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Glycerol-3-phosphate acyltransferase 1, mitochondrial (GPAM) is an enzyme located in the mitochondrial outer membrane that catalyzes the first and rate-limiting step in glycerolipid biosynthesis: the acylation of glycerol-3-phosphate with long-chain acyl-CoA to produce lysophosphatidic acid[1][2][3][5]. GPAM is especially active with saturated fatty acids and is highly expressed in liver and adipose tissues, playing a major role in triglyceride and phospholipid synthesis and regulating systemic energy homeostasis[3][5]. It influences biological processes including adipocyte differentiation, lipid metabolism, immune cell function, and disease susceptibility, particularly impacting metabolic disorders, liver disease, and insulin resistance[1][3]. GPAM activity is controlled by both transcriptional and post-transcriptional mechanisms involving key metabolic regulators such as SREBP-1c, ChREBP, LXR, insulin, and AMPK[1].
Drugs or modulators targeting GPAM (not named in the results) work by inhibiting or activating its enzymatic activity, thereby altering lipid synthesis and downstream cellular energy metabolism[1][3].
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