Type 1 diabetes (T1D) is a chronic autoimmune disease characterized by the destruction of insulin-producing β-cells. Emerging evidence highlights the pivotal role of CD4+ T cell subsets in driving T1D pathogenesis, where their activation, proliferation, and differentiation are tightly regulated by glucose metabolic pathways. Recent studies demonstrate that key enzymes and intermediates of glycolysis, OXPHOS, and other metabolic pathways critically modulate CD4+ T cell functions. In this review, we discuss how glucose metabolic pathways affect CD4+ T cell differentiation and functions. We also summarize the latest progress regarding glucose metabolism intervention to control the T cell immune response in T1D, with the expectation of providing new insights into T1D progression and treatment.