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Emerging evidence indicates that the hypothalamus, a central regulator of energy and glucose homeostasis, undergoes age-associated inflammatory remodeling that contributes to metabolic dysfunction. In particular, glial cells, including microglia, astrocytes, tanycytes, and neural stem cells, acquire senescence-associated phenotypes characterized by impaired homeostatic functions and increased secretion of pro-inflammatory mediators. These changes disrupt hypothalamic neuronal circuits involved in glucose sensing, energy balance, and insulin responsiveness, thereby potentially promoting systemic insulin resistance and T2DM progression. In this review, we summarize current evidence on the cellular and molecular mechanisms of hypothalamic glial inflammaging and discuss how age-related glial dysfunction may contribute to metabolic abnormalities. 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