Nathalie Rohmann , Paula Stürmer , Corinna Geisler , Kristina Schlicht , Carina Knappe , Katharina Hartmann , Kathrin Türk , Tim Hollstein , Alexia Beckmann , Anna K. Seoudy , Ulla Becker , Perdita Wietzke-Braun , Ute Settgast , Florian Tran , Philip Rosenstiel , Jan H. Beckmann , Witigo von Schönfels , Stephan Seifert , Jan Heyckendorf , Andre Franke , Matthias Laudes
{"title":"生活方式和相关疾病对血清 CC16 的影响表明，新陈代谢、心脏和肺之间存在复杂的相互作用","authors":"Nathalie Rohmann , Paula Stürmer , Corinna Geisler , Kristina Schlicht , Carina Knappe , Katharina Hartmann , Kathrin Türk , Tim Hollstein , Alexia Beckmann , Anna K. Seoudy , Ulla Becker , Perdita Wietzke-Braun , Ute Settgast , Florian Tran , Philip Rosenstiel , Jan H. Beckmann , Witigo von Schönfels , Stephan Seifert , Jan Heyckendorf , Andre Franke , Matthias Laudes","doi":"10.1016/j.jare.2023.06.005","DOIUrl":null,"url":null,"abstract":"<div><h3>Introduction</h3><p>Clara cell 16-kDa protein (CC16) is an anti-inflammatory, immunomodulatory secreted pulmonary protein with reduced serum concentrations in obesity according to recent data.</p></div><div><h3>Objective</h3><p>Studies focused solely on bodyweight, which does not properly reflect obesity-associated implications of the metabolic and reno-cardio-vascular system. The purpose of this study was therefore to examine CC16 in a broad physiological context considering cardio-metabolic comorbidities of primary pulmonary diseases.</p></div><div><h3>Methods</h3><p>CC16 was quantified in serum samples in a subset of the FoCus (N = 497) and two weight loss intervention cohorts (N = 99) using ELISA. Correlation and general linear regression analyses were applied to assess CC16 effects of lifestyle, gut microbiota, disease occurrence and treatment strategies. Importance and intercorrelation of determinants were validated using random forest algorithms.</p></div><div><h3>Results</h3><p>CC16 A38G gene mutation, smoking and low microbial diversity significantly decreased CC16. Pre-menopausal female displayed lower CC16 compared to post-menopausal female and male participants. Biological age and uricosuric medications increased CC16 (all <em>p</em> < 0.01). Adjusted linear regression revealed CC16 lowering effects of high waist-to-hip ratio (est. −11.19 [−19.4; −2.97], <em>p</em> = 7.99 × 10<sup>−3</sup>), severe obesity (est. −2.58 [−4.33; −0.82], <em>p</em> = 4.14 × 10<sup>−3</sup>) and hypertension (est. −4.31 [−7.5; −1.12], <em>p</em> = 8.48 × 10<sup>−3</sup>). ACEi/ARB medication (<em>p</em> = 2.5 × 10<sup>−2</sup>) and chronic heart failure (est. 4.69 [1.37; 8.02], <em>p</em> = 5.91 × 10<sup>−3</sup>) presented increasing effects on CC16. Mild associations of CC16 were observed with blood pressure, HOMA-IR and NT-proBNP, but not manifest hyperlipidemia, type 2 diabetes, diet quality and dietary weight loss intervention.</p></div><div><h3>Conclusion</h3><p>A role of metabolic and cardiovascular abnormalities in the regulation of CC16 and its modifiability by behavioral and pharmacological interventions is indicated. Alterations by ACEi/ARB and uricosurics could point towards regulatory axes comprising the renin-angiotensin-aldosterone system and purine metabolism. Findings altogether strengthen the importance of interactions among metabolism, heart and lungs.</p></div>","PeriodicalId":14952,"journal":{"name":"Journal of Advanced Research","volume":"59 ","pages":"Pages 161-171"},"PeriodicalIF":11.4000,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2090123223001686/pdfft?md5=63492328022031a161b8be41b7c6e912&pid=1-s2.0-S2090123223001686-main.pdf","citationCount":"0","resultStr":"{\"title\":\"Effects of lifestyle and associated diseases on serum CC16 suggest complex interactions among metabolism, heart and lungs\",\"authors\":\"Nathalie Rohmann , Paula Stürmer , Corinna Geisler , Kristina Schlicht , Carina Knappe , Katharina Hartmann , Kathrin Türk , Tim Hollstein , Alexia Beckmann , Anna K. Seoudy , Ulla Becker , Perdita Wietzke-Braun , Ute Settgast , Florian Tran , Philip Rosenstiel , Jan H. Beckmann , Witigo von Schönfels , Stephan Seifert , Jan Heyckendorf , Andre Franke , Matthias Laudes\",\"doi\":\"10.1016/j.jare.2023.06.005\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Introduction</h3><p>Clara cell 16-kDa protein (CC16) is an anti-inflammatory, immunomodulatory secreted pulmonary protein with reduced serum concentrations in obesity according to recent data.</p></div><div><h3>Objective</h3><p>Studies focused solely on bodyweight, which does not properly reflect obesity-associated implications of the metabolic and reno-cardio-vascular system. The purpose of this study was therefore to examine CC16 in a broad physiological context considering cardio-metabolic comorbidities of primary pulmonary diseases.