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This study investigated whether alpha\u2010lipoic acid (ALA), a redox\u2010active compound with established anti\u2010inflammatory properties, can inhibit the activation of the nucleotide\u2010binding oligomerization domain\u2010like receptor family pyrin domain\u2010containing 3 (NLRP3) inflammasome in lipopolysaccharide (LPS)\u2010stimulated Kupffer cells and mitigate inflammation\u2010induced insulin resistance in FL83B hepatocytes. Kupffer cells were pretreated with ALA prior to exposure to LPS and either adenosine triphosphate or nigericin to activate NLRP3 inflammasome. The resulting conditioned medium was collected for cytokine analysis and subsequently used to treat FL83B hepatocytes. ALA reduced LPS\u2010induced interleukin\u20101\u03b2 (IL\u20101\u03b2) secretion in a concentration\u2010dependent manner, whereas a modest but significant decrease in tumor necrosis factor\u2010alpha (TNF\u2010\u03b1) was observed only at the highest dose (2000\u2009\u03bcM;\n                    <jats:italic>p<\/jats:italic>\n                    \u2009&lt;\u20090.05). Western blot analysis demonstrated that ALA suppressed the expression of NLRP3 and nuclear factor\u2010kappa B (NF\u2010\u03baB) (\n                    <jats:italic>p<\/jats:italic>\n                    \u2009&lt;\u20090.05) and inhibited the phosphorylation of extracellular signal\u2010regulated kinase (ERK). Additionally, ALA preserved mitochondrial membrane potential in Kupffer cells. Kupffer cells treated with ALA (100\u2009\u03bcM) prior to LPS stimulation significantly enhanced glucose uptake and upregulated the expression of insulin signaling related proteins, including phosphorylated phosphoinositide 3\u2010kinase (p\u2010PI3K), phosphorylated protein kinase B (p\u2010Akt) and glucose transporter type 2 (GLUT2) expression, in FL83B hepatocytes cultured with a conditioned medium from LPS\u2010primed and ATP\/nigericin\u2010stimulated Kupffer cells (\n                    <jats:italic>p<\/jats:italic>\n                    \u2009&lt;\u20090.05). These findings highlight the potential of ALA as a modulator of hepatic immune\u2010metabolic interactions and support its therapeutic relevance for managing insulin resistance in T2DM.\n                  <\/jats:p>","DOI":"10.1002\/fsn3.71517","type":"journal-article","created":{"date-parts":[[2026,2,4]],"date-time":"2026-02-04T06:27:49Z","timestamp":1770186469000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Alpha\u2010Lipoic Acid Reduces\n                    <scp>NLRP3<\/scp>\n                    \/\n                    <scp>ASC<\/scp>\n                    Expression and\n                    <scp>IL<\/scp>\n                    \u20101\u03b2 Release in Kupffer Cells and Improves Insulin Signaling in\n                    <scp>FL83B<\/scp>\n                    Hepatocytes Exposed to a Conditioned 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