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The role of breast milk exosomes in diabetes prevention and the impact of cow milk exosomes on andbeta;-cell dedifferentiation later in life
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Journal of Diabetic Complications & Medicine

ISSN: 2475-3211

Open Access

The role of breast milk exosomes in diabetes prevention and the impact of cow milk exosomes on β-cell dedifferentiation later in life


4th Annual Conference on Diabetes

June 15, 2023 | Webinar

Bodo C. Melnik

University of Osnabrueck, Germany

Scientific Tracks Abstracts: J Diabetic Complications Med

Abstract :

Recent evidence points to an intensive exosome cross-talk between pancreatic β-cells and towards β-cells by transmitted exosomes from adipocytes, skeletal muscle cells, macrophages and T-lymphcytes. It is thus conceivable that milk exosomes (MEX) of human breast milk and their microRNA (miR) cargo also affect postnatal β-cells and promote their proliferation and mass expansion. Translational evidence indicates that human MEX miRs enhance mTORC1/c-Myc-driven β-cell proliferation. It is a matter of concern that maternal obesity, gestational diabetes, caesarean delivery and especially MEX-deficient infant formula feeding disturb physiological MEX miR signalling during the postnatal period thereby increasing the risk of type 2 diabetes later in life. In all mammals, MEX miR signalling fades after weaning. However, humans, who regularly consume pasteurized cow milk are continuously exposed to bioavailable bovine MEX miRs, which are identical in nucleotide sequence with human MEX miRs. Circumstantial evidence supports the view that bovine MEX miRs promote β-cell dedifferentiation back to the mTORC1-driven neonatal immature phenotype with reduced glucose-stimulated insulin secretion.1 MEX miR signalling, beneficial for the immature postnatal β-cell, turns into a pathogen for the mature adult β-cell.2 The human consumer should not be exposed to diabetogenic MEX and their miRs after the weaning period.2,3 Thus, the elimination of bovine MEX and their bioactive miRs is a promising approach for the prevention of type 2 diabetes and other MEX-related diseases of civilization.2,4,5.

Biography :

BODO C. MELNIK has completed his medical studies and MD thesis at the age of 26 years from the University of Münster in Germany and thereafter was postdoctoral research fellow at UCSF, School of Medicine. He is senior lecturer at the University of Osnabrück, has published more than 100 papers in reputed journals, and is author of several scientific books and editorial board member of the Journal of Translational Medicine. His major research interest is the molecular biology of milk, milk exosomal RNAs and their function in health and disease, especially type 2 diabetes mellitus.

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