</p></div><div><h3>Methods</h3><p>CC16 was quantified in serum samples in a subset of the FoCus (N = 497) and two weight loss intervention cohorts (N = 99) using ELISA. Correlation and general linear regression analyses were applied to assess CC16 effects of lifestyle, gut microbiota, disease occurrence and treatment strategies. Importance and intercorrelation of determinants were validated using random forest algorithms.</p></div><div><h3>Results</h3><p>CC16 A38G gene mutation, smoking and low microbial diversity significantly decreased CC16. Pre-menopausal female displayed lower CC16 compared to post-menopausal female and male participants. Biological age and uricosuric medications increased CC16 (all <em>p</em> < 0.01). Adjusted linear regression revealed CC16 lowering effects of high waist-to-hip ratio (est. −11.19 [−19.4; −2.97], <em>p</em> = 7.99 × 10<sup>−3</sup>), severe obesity (est. −2.58 [−4.33; −0.82], <em>p</em> = 4.14 × 10<sup>−3</sup>) and hypertension (est. −4.31 [−7.5; −1.12], <em>p</em> = 8.48 × 10<sup>−3</sup>). ACEi/ARB medication (<em>p</em> = 2.5 × 10<sup>−2</sup>) and chronic heart failure (est. 4.69 [1.37; 8.02], <em>p</em> = 5.91 × 10<sup>−3</sup>) presented increasing effects on CC16. Mild associations of CC16 were observed with blood pressure, HOMA-IR and NT-proBNP, but not manifest hyperlipidemia, type 2 diabetes, diet quality and dietary weight loss intervention.</p></div><div><h3>Conclusion</h3><p>A role of metabolic and cardiovascular abnormalities in the regulation of CC16 and its modifiability by behavioral and pharmacological interventions is indicated. Alterations by ACEi/ARB and uricosurics could point towards regulatory axes comprising the renin-angiotensin-aldosterone system and purine metabolism. 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Effects of lifestyle and associated diseases on serum CC16 suggest complex interactions among metabolism, heart and lungs
Introduction
Clara cell 16-kDa protein (CC16) is an anti-inflammatory, immunomodulatory secreted pulmonary protein with reduced serum concentrations in obesity according to recent data.
Objective
Studies focused solely on bodyweight, which does not properly reflect obesity-associated implications of the metabolic and reno-cardio-vascular system. The purpose of this study was therefore to examine CC16 in a broad physiological context considering cardio-metabolic comorbidities of primary pulmonary diseases.
Methods
CC16 was quantified in serum samples in a subset of the FoCus (N = 497) and two weight loss intervention cohorts (N = 99) using ELISA. Correlation and general linear regression analyses were applied to assess CC16 effects of lifestyle, gut microbiota, disease occurrence and treatment strategies. Importance and intercorrelation of determinants were validated using random forest algorithms.
Results
CC16 A38G gene mutation, smoking and low microbial diversity significantly decreased CC16. Pre-menopausal female displayed lower CC16 compared to post-menopausal female and male participants. Biological age and uricosuric medications increased CC16 (all p < 0.01). Adjusted linear regression revealed CC16 lowering effects of high waist-to-hip ratio (est. −11.19 [−19.4; −2.97], p = 7.99 × 10−3), severe obesity (est. −2.58 [−4.33; −0.82], p = 4.14 × 10−3) and hypertension (est. −4.31 [−7.5; −1.12], p = 8.48 × 10−3). ACEi/ARB medication (p = 2.5 × 10−2) and chronic heart failure (est. 4.69 [1.37; 8.02], p = 5.91 × 10−3) presented increasing effects on CC16. Mild associations of CC16 were observed with blood pressure, HOMA-IR and NT-proBNP, but not manifest hyperlipidemia, type 2 diabetes, diet quality and dietary weight loss intervention.
Conclusion
A role of metabolic and cardiovascular abnormalities in the regulation of CC16 and its modifiability by behavioral and pharmacological interventions is indicated. Alterations by ACEi/ARB and uricosurics could point towards regulatory axes comprising the renin-angiotensin-aldosterone system and purine metabolism. Findings altogether strengthen the importance of interactions among metabolism, heart and lungs.
期刊介绍：
Journal of Advanced Research (J. Adv. Res.) is an applied/natural sciences, peer-reviewed journal that focuses on interdisciplinary research. The journal aims to contribute to applied research and knowledge worldwide through the publication of original and high-quality research articles in the fields of Medicine, Pharmaceutical Sciences, Dentistry, Physical Therapy, Veterinary Medicine, and Basic and Biological Sciences.
The following abstracting and indexing services cover the Journal of Advanced Research: PubMed/Medline, Essential Science Indicators, Web of Science, Scopus, PubMed Central, PubMed, Science Citation Index Expanded, Directory of Open Access Journals (DOAJ), and INSPEC.
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