TY - JOUR
T1 - Interorgan crosstalk in pancreatic islet function and pathology
AU - Evans, Ronald M.
AU - Wei, Zong
N1 - Funding Information:
Due to the limits on space, we were not able to include all important papers in the field. We apologize to those whose work was not cited directly. We thank C. Brondos for administrative help. Work in R.M.E's laboratory is supported by grants from the NIH (HL088093, HL105278, R01DK120480, R01DK057978, P42ES010337), the Glenn Foundation for Medical Research, the Leona M. and Harry B. Helmsley Charitable Trust (#2017PG-MED001), Ipsen/Biomeasure, California Institute for Regenerative Medicine and the Ellison Medical Foundation. R.M.E is a NOMIS Foundation Distinguished Scientist and Scholar at the Salk Institute. Work in Z.W.'s laboratory is supported by NIH (K01DK120808), Mayo Clinic Center for Biomedical Discovery, ASU-Mayo Collaborative Fund, Roubos Family Fund in Research and Integrated Islet Distribution Program. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.
Funding Information:
Due to the limits on space, we were not able to include all important papers in the field. We apologize to those whose work was not cited directly. We thank C. Brondos for administrative help. Work in R.M.E's laboratory is supported by grants from the NIH (HL088093, HL105278, R01DK120480, R01DK057978, P42ES010337), the Glenn Foundation for Medical Research, the Leona M. and Harry B. Helmsley Charitable Trust (#2017PG‐MED001), Ipsen/Biomeasure, California Institute for Regenerative Medicine and the Ellison Medical Foundation. R.M.E is a NOMIS Foundation Distinguished Scientist and Scholar at the Salk Institute. Work in Z.W.'s laboratory is supported by NIH (K01DK120808), Mayo Clinic Center for Biomedical Discovery, ASU‐Mayo Collaborative Fund, Roubos Family Fund in Research and Integrated Islet Distribution Program. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.
Publisher Copyright:
© 2022 Federation of European Biochemical Societies
PY - 2022/3
Y1 - 2022/3
N2 - Pancreatic β cells secrete insulin in response to glucose, a process that is regulated at multiple levels, including a network of input signals from other organ systems. Impaired islet function contributes to the pathogenesis of type 2 diabetes mellitus (T2DM), and targeting inter-organ communications, such as GLP-1 signalling, to enhance β-cell function has been proven to be a successful therapeutic strategy in the last decade. In this review, we will discuss recent advances in inter-organ communication from the metabolic, immune and neural system to pancreatic islets, their biological implication in normal pancreas endocrine function and their role in the (mal)adaptive responses of islet to nutrition-induced stress.
AB - Pancreatic β cells secrete insulin in response to glucose, a process that is regulated at multiple levels, including a network of input signals from other organ systems. Impaired islet function contributes to the pathogenesis of type 2 diabetes mellitus (T2DM), and targeting inter-organ communications, such as GLP-1 signalling, to enhance β-cell function has been proven to be a successful therapeutic strategy in the last decade. In this review, we will discuss recent advances in inter-organ communication from the metabolic, immune and neural system to pancreatic islets, their biological implication in normal pancreas endocrine function and their role in the (mal)adaptive responses of islet to nutrition-induced stress.
KW - GLP-1
KW - inter-organ crosstalk
KW - pancreatic β cells
KW - type 2 diabetes mellitus
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U2 - 10.1002/1873-3468.14282
DO - 10.1002/1873-3468.14282
M3 - Review article
C2 - 35014695
AN - SCOPUS:85122930195
SN - 0014-5793
VL - 596
SP - 607
EP - 619
JO - FEBS Letters
JF - FEBS Letters
IS - 5
ER -