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Metformin (MF), an FDA\u2010approved medication for type II diabetes mellitus, has recently gained attention for its promising anti\u2010aging properties, acting as a calorie restriction mimetic, and delaying precocious puberty. Additionally, trodusquemine (MSI\u20101436), an investigational drug, has been shown to combat obesity and metabolic disorders by inhibiting the enzyme protein tyrosine phosphatase 1b (<jats:italic>Ptp1b<\/jats:italic>), consequently reducing hepatic lipogenesis and counteracting insulin and leptin resistance. In this study, we aimed to further explore the effects of these compounds on young, developing mice to uncover biomolecular signatures that are central to liver metabolic processes. We found that MSI\u20101436 more potently alters mRNA and miRNA expression in the liver compared with MF, with bioinformatic analysis suggesting that cohorts of differentially expressed miRNAs inhibit the action of phosphoinositide 3\u2010kinase (<jats:italic>Pi3k<\/jats:italic>), protein kinase B (<jats:italic>Akt<\/jats:italic>), and mammalian target of rapamycin (<jats:italic>Mtor<\/jats:italic>) to regulate the downstream processes of de novo lipogenesis, fatty acid oxidation, very\u2010low\u2010density lipoprotein transport, and cholesterol biosynthesis and efflux. In summary, our study demonstrates that administering these compounds during the postnatal window metabolically reprograms the liver through induction of potent epigenetic changes in the transcriptome, potentially forestalling the onset of age\u2010related diseases and enhancing longevity. 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