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Nineteen young, healthy adults underwent randomized crossover lipid infusion or saline, with plasma ketones and inflammatory markers measured via colorimetric and multiplex assays. Hepatic and peripheral insulin sensitivity was evaluated using a hyperinsulinemic–euglycemic clamp, and skeletal muscle biopsies assessed gene expression linked to ketone metabolism and inflammation.",{"@graph":69,"@context":121},[70,84,104],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":40,"@type":76,"position":81},"https://docshare.wps.com/document/research-report/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/ketogenic-propensity-is-differentially-related-to-lipid-induced-hepatic-and-peripheral-insulin-resistance/433406/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":98,"encodingFormat":97,"isAccessibleForFree":99,"interactionStatistic":100},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/ketogenic-propensity-is-differentially-related-to-lipid-induced-hepatic-and-peripheral-insulin-resistance/433406.png","ImageObject",300,407,{"name":92,"@type":93},"CatatanPagi","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-09-29",true,{"@type":101,"interactionType":102,"userInteractionCount":81},"InteractionCounter",{"@type":103},"ViewAction",{"@type":105,"mainEntity":106},"FAQPage",[107,113,117],{"name":108,"@type":109,"acceptedAnswer":110},"What was the study’s primary aim?","Question",{"text":111,"@type":112},"To determine the ketogenic response, tracked by β-hydroxybutyrate as a surrogate for hepatic ketogenesis, in relation to a controlled lipid overload in humans.","Answer",{"name":114,"@type":109,"acceptedAnswer":115},"How was insulin sensitivity measured?",{"text":116,"@type":112},"Hepatic and peripheral insulin sensitivity were assessed using the hyperinsulinemic–euglycemic clamp, alongside measured plasma ketones and inflammatory markers.",{"name":118,"@type":109,"acceptedAnswer":119},"What did the results show about ketones and insulin resistance under lipid vs saline conditions?",{"text":120,"@type":112},"During lipid overload, ketones increased with hyperlipidemia and decreased with hyperinsulinemia; ketones correlated positively with hepatic insulin sensitivity and inversely with peripheral insulin sensitivity, while in saline controls ketones did not correlate with insulin sensitivity measures.","https://schema.org",{"og:url":83,"og:type":123,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":125,"canonical":83},"index,follow",{"doc_id":127,"site_id":62},433406,1790704840,{"code":4,"msg":5,"data":130},{"doc_id":127,"user_id":131,"nickname":92,"user_avatar":132,"doc_module":4,"category_id":39,"category_name":40,"doc_title":65,"doc_description":67,"doc_content":133,"file_id":134,"file_url":135,"file_type":136,"file_size":137,"view_count":81,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":138,"language":139,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":140,"faqs":141,"seo_title":142,"seo_description":67,"update_tm":143,"read_time":144},962090894170,"https://ap-avatar.wpscdn.com/davatar_6f874abed73319feea01a86fa6f0fab8","Author Manuscript Author Manuscript Author Manuscript Author Manuscript  \n\n| | HHS Public Access\u003Cbr>Author manuscript\u003Cbr>Acta Physiol (Oxf). Author manuscript; available in PMC 2026 January 05. |\n| --- | --- |\n\nPublished in final edited form as:  \nActa Physiol (Oxf). 2023 December ; 239(4): e14054 . doi:10.1111/apha.14054 .  \nKetogenic propensity is differentially related to lipid-induced hepatic and peripheral insulin resistance  \nJ. T. Mey,  \nB. Vandagmansar,  \nW. S. Dantas,  \nK. P. Belmont,  \nC. L. Axelrod,  \nJ. P. Kirwan  \nPennington Biomedical Research Center, Baton Rouge, Louisiana, USA  \nAbstract  \nAim: Determine the ketogenic response (β-hydroxybutyrate, a surrogate of hepatic ketogenesis) toa controlled lipid overload in humans.  \nMethods: In total, nineteen young, healthy adults (age: 28.4 ± 1.7 years; BMI: 22.7 ± 0.3  \nkg/m2) received either a 12 h overnight lipid infusion or saline in a randomized, crossover design. Plasma ketones and inflammatory markers were quantified by colorimetric and multiplex assays. Hepatic and peripheral insulin sensitivity was assessed by the hyperinsulinemic–euglycemicclamp. Skeletal muscle biopsies were obtained to quantify gene expression related to ketone body metabolism and inflammation.  \nResults: By design, the lipid overload-induced hepatic (50%, p \u003C 0 .001) and peripheral insulin resistance (73%, p \u003C 0.01) in healthy adults. Ketones increased with hyperlipidemia and were subsequently reduced with hyperinsulinemia during the clamp procedure (Saline: Basal = 0.22 mM, Insulin = 0.07 mM; Lipid: Basal = 0.78 mM, Insulin = 0.51 mM; 2-way ANOVA: Lipid p \u003C 0.001, Insulin p \u003C 0.001, Interaction p = 0.07) . In the saline control condition, ketones did not correlate with hepatic or peripheral insulin sensitivity. Conversely, in the lipid condition, ketones were positively correlated with hepatic insulin sensitivity (r = 0.59, p \u003C 0.01), but inversely  \nThis is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.  \nCorrespondence, J. P. Kirwan, Integrated Physiology and Molecular Medicine, Pennington Biomedical Research Center, 6400 Perkins Road, Baton Rouge, LA 70808, [USA. john.kirwan@pbrc.edu](USA. john.kirwan@pbrc.edu).  \nAUTHOR CONTRIBUTIONS  \nJ. T. Mey: Conceptualization; Investigation; Formal analysis; Visualization; Writing—original draft; Writing—review & editing; Data curation; Methodology. B. Vandagmansar: Conceptualization; Data curation; Formal analysis; Visualization; Methodology; Investigation; Writing—review & editing. W. S. Dantas: Conceptualization; Data curation; Formal analysis; Visualization; Methodology; Investigation; Writing—review & editing. K. P. Belmont: Data curation; Formal analysis; Investigation; Writing—review & editing. C. L. Axelrod: Conceptualization; Data curation; Formal analysis; Visualization; Methodology; Investigation; Supervision; Project administration; Writing—review & editing. J. P. Kirwan: Conceptualization; Data curation; Formal analysis; Visualization; Methodology; Investigation; Supervision; Project administration; Writing—review & editing; Funding acquisition; Resources.  \nCONFLICT OF INTEREST STATEMENT  \nThe authors declare that they have no conflicts of interest with this work.  \nAuthor Manuscript Author Manuscript Author Manuscript Author Manuscript  \nMey et al. Page 2  \nrelated to peripheral insulin sensitivity (r = −0.64, p \u003C 0.01). Hyperlipidemia increased plasma inflammatory markers, but did not impact skeletal muscle inflammatory gene expression. Gene expression related to ketone and fatty acid metabolism in skeletal muscle increased in response to hyperlipidemia.  \nConclusion: This work provides important insight into the role of ketones in human health and suggests that ketone body metabolism is altered at the ons","cbCaipniJgjYRfu1","https://ap.wps.com/l/cbCaipniJgjYRfu1","pdf",1335750,22,"English","# Abstract\n## Aim\n## Methods\n## Results\n## Conclusion\n# Introduction\n## Background and rationale\n## Countermeasures and prior findings\n## Lipid-induced insulin resistance mechanisms","[{\"question\":\"What was the study’s primary aim?\",\"answer\":\"To determine the ketogenic response, tracked by β-hydroxybutyrate as a surrogate for hepatic ketogenesis, in relation to a controlled lipid overload in humans.\"},{\"question\":\"How was insulin sensitivity measured?\",\"answer\":\"Hepatic and peripheral insulin sensitivity were assessed using the hyperinsulinemic–euglycemic clamp, alongside measured plasma ketones and inflammatory markers.\"},{\"question\":\"What did the results show about ketones and insulin resistance under lipid vs saline conditions?\",\"answer\":\"During lipid overload, ketones increased with hyperlipidemia and decreased with hyperinsulinemia; ketones correlated positively with hepatic insulin sensitivity and inversely with peripheral insulin sensitivity, while in saline controls ketones did not correlate with insulin sensitivity measures.\"}]","Ketogenic propensity is differentially related to lipid-induced hepatic and peripheral insulin resistance | PDF",1790664006,55]