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Beta-cell, but not autonomic nervous system, function is related to MAFLD in early stages of glucose intolerance
IntroductionPrevious studies have suggested an association between beta-cell and autonomic function and metabolic-associated fatty liver disease (MAFLD). We explored the association between controlled attenuated parameter (CAP) and insulin secretion and action, as well as sympathetic and parasympath...
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description | IntroductionPrevious studies have suggested an association between beta-cell and autonomic function and metabolic-associated fatty liver disease (MAFLD). We explored the association between controlled attenuated parameter (CAP) and insulin secretion and action, as well as sympathetic and parasympathetic activity in normal (NGT) and impaired (IGT) glucose tolerance.Research design and methodsTwenty-five NGT (age 44.8±9.6 years; body mass index (BMI) 32.3±6.9 kg/m2) and 27 IGT (47.6±11.8 years; 31.0±6.5 kg/m2) subjects underwent a 75 g oral glucose tolerance test (OGTT) and a mixed meal tolerance test (MMTT) for assessment of glucose and insulin secretion. Parameters of beta-cell function and insulin sensitivity were calculated. Body composition was assessed by bioimpedance analysis (Inbody720). Autonomic function was assessed by ANX V.3.0 monitoring system. CAP was determined by Fibroscan (Echosense) and presence of MAFLD was defined as CAP >233 dB/m.ResultsA CAP >233 dB/m was found in 72% of subjects with NGT and 67% of subjects with IGT. Subjects with MAFLD, irrespective of glucose tolerance, had higher BMI and waist circumference, lower insulin secretion and action, and lower parasympathetic activity. On a matrix analysis, after adjustment for age and BMI, CAP was positively related to systolic blood pressure (SBP); insulin action was negatively related to parasympathetic activity. Regression analysis showed that AUC-insulin MMTT remained independently related to MAFLD: OR 24.4 (95% CI 2.17 to 274.77; p=0.010). A “cut-off” value of 15,620 uIU/mL-1*180 min-1 provided a 75% sensitivity and 75% specificity for CAP >233 dB/m.ConclusionsOur results do not support a role for parasympathetic activity in MAFLD. Rather, they show that stimulated hyperinsulinemia may be associated with greater risk of MAFLD irrespective of glucose tolerance in a high-risk population without diabetes. |
doi_str_mv | 10.1136/bmjdrc-2024-004542 |
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We explored the association between controlled attenuated parameter (CAP) and insulin secretion and action, as well as sympathetic and parasympathetic activity in normal (NGT) and impaired (IGT) glucose tolerance.Research design and methodsTwenty-five NGT (age 44.8±9.6 years; body mass index (BMI) 32.3±6.9 kg/m2) and 27 IGT (47.6±11.8 years; 31.0±6.5 kg/m2) subjects underwent a 75 g oral glucose tolerance test (OGTT) and a mixed meal tolerance test (MMTT) for assessment of glucose and insulin secretion. Parameters of beta-cell function and insulin sensitivity were calculated. Body composition was assessed by bioimpedance analysis (Inbody720). Autonomic function was assessed by ANX V.3.0 monitoring system. CAP was determined by Fibroscan (Echosense) and presence of MAFLD was defined as CAP >233 dB/m.ResultsA CAP >233 dB/m was found in 72% of subjects with NGT and 67% of subjects with IGT. Subjects with MAFLD, irrespective of glucose tolerance, had higher BMI and waist circumference, lower insulin secretion and action, and lower parasympathetic activity. On a matrix analysis, after adjustment for age and BMI, CAP was positively related to systolic blood pressure (SBP); insulin action was negatively related to parasympathetic activity. Regression analysis showed that AUC-insulin MMTT remained independently related to MAFLD: OR 24.4 (95% CI 2.17 to 274.77; p=0.010). A “cut-off” value of 15,620 uIU/mL-1*180 min-1 provided a 75% sensitivity and 75% specificity for CAP >233 dB/m.ConclusionsOur results do not support a role for parasympathetic activity in MAFLD. Rather, they show that stimulated hyperinsulinemia may be associated with greater risk of MAFLD irrespective of glucose tolerance in a high-risk population without diabetes.