Abstract
The functional maturation of insulin-secreting β-cells is initiated before birth and is completed in early postnatal life. This process has a critical impact on the acquisition of an adequate functional β-cell mass and on the capacity to meet and adapt to insulin needs later in life. Many cellular pathways playing a role in postnatal β-cell development have already been identified. However, single-cell transcriptomic and proteomic analyses continue to reveal new players contributing to the acquisition of β-cell identity. In this review, we provide an updated picture of the mechanisms governing postnatal β-cell mass expansion and the transition of insulin-secreting cells from an immature to a mature state. We then highlight the contribution of the environment to β-cell maturation and discuss the adverse impact of an in utero and neonatal environment characterized by calorie and fat overload or by protein deficiency and undernutrition. Inappropriate nutrition early in life constitutes a risk factor for developing diabetes in adulthood and can affect the β-cells of the offspring over two generations. A better understanding of these events occurring in the neonatal period will help developing better strategies to produce functional β-cells and to design novel therapeutic approaches for the prevention and treatment of diabetes.
Highlights
The acquisition of a suitable and fully functional adult pancreatic β-cell mass is a fundamental prerequisite for the maintenance of carbohydrate homeostasis and for facing the pathophysiological challenges encountered by our organism throughout life [1,2]
The postnatal period is a critical stage for the proper development of an organism, especially in the perspective of acquiring cells and organs capable of adapting and compensating for any physio-pathological challenge that may arise in adulthood
An essential point that remains to be further investigated is the impact on β-cell maturation of a deleterious environment restricted either to the prenatal period or to the postnatal period
Summary
The acquisition of a suitable and fully functional adult pancreatic β-cell mass is a fundamental prerequisite for the maintenance of carbohydrate homeostasis and for facing the pathophysiological challenges encountered by our organism throughout life [1,2]. At P0, P3, and P9, a first group of β-cells show a high abundance of genes associated with an immature phenotype such as Mafb (basic leucine zipper (bZIP) transcription factor B), Pyy (peptide YY), and Fev (fifth ewing variant) while a second group of cells express predominantly genes such as Trpm (transient receptor potential cation channel subfamily M member 5), Vipr (vasoactive intestinal polypeptide receptor 1), and Prlr (prolactin receptor), known to be abundant in so-called mature and fully operational cells Despite this identified transcriptomic heterogeneity, neonatal β-cells appear to follow a synchronous functional maturation process. It is likely that the WNT/PCP pathway drives the establishment of planar polarization and the acquisition of a mature cell phenotype by regulating post-transcriptional rather than transcriptional events [15]
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