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Significant alterations in cellular metabolism often accompany these inflammatory changes. Although considerable research has focused on understanding these metabolic shifts in astrocytes and microglia, the precise mechanisms linking neuroinflammation and cellular metabolism in neurons remain poorly understood. This study explores the connection between neuroinflammation and neuronal cell metabolism through a lipopolysaccharide (LPS)\u2010induced neuroinflammation model utilizing GT1\u20107 hypothalamic neuron cultures. Our findings indicate that LPS\u2010induced neuroinflammation in GT1\u20107 hypothalamic neurons is marked by reduced oxidative phosphorylation (OXPHOS) and decreased endogenous fatty acid oxidation (FAO). In contrast, exogenous FAO increases, leading to elevated ATP production, while glycolysis remains unchanged. These metabolic changes are associated with increased inflammatory markers (IL\u20106, TNF\u2010\u03b1) and oxidative stress indicators (ROS, NO), as well as decreased synaptic plasticity (as indicated by synaptophysin) and impaired cellular function, as evidenced by reduced gonadotropin\u2010releasing hormone (GnRH) release. Our study highlights the intricate interplay between neuroinflammation and neuronal cell metabolism. 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