</description><identifier>ISSN: 2052-4897</identifier><identifier>EISSN: 2052-4897</identifier><identifier>DOI: 10.1136/bmjdrc-2024-004542</identifier><identifier>PMID: 39706674</identifier><language>eng</language><publisher>England: American Diabetes Association</publisher><subject>Adult ; Autonomic Function ; Autonomic Nervous System - physiopathology ; Biomarkers - analysis ; Blood Glucose - analysis ; Body Mass Index ; Cardiovascular and Metabolic Risk ; Clinical medicine ; Diabetes ; Female ; Follow-Up Studies ; Glucose ; Glucose Intolerance - physiopathology ; Glucose Tolerance Test ; Humans ; Hyperinsulinemia ; Impaired Glucose Tolerance ; Insulin - metabolism ; Insulin resistance ; Insulin Resistance - physiology ; Insulin Secretion ; Insulin-Secreting Cells - metabolism ; Insulin-Secreting Cells - physiology ; Liver diseases ; Male ; Metabolism ; Middle Aged ; Nervous system ; Non-alcoholic Fatty Liver Disease - physiopathology ; Original Research ; Pathogenesis ; Peptides ; Prognosis ; Respiration ; Software ; Statistical analysis ; Variance analysis</subject><ispartof>BMJ open diabetes research & care, 2024-12, Vol.12 (6), p.e004542</ispartof><rights>Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ Group.</rights><rights>2024 Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ Group. http://creativecommons.org/licenses/by-nc/4.0/ This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/ . Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Copyright © Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ Group. 2024</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-b3322-7d7639df78f53fb4965331169e5cbf449cdc97a970b305aa2f36a500ba0009343</cites><orcidid>0000-0003-2838-4344 ; 0000-0002-5388-0270</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/3147734508/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/3147734508?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25751,27922,27923,37010,37011,44588,53789,53791,55348,74896,77430,77456</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39706674$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dimova, Rumyana</creatorcontrib><creatorcontrib>Chakarova, Nevena</creatorcontrib><creatorcontrib>Serdarova, Mina</creatorcontrib><creatorcontrib>Marinova, Cvetelina</creatorcontrib><creatorcontrib>Popov, Dimitar</creatorcontrib><creatorcontrib>Del Prato, Stefano</creatorcontrib><creatorcontrib>Tankova, Tsvetalina</creatorcontrib><title>Beta-cell, but not autonomic nervous system, function is related to MAFLD in early stages of glucose intolerance</title><title>BMJ open diabetes research & care</title><addtitle>BMJ Open Diab Res Care</addtitle><addtitle>BMJ Open Diabetes Res Care</addtitle><description>IntroductionPrevious studies have suggested an association between beta-cell and autonomic function and metabolic-associated fatty liver disease (MAFLD). We explored the association between controlled attenuated parameter (CAP) and insulin secretion and action, as well as sympathetic and parasympathetic activity in normal (NGT) and impaired (IGT) glucose tolerance.Research design and methodsTwenty-five NGT (age 44.8±9.6 years; body mass index (BMI) 32.3±6.9 kg/m2) and 27 IGT (47.6±11.8 years; 31.0±6.5 kg/m2) subjects underwent a 75 g oral glucose tolerance test (OGTT) and a mixed meal tolerance test (MMTT) for assessment of glucose and insulin secretion. Parameters of beta-cell function and insulin sensitivity were calculated. Body composition was assessed by bioimpedance analysis (Inbody720). Autonomic function was assessed by ANX V.3.0 monitoring system. CAP was determined by Fibroscan (Echosense) and presence of MAFLD was defined as CAP >233 dB/m.ResultsA CAP >233 dB/m was found in 72% of subjects with NGT and 67% of subjects with IGT. Subjects with MAFLD, irrespective of glucose tolerance, had higher BMI and waist circumference, lower insulin secretion and action, and lower parasympathetic activity. On a matrix analysis, after adjustment for age and BMI, CAP was positively related to systolic blood pressure (SBP); insulin action was negatively related to parasympathetic activity. Regression analysis showed that AUC-insulin MMTT remained independently related to MAFLD: OR 24.4 (95% CI 2.17 to 274.77; p=0.010). A “cut-off” value of 15,620 uIU/mL-1*180 min-1 provided a 75% sensitivity and 75% specificity for CAP >233 dB/m.ConclusionsOur results do not support a role for parasympathetic activity in MAFLD. Rather, they show that stimulated hyperinsulinemia may be associated with greater risk of MAFLD irrespective of glucose tolerance in a high-risk population without diabetes.