<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>10(12)</volume><submitter>Horn P</submitter><pubmed_abstract>Sepsis is defined by life-threatening organ dysfunction mediated by the host’s response to infection. This can result in septic dyslipidemia, which is involved in the neutralization of pathogen-related lipids. Knowledge of the regulatory mechanisms of septic dyslipidemia is incomplete. The cytokine betatrophin/Angiopoietin-like protein 8 (ANGPTL8) plays a role in the regulation of triacylglyceride metabolism, though its function in septic dyslipidemia remains unknown. Sixty-six patients were enrolled in a cross-sectional study. Circulating concentrations and adipose tissue (AT) mRNA expression of betatrophin/ANGPTL8 were studied in patients suffering from peritoneal sepsis. Insulin-resistant individuals and subjects without metabolic derangement/systemic inflammation were enrolled as controls. All underwent open abdominal surgery. Circulating betatrophin/ANGPTL8 was analyzed by an enzyme-linked immunosorbent assay and AT mRNA expression levels were assessed by real-time PCR. Standard laboratory analyses including lipid electrophoresis were evaluated. Sepsis patients showed pronounced septic dyslipidemia (p &lt; 0.05 for all major lipid classes). Despite comparable betatrophin/ANGPTL8 mRNA expression in AT (p = 0.24), we found significantly increased circulating betatrophin/ANGPTL8 with septic dyslipidemia (p = 0.009). Expression levels of betatrophin/ANGPTL8 in AT correlated with circulating concentrations in both control groups (r = 0.61; p = 0.008 and r = 0.43; p = 0.034), while this association was undetectable in sepsis. After stratification, betatrophin/ANGPTL8 remained associated with hypertriacylglyceridemia (p &lt; 0.05).</pubmed_abstract><journal>Biomedicines</journal><pagination>3151</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9775570</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Associations of Betatrophin/ANGPTL8 with Septic Dyslipidemia in Human Peritonitis: An Explorative Analysis.</pubmed_title><pmcid>PMC9775570</pmcid><pubmed_authors>Claus RA</pubmed_authors><pubmed_authors>Sponholz C</pubmed_authors><pubmed_authors>Roth J</pubmed_authors><pubmed_authors>Metzing UB</pubmed_authors><pubmed_authors>Sommerfeld O</pubmed_authors><pubmed_authors>Radtke S</pubmed_authors><pubmed_authors>Steidl R</pubmed_authors><pubmed_authors>Horn P</pubmed_authors><pubmed_authors>Birkenfeld AL</pubmed_authors><pubmed_authors>Settmacher U</pubmed_authors><pubmed_authors>Rauchfuß F</pubmed_authors><pubmed_authors>von Loeffelholz C</pubmed_authors></additional><is_claimable>false</is_claimable><name>Associations of Betatrophin/ANGPTL8 with Septic Dyslipidemia in Human Peritonitis: An Explorative Analysis.</name><description>Sepsis is defined by life-threatening organ dysfunction mediated by the host’s response to infection. This can result in septic dyslipidemia, which is involved in the neutralization of pathogen-related lipids. Knowledge of the regulatory mechanisms of septic dyslipidemia is incomplete. The cytokine betatrophin/Angiopoietin-like protein 8 (ANGPTL8) plays a role in the regulation of triacylglyceride metabolism, though its function in septic dyslipidemia remains unknown. Sixty-six patients were enrolled in a cross-sectional study. Circulating concentrations and adipose tissue (AT) mRNA expression of betatrophin/ANGPTL8 were studied in patients suffering from peritoneal sepsis. Insulin-resistant individuals and subjects without metabolic derangement/systemic inflammation were enrolled as controls. All underwent open abdominal surgery. Circulating betatrophin/ANGPTL8 was analyzed by an enzyme-linked immunosorbent assay and AT mRNA expression levels were assessed by real-time PCR. Standard laboratory analyses including lipid electrophoresis were evaluated. Sepsis patients showed pronounced septic dyslipidemia (p &lt; 0.05 for all major lipid classes). Despite comparable betatrophin/ANGPTL8 mRNA expression in AT (p = 0.24), we found significantly increased circulating betatrophin/ANGPTL8 with septic dyslipidemia (p = 0.009). Expression levels of betatrophin/ANGPTL8 in AT correlated with circulating concentrations in both control groups (r = 0.61; p = 0.008 and r = 0.43; p = 0.034), while this association was undetectable in sepsis. After stratification, betatrophin/ANGPTL8 remained associated with hypertriacylglyceridemia (p &lt; 0.05).</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Dec</publication><modification>2025-04-19T14:16:05.336Z</modification><creation>2025-04-19T14:16:05.336Z</creation></dates><accession>S-EPMC9775570</accession><cross_references><pubmed>36551906</pubmed><doi>10.3390/biomedicines10123151</doi></cross_references></HashMap>