{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T05:26:28Z","timestamp":1787030788878,"version":"build-2736575974"},"reference-count":51,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2026,2,12]],"date-time":"2026-02-12T00:00:00Z","timestamp":1770854400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,2,12]],"date-time":"2026-02-12T00:00:00Z","timestamp":1770854400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["dom-pubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Diabetes Obesity Metabolism"],"published-print":{"date-parts":[[2026,5]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>De novo lipogenesis (DNL) is an important cause of lipid deposition in metabolic dysfunction\u2010associated fatty liver disease (MAFLD), and recent studies report that lactate is a major substrate for DNL in MAFLD. High\u2010intensity interval training (HIIT) has a powerful regulatory effect on lactate metabolism, but whether it can alleviate MAFLD by regulating lactate metabolism has not been reported.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>High\u2010fat diet (HFD)\u2010induced MAFLD mice were used as a model and underwent performed 8\u2009weeks of HIIT. Serum and liver tissues were collected and analysed by biochemical assay, histology, quantitative real\u2010time polymerase chain reaction, western blot, coimmunoprecipitation, isotope tracing and ultra\u2010performance liquid chromatography\u2013tandem mass spectrometry analysis. HepG2 cells were treated in vitro with oleic acid\/palmitic acid (OA\/PA) to mimic\/inhibit lactate dehydrogenase B (LDHB) lactylation (Kla) by mutations and to observe changes in lipid deposition.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Here, hepatic lactate metabolism in MAFLD mice is characterised by increased endogenous lactate and involvement in DNL. In contrast, decreased hepatic lipid deposition in MAFLD mice after HIIT inhibits lactate\u2010involved DNL, and lactate enters the tricarboxylic acid cycle with increased oxidative catabolism. MAFLD model mice have decreased LDHB Kla and increased LDHB activity in liver and OA\/PA\u2010induced hepatocytes. LDHB lactylation increases and LDHB activity decreases after HIIT. LDHB K82 is a lactylation site that affects LDHB activity, and in vitro LDHB K82 lactylation inhibition increases LDHB activity, leading to OA\/PA\u2010induced lipid deposition in HepG2 cells, whereas LDHB K82La enhancement decreases lipid deposition.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>HIIT effectively alleviates HFD\u2010induced MAFLD in mice by regulating hepatic lactate metabolism to inhibit lactate\u2010substrate DNL, and the ability of LDHB K82La to regulate LDHB activity may be one of the mechanisms by which HIIT exerts the above effects.<\/jats:p>\n                  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