</description><subject>Adult</subject><subject>Autonomic Function</subject><subject>Autonomic Nervous System - physiopathology</subject><subject>Biomarkers - analysis</subject><subject>Blood Glucose - analysis</subject><subject>Body Mass Index</subject><subject>Cardiovascular and Metabolic Risk</subject><subject>Clinical medicine</subject><subject>Diabetes</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>Glucose</subject><subject>Glucose Intolerance - physiopathology</subject><subject>Glucose Tolerance Test</subject><subject>Humans</subject><subject>Hyperinsulinemia</subject><subject>Impaired Glucose Tolerance</subject><subject>Insulin - metabolism</subject><subject>Insulin resistance</subject><subject>Insulin Resistance - physiology</subject><subject>Insulin Secretion</subject><subject>Insulin-Secreting Cells - metabolism</subject><subject>Insulin-Secreting Cells - physiology</subject><subject>Liver diseases</subject><subject>Male</subject><subject>Metabolism</subject><subject>Middle Aged</subject><subject>Nervous system</subject><subject>Non-alcoholic Fatty Liver Disease - physiopathology</subject><subject>Original Research</subject><subject>Pathogenesis</subject><subject>Peptides</subject><subject>Prognosis</subject><subject>Respiration</subject><subject>Software</subject><subject>Statistical analysis</subject><subject>Variance analysis</subject><issn>2052-4897</issn><issn>2052-4897</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>9YT</sourceid><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNp9kk9v1DAQxSMEolXpF-CALHHh0BTHf-L4hNpCodIiLnC2xo69ZJXYi-1U2m-P05TScuBky_Pm55mnV1WvG3zeNLR9r6ddH01NMGE1xowz8qw6JpiTmnVSPH90P6pOU9phjEtbQzv-sjqiUuC2Fey42l_aDLWx43iG9JyRDxnBnIMP02CQt_E2zAmlQ8p2OkNu9iYPwaMhoWhHyLZHOaCvF9ebj2jwyEIcDyhl2NqEgkPbcTYh2VLKYbQRvLGvqhcOxmRP78-T6sf1p-9XX-rNt883VxebWlNKSC160VLZO9E5Tp1msuWUNk0rLTfaMSZNb6SAsoemmAMQR1vgGGsoi0rK6El1s3L7ADu1j8ME8aACDOruIcStgpgHM1rVQWu6xnWOyI51WkotjHAgpGGaAe8K68PK2s96sr2xPkcYn0CfVvzwU23DrSoDF5fJQnh3T4jh12xTVtOQFtfB22Kwog0TUlAscZG-_Ue6C3P0xas7laCM4wVIVpWJIaVo3cM0DVZLQNQaELUERK0BKU1vHu_x0PInDkVwvgpK899v_0P8Day_xgI</recordid><startdate>20241220</startdate><enddate>20241220</enddate><creator>Dimova, Rumyana</creator><creator>Chakarova, Nevena</creator><creator>Serdarova, Mina</creator><creator>Marinova, Cvetelina</creator><creator>Popov, Dimitar</creator><creator>Del Prato, Stefano</creator><creator>Tankova, Tsvetalina</creator><general>American Diabetes Association</general><general>BMJ Publishing Group LTD</general><general>BMJ Publishing Group</general><scope>9YT</scope><scope>ACMMV</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>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>NAPCQ</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0003-2838-4344</orcidid><orcidid>https://orcid.org/0000-0002-5388-0270</orcidid></search><sort><creationdate>20241220</creationdate><title>Beta-cell, but not autonomic nervous system, function is related to MAFLD in early stages of glucose intolerance</title><author>Dimova, Rumyana ; Chakarova, Nevena ; Serdarova, Mina ; Marinova, Cvetelina ; Popov, Dimitar ; Del Prato, Stefano ; Tankova, Tsvetalina</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b3322-7d7639df78f53fb4965331169e5cbf449cdc97a970b305aa2f36a500ba0009343</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Adult</topic><topic>Autonomic Function</topic><topic>Autonomic Nervous System - physiopathology</topic><topic>Biomarkers - analysis</topic><topic>Blood Glucose - analysis</topic><topic>Body Mass Index</topic><topic>Cardiovascular and Metabolic Risk</topic><topic>Clinical medicine</topic><topic>Diabetes</topic><topic>Female</topic><topic>Follow-Up Studies</topic><topic>Glucose</topic><topic>Glucose Intolerance - physiopathology</topic><topic>Glucose Tolerance Test</topic><topic>Humans</topic><topic>Hyperinsulinemia</topic><topic>Impaired Glucose Tolerance</topic><topic>Insulin - metabolism</topic><topic>Insulin resistance</topic><topic>Insulin Resistance - physiology</topic><topic>Insulin Secretion</topic><topic>Insulin-Secreting Cells - metabolism</topic><topic>Insulin-Secreting Cells - physiology</topic><topic>Liver diseases</topic><topic>Male</topic><topic>Metabolism</topic><topic>Middle Aged</topic><topic>Nervous system</topic><topic>Non-alcoholic Fatty Liver Disease - physiopathology</topic><topic>Original Research</topic><topic>Pathogenesis</topic><topic>Peptides</topic><topic>Prognosis</topic><topic>Respiration</topic><topic>Software</topic><topic>Statistical analysis</topic><topic>Variance analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dimova, Rumyana</creatorcontrib><creatorcontrib>Chakarova, Nevena</creatorcontrib><creatorcontrib>Serdarova, Mina</creatorcontrib><creatorcontrib>Marinova, Cvetelina</creatorcontrib><creatorcontrib>Popov, Dimitar</creatorcontrib><creatorcontrib>Del