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Updated: Mar 1, 2026

Isolating and Analyzing Cells of the Pancreas Mesenchyme by Flow Cytometry
05:38

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Published on: January 28, 2017

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Distinct roles for the mTOR pathway in postnatal morphogenesis, maturation and function of pancreatic islets

Katie L Sinagoga1, William J Stone1, Jacqueline V Schiesser1

  • 1Division of Developmental