ArticleFrontiers in endocrinology2026
Mitochondrial development and remodeling occur at pancreatic progenitor stage during induction of stem cell-derived islet organoids.
Article in Frontiers in endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Despite decades of research, there is still no effective cure for type 1 diabetes, except islet transplantation, which is limited by healthy islet donors' shortage. Transplantation of surrogate insulin-producing β-cells from human pluripotent stem cells (hPSC) may provide an alternative solution when endogenous β-cells are nearly depleted. However, most differentiation protocols generate immature β-cells with impaired glucose-stimulated insulin secretion (GSIS) compared to primary β-cells. During β-cell development, there is a metabolic shift from glycolysis to OXPHOS metabolism to meet the increasing energy demand, suggesting that mitochondrial function is essential for hPSC-derived β-cell differentiation. This study investigated mitochondrial development and function during the differentiation process of hPSC into islet organoids. Two hPSC cell lines (HUES8 and iPSC824) were differentiated into islet organoids using a 6-stage differentiation protocol. Relevant stage-specific markers and GSIS were measured. Mitochondrial biogenesis, dynamics, morphological remodeling, and function were assessed to investigate mitochondria role in β-cell development. Mitochondrial contribution to total ATP production and lactate production were measured to assess the metabolic shift. The results showed, in both cell lines, >96% OCT4
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