{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T19:18:08Z","timestamp":1790709488680,"version":"4.1.0"},"reference-count":130,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"637","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Sci. Transl. Med."],"published-print":{"date-parts":[[2022,3,23]]},"abstract":"<jats:p>\n            Inflammation has profound but poorly understood effects on metabolism, especially in the context of obesity and nonalcoholic fatty liver disease (NAFLD). Here, we report that hepatic interferon regulatory factor 3 (IRF3) is a direct transcriptional regulator of glucose homeostasis through induction of\n            <jats:italic>Ppp2r1b<\/jats:italic>\n            , a component of serine\/threonine phosphatase PP2A, and subsequent suppression of glucose production. Global ablation of IRF3 in mice on a high-fat diet protected against both steatosis and dysglycemia, whereas hepatocyte-specific loss of IRF3 affects only dysglycemia. Integration of the IRF3-dependent transcriptome and cistrome in mouse hepatocytes identifies\n            <jats:italic>Ppp2r1b<\/jats:italic>\n            as a direct IRF3 target responsible for mediating its metabolic actions on glucose homeostasis. IRF3-mediated induction of\n            <jats:italic>Ppp2r1b<\/jats:italic>\n            amplified PP2A activity, with subsequent dephosphorylation of AMPK\u03b1 and AKT. Furthermore, suppression of hepatic\n            <jats:italic>Irf3<\/jats:italic>\n            expression with antisense oligonucleotides reversed obesity-induced insulin resistance and restored glucose homeostasis in obese mice. Obese humans with NAFLD displayed enhanced activation of liver IRF3, with reversion after bariatric surgery. Hepatic\n            <jats:italic>PPP2R1B<\/jats:italic>\n            expression correlated with HgbA1C and was elevated in obese humans with impaired fasting glucose. We therefore identify the hepatic IRF3-PPP2R1B axis as a causal link between obesity-induced inflammation and dysglycemia and suggest an approach for limiting the metabolic dysfunction accompanying obesity-associated NAFLD.\n          <\/jats:p>","DOI":"10.1126\/scitranslmed.abh3831","type":"journal-article","created":{"date-parts":[[2022,3,23]],"date-time":"2022-03-23T17:56:44Z","timestamp":1648058204000},"source":"Crossref","is-referenced-by-count":42,"title":["Hepatic IRF3 fuels dysglycemia in obesity through direct regulation of\n            <i>Ppp2r1b<\/i>"],"prefix":"10.1126","volume":"14","author":[{"given":"Suraj J.","family":"Patel","sequence":"first","affiliation":[{"name":"Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA."},{"name":"Division of Endocrinology, Diabetes, and Metabolism, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA."},{"name":"Division of Gastroenterology, Massachusetts General Hospital, 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