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Although<jats:italic>Pgc1\u03b1<\/jats:italic>is regarded as the main regulator of mitochondrial function, downstream<jats:italic>Nrf1<\/jats:italic>is the key regulator of mitochondrial biogenesis.<jats:italic>Nrf1<\/jats:italic>is also involved in a wide range of other processes, including proliferation, innate immune response, and apoptosis. To determine transcriptional targets of<jats:italic>Nrf1<\/jats:italic>, 3T3\u2010L1 preadipocytes were transfected with either pNrf1 or a control vector. Two days post\u2010confluence, 3T3\u2010L1 preadipocytes were allowed to differentiate. At day 8 of differentiation,<jats:italic>Nrf1<\/jats:italic>overexpressing cells had an increased mtDNA copy number and reduced lipid content. This was not associated with an increased ATP production rate per cell. Using global gene expression analysis, we observed that<jats:italic>Nrf1<\/jats:italic>overexpression stimulated cell proliferation, apoptosis, and cytokine expression. In addition, prolonged<jats:italic>Nrf1<\/jats:italic>induced an adipokine expression profile of insulin resistant adipocytes.<jats:italic>Nrf1<\/jats:italic>has a wide range of transcriptional targets, stimulators as well as inhibitors of adipose tissue functioning. Therefore, post\u2010transcriptional regulation of<jats:italic>Nrf1<\/jats:italic>, or stimulating specific<jats:italic>Nrf1<\/jats:italic>targets may be a more suitable approach for stimulating mitochondrial biogenesis and treating adipose tissue defects, instead of directly stimulating<jats:italic>Nrf1<\/jats:italic>expression. In addition, our results show that short\u2010term effects can drastically differ from long\u2010term effects. J. Cell. 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