Prostate cancer is a common cancer in men and a major cause of cancer-related deaths worldwide. Recent research highlights the role of metabolism in this disease, as tumors adapt their metabolic processes to meet biosynthetic needs. Metabolites also support cell survival and reshape the tumor microenvironment, making metabolism a key hallmark of cancer. Prostate cancer is uniquely driven by androgen receptor (AR) signaling, influencing cancer metabolism research. This review explores metabolic adaptations beyond AR signaling, focusing on intrinsic and extrinsic pathways in prostate cancer cells. The androgen receptor regulates the expression of genes involved in various metabolic processes, including glycolysis. Cancer cells often exhibit increased glycolytic activity, even in the presence of oxygen, known as the Warburg effect. This metabolic adaptation is linked to prostate cancer progression, and therapies targeting glycolysis, such as MCT4 inhibition, are being explored. Despite the relevance of glycolysis, evidence shows that the tricarboxylic acid (TCA) cycle and oxidative phosphorylation (OXPHOS) are still active in metastatic settings, complicating lactate-targeted therapies. The TCA cycle and OXPHOS are essential for energy production and metabolic intermediates. Mutations in the TCA cycle or electron transport chain machinery can lead to alternative metabolic routes, such as reductive carboxylation. Prostate epithelial cells have a truncated TCA cycle, leading to citrate accumulation and secretion. AR signaling reprograms metabolism, increasing mitochondrial zinc levels and restoring TCA cycle activity. The pentose phosphate pathway (PPP) is crucial for NADPH production and nucleotide precursors, supporting tumor cell redox balance. G6PD, a key enzyme in the PPP, is upregulated in various cancers, including prostate cancer. Targeting G6PD and 6PGD has shown promise in reducing cancer growth and improving therapeutic outcomes. The hexosamine biosynthetic pathway (HBP) redirects glucose-derived carbons away from glycolysis. Increased HBP activity is associated with O-GlcNAcylation, which influences protein structure and function. Targeting HBP could be a novel strategy for cancer therapy. Lipid metabolism is also crucial in prostate cancer, with increased de novo lipogenesis and altered lipid uptake and utilization. SREBPs regulate lipid synthesis, and inhibitors like fatostatin and FASN inhibitors are being explored. Lipolysis and fatty acid oxidation (FAO) are also important, with enzymes like CPT1 and CD36 playing roles in lipid metabolism. Cholesterol metabolism is vital for steroid hormone synthesis and lipid raft dynamics. Statins and SQLE inhibitors are being studied for their potential in prostate cancer treatment. The TME also influences lipid metabolism, with macrophages contributing to cholesterol supply for cancer cells. One-carbon (1C) metabolism is essential for DNA synthesis, redox balance, and methylation. SAM homeostasis and the transProstate cancer is a common cancer in men and a major cause of cancer-related deaths worldwide. Recent research highlights the role of metabolism in this disease, as tumors adapt their metabolic processes to meet biosynthetic needs. Metabolites also support cell survival and reshape the tumor microenvironment, making metabolism a key hallmark of cancer. Prostate cancer is uniquely driven by androgen receptor (AR) signaling, influencing cancer metabolism research. This review explores metabolic adaptations beyond AR signaling, focusing on intrinsic and extrinsic pathways in prostate cancer cells. The androgen receptor regulates the expression of genes involved in various metabolic processes, including glycolysis. Cancer cells often exhibit increased glycolytic activity, even in the presence of oxygen, known as the Warburg effect. This metabolic adaptation is linked to prostate cancer progression, and therapies targeting glycolysis, such as MCT4 inhibition, are being explored. Despite the relevance of glycolysis, evidence shows that the tricarboxylic acid (TCA) cycle and oxidative phosphorylation (OXPHOS) are still active in metastatic settings, complicating lactate-targeted therapies. The TCA cycle and OXPHOS are essential for energy production and metabolic intermediates. Mutations in the TCA cycle or electron transport chain machinery can lead to alternative metabolic routes, such as reductive carboxylation. Prostate epithelial cells have a truncated TCA cycle, leading to citrate accumulation and secretion. AR signaling reprograms metabolism, increasing mitochondrial zinc levels and restoring TCA cycle activity. The pentose phosphate pathway (PPP) is crucial for NADPH production and nucleotide precursors, supporting tumor cell redox balance. G6PD, a key enzyme in the PPP, is upregulated in various cancers, including prostate cancer. Targeting G6PD and 6PGD has shown promise in reducing cancer growth and improving therapeutic outcomes. The hexosamine biosynthetic pathway (HBP) redirects glucose-derived carbons away from glycolysis. Increased HBP activity is associated with O-GlcNAcylation, which influences protein structure and function. Targeting HBP could be a novel strategy for cancer therapy. Lipid metabolism is also crucial in prostate cancer, with increased de novo lipogenesis and altered lipid uptake and utilization. SREBPs regulate lipid synthesis, and inhibitors like fatostatin and FASN inhibitors are being explored. Lipolysis and fatty acid oxidation (FAO) are also important, with enzymes like CPT1 and CD36 playing roles in lipid metabolism. Cholesterol metabolism is vital for steroid hormone synthesis and lipid raft dynamics. Statins and SQLE inhibitors are being studied for their potential in prostate cancer treatment. The TME also influences lipid metabolism, with macrophages contributing to cholesterol supply for cancer cells. One-carbon (1C) metabolism is essential for DNA synthesis, redox balance, and methylation. SAM homeostasis and the trans