Partial clinical remission in Type 1 diabetes (T1D) refers to a transient phase of improved glucose control following diagnosis. During this period, endogenous islet β-cells continue to produce and secrete insulin, resulting in lower exogenous insulin requirements and improved glycaemic status. Partial remission is often described colloquially as the 'honeymoon phase', a period lasting from months to years which is heterogeneous across patient groups. In this review, we discuss the immunometabolic events that may control the duration of the partial remission period by highlighting how glucose metabolism supports immune cell-driven inflammatory and autoimmune events. We thus propose that precise control of blood glucose within a healthy range delays the deleterious consequences that arise from autoimmune mechanisms within pancreatic islets, ultimately leading to the extension of the honeymoon phase. We further discuss data supporting the notion that managing blood glucose effectively also improves islet β-cell mass, function and maturity markers. Collectively, these paradigms help explain the success of recent clinical trial outcomes and offer novel opportunities to intervene in future study designs.
Keywords: beta cell function; endocrine therapy; glycaemic control; insulin secretion; islets.
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