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While anti-tuberculosis (TB) drug therapy is directed toward eliminating bacilli, the treatment regimen ignores the systemic pathogenic derailments that probably dictate TB-associated mortality and morbidity. Presently, it is not understood whether Mtb spreads to metabolic organs and brings about these impairments. Here, we show that Mtb creates a replication-conducive milieu of lipid droplets in hepatocytes by upregulating transcription factor PPAR\u03b3 and scavenging lipids from the host cells. In hepatocytes, Mtb shields itself against the common anti-TB drugs by inducing drug-metabolizing enzymes. Infection of the hepatocytes in the in vivo aerosol mice model can be consistently observed post-week, 4 along with enhanced expression of PPAR\u03b3 and drug-metabolizing enzymes. Moreover, histopathological analysis indeed shows the presence of Mtb in hepatocytes along with granuloma-like structures in human biopsied liver sections. Hepatotropism of Mtb during the chronic infectious cycle results in immuno-metabolic dysregulation that could magnify local and systemic pathogenicity, altering clinical presentations.\n                  <\/jats:p>","DOI":"10.7554\/elife.103817","type":"journal-article","created":{"date-parts":[[2025,1,6]],"date-time":"2025-01-06T12:25:48Z","timestamp":1736166348000},"update-policy":"https:\/\/doi.org\/10.7554\/elife.103817","source":"Crossref","is-referenced-by-count":3,"title":["PPAR\u03b3 mediated enhanced lipid biogenesis fuels Mycobacterium tuberculosis growth in a drug-tolerant hepatocyte environment"],"prefix":"10.7554","volume":"14","author":[{"ORCID":"https:\/\/orcid.org\/0009-0009-3366-4851","authenticated-orcid":true,"given":"Binayak","family":"Sarkar","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/04fhee747","id-type":"ROR","asserted-by":"publisher"}],"name":"Immunometabolism Laboratory, National Institute of Immunology","place":["New Delhi, 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