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-6582-907X</orcidid></search><sort><creationdate>202407</creationdate><title>In severe acne vulgaris, TNF‐α gene variants are connected to increased TNF‐α gene expression and insulin resistance</title><author>AbdElneam, Ahmed Ibrahim ; Alhajlah, Sharif ; Al‐Dhubaibi, Mohammed Saleh ; Bahaj, Saleh Salem ; Mohammed, Ghada Farouk ; Alantry, Ahmed Kaid ; Atef, Lina Mohammed</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4041-8272752d13a299f52acf5955fa50c6d77a4446374f5759a7ff524c3019f9a07a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Acne</topic><topic>acne vulgaris</topic><topic>Acne Vulgaris - blood</topic><topic>Acne Vulgaris - genetics</topic><topic>Adolescent</topic><topic>Adult</topic><topic>Biochemical analysis</topic><topic>Blood levels</topic><topic>Case-Control Studies</topic><topic>Comedones</topic><topic>Cross-Sectional Studies</topic><topic>Fasting</topic><topic>Female</topic><topic>Folding</topic><topic>Gene expression</topic><topic>Gene polymorphism</topic><topic>Genetic diversity</topic><topic>Genetic Predisposition to Disease - genetics</topic><topic>Genetic variance</topic><topic>Glucose</topic><topic>Humans</topic><topic>Hyperpigmentation</topic><topic>Inflammation</topic><topic>Insulin</topic><topic>Insulin resistance</topic><topic>Insulin Resistance - genetics</topic><topic>Laboratory testing</topic><topic>Male</topic><topic>Nodules</topic><topic>Original</topic><topic>Polymorphism</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Psychology</topic><topic>serum TNF‐α</topic><topic>Severity of Illness Index</topic><topic>Skin diseases</topic><topic>Skin resistance</topic><topic>TNF‐α gene</topic><topic>TNF‐α gene expression</topic><topic>Torso</topic><topic>Tumor necrosis factor</topic><topic>Tumor Necrosis Factor-alpha - blood</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><topic>Tumor necrosis factor-TNF</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>AbdElneam, Ahmed Ibrahim</creatorcontrib><creatorcontrib>Alhajlah, Sharif</creatorcontrib><creatorcontrib>Al‐Dhubaibi, Mohammed Saleh</creatorcontrib><creatorcontrib>Bahaj, Saleh Salem</creatorcontrib><creatorcontrib>Mohammed, Ghada Farouk</creatorcontrib><creatorcontrib>Alantry, Ahmed Kaid</creatorcontrib><creatorcontrib>Atef, Lina Mohammed</creatorcontrib><collection>Wiley Online Library Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Skin research and technology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>AbdElneam, Ahmed Ibrahim</au><au>Alhajlah, Sharif</au><au>Al‐Dhubaibi, Mohammed Saleh</au><au>Bahaj, Saleh Salem</au><au>Mohammed, Ghada Farouk</au><au>Alantry, Ahmed Kaid</au><au>Atef, Lina Mohammed</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>In severe acne vulgaris, TNF‐α gene variants are connected to increased TNF‐α gene expression and insulin resistance</atitle><jtitle>Skin research and technology</jtitle><addtitle>Skin Res Technol</addtitle><date>2024-07</date><risdate>2024</risdate><volume>30</volume><issue>7</issue><spage>e13811</spage><epage>n/a</epage><pages>e13811-n/a</pages><issn>0909-752X</issn><issn>1600-0846</issn><eissn>1600-0846</eissn><abstract>Background
Acne vulgaris (AV) is a chronic inflammatory skin condition affecting the pilosebaceous unit, commonly presenting as comedones, papules, pustules, or nodules on the face, upper limbs, torso, and back, with comedones formation being the primary pathology leading to disfiguring inflammation, hyperpigmentation, scarring, and psychological impact.
Aim
The purpose of this study was to investigate the significance of two genetic variants in the promoter region of the tumor necrosis factor‐alpha (TNF‐α) gene and their association with insulin resistance (IR) in acne patients. To understand how these variants contribute to AV and its associated IR.
Subjects and methods
An analytical cross‐sectional study with a case‐control design and research evaluation was carried out on 87 AV patients and 73 healthy volunteers. The medical histories of both groups were obtained, as well as the severity and duration of inflammation among acne sufferers, as well as demographic data. Biochemical analysis was performed on both sets of participants, including fasting blood glucose levels, insulin levels while fasting, IR, and serum TNF‐α. PCR‐RFLP analysis identified −863 G > A (rs1800630) and −308 G > A (rs1800629) variations, and real‐time PCR analysis evaluated TNF‐α gene expression in both patients and healthy people.
Results
Acne patients exhibited significantly higher levels of IR, fasting glucose, fasting insulin, serum TNF‐α, and TNF‐α folding change, when compared to healthy controls. The co‐dominant model for −863 G > A and −308 G > A variants exhibited significant variations between the two groups. Severe acne patients who had the A/A genotype for −308 variants exhibited higher levels of IR, serum TNF‐α, and TNF‐α folding change. Highly significant positive linear correlation between IR, serum TNF‐α, and TNF‐α folding change in severe AV.
Conclusion
There is a correlation between AV, especially severe acne, and the −863 G > A and −308 G > A polymorphism, which influences TNF‐α gene expression and serum TNF‐α levels.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>38923681</pmid><doi>10.1111/srt.13811</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0001-6582-907X</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Acne acne vulgaris Acne Vulgaris - blood Acne Vulgaris - genetics Adolescent Adult Biochemical analysis Blood levels Case-Control Studies Comedones Cross-Sectional Studies Fasting Female Folding Gene expression Gene polymorphism Genetic diversity Genetic Predisposition to Disease - genetics Genetic variance Glucose Humans Hyperpigmentation Inflammation Insulin Insulin resistance Insulin Resistance - genetics Laboratory testing Male Nodules Original Polymorphism Polymorphism, Single Nucleotide Psychology serum TNF‐α Severity of Illness Index Skin diseases Skin resistance TNF‐α gene TNF‐α gene expression Torso Tumor necrosis factor Tumor Necrosis Factor-alpha - blood Tumor Necrosis Factor-alpha - genetics Tumor necrosis factor-TNF Young Adult |
title | In severe acne vulgaris, TNF‐α gene variants are connected to increased TNF‐α gene expression and insulin resistance |
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