Prato, Stefano</creatorcontrib><creatorcontrib>Tankova, Tsvetalina</creatorcontrib><collection>British Medical Journal Open Access Journals</collection><collection>BMJ Journals: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>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database (ProQuest)</collection><collection>ProQuest_Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Nursing & Allied Health Premium</collection><collection>Publicly Available Content Database (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>Directory of Open Access Journals</collection><jtitle>BMJ open diabetes research & care</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dimova, Rumyana</au><au>Chakarova, Nevena</au><au>Serdarova, Mina</au><au>Marinova, Cvetelina</au><au>Popov, Dimitar</au><au>Del Prato, Stefano</au><au>Tankova, Tsvetalina</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Beta-cell, but not autonomic nervous system, function is related to MAFLD in early stages of glucose intolerance</atitle><jtitle>BMJ open diabetes research & care</jtitle><stitle>BMJ Open Diab Res Care</stitle><addtitle>BMJ Open Diabetes Res Care</addtitle><date>2024-12-20</date><risdate>2024</risdate><volume>12</volume><issue>6</issue><spage>e004542</spage><pages>e004542-</pages><issn>2052-4897</issn><eissn>2052-4897</eissn><abstract>IntroductionPrevious studies have suggested an association between beta-cell and autonomic function and metabolic-associated fatty liver disease (MAFLD). We explored the association between controlled attenuated parameter (CAP) and insulin secretion and action, as well as sympathetic and parasympathetic activity in normal (NGT) and impaired (IGT) glucose tolerance.Research design and methodsTwenty-five NGT (age 44.8±9.6 years; body mass index (BMI) 32.3±6.9 kg/m2) and 27 IGT (47.6±11.8 years; 31.0±6.5 kg/m2) subjects underwent a 75 g oral glucose tolerance test (OGTT) and a mixed meal tolerance test (MMTT) for assessment of glucose and insulin secretion. Parameters of beta-cell function and insulin sensitivity were calculated. Body composition was assessed by bioimpedance analysis (Inbody720). Autonomic function was assessed by ANX V.3.0 monitoring system. CAP was determined by Fibroscan (Echosense) and presence of MAFLD was defined as CAP >233 dB/m.ResultsA CAP >233 dB/m was found in 72% of subjects with NGT and 67% of subjects with IGT. Subjects with MAFLD, irrespective of glucose tolerance, had higher BMI and waist circumference, lower insulin secretion and action, and lower parasympathetic activity. On a matrix analysis, after adjustment for age and BMI, CAP was positively related to systolic blood pressure (SBP); insulin action was negatively related to parasympathetic activity. Regression analysis showed that AUC-insulin MMTT remained independently related to MAFLD: OR 24.4 (95% CI 2.17 to 274.77; p=0.010). A “cut-off” value of 15,620 uIU/mL-1*180 min-1 provided a 75% sensitivity and 75% specificity for CAP >233 dB/m.ConclusionsOur results do not support a role for parasympathetic activity in MAFLD. Rather, they show that stimulated hyperinsulinemia may be associated with greater risk of MAFLD irrespective of glucose tolerance in a high-risk population without diabetes.</abstract><cop>England</cop><pub>American Diabetes Association</pub><pmid>39706674</pmid><doi>10.1136/bmjdrc-2024-004542</doi><orcidid>https://orcid.org/0000-0003-2838-4344</orcidid><orcidid>https://orcid.org/0000-0002-5388-0270</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Adult Autonomic Function Autonomic Nervous System - physiopathology Biomarkers - analysis Blood Glucose - analysis Body Mass Index Cardiovascular and Metabolic Risk Clinical medicine Diabetes Female Follow-Up Studies Glucose Glucose Intolerance - physiopathology Glucose Tolerance Test Humans Hyperinsulinemia Impaired Glucose Tolerance Insulin - metabolism Insulin resistance Insulin Resistance - physiology Insulin Secretion Insulin-Secreting Cells - metabolism Insulin-Secreting Cells - physiology Liver diseases Male Metabolism Middle Aged Nervous system Non-alcoholic Fatty Liver Disease - physiopathology Original Research Pathogenesis Peptides Prognosis Respiration Software Statistical analysis Variance analysis |
title | Beta-cell, but not autonomic nervous system, function is related to MAFLD in early stages of glucose intolerance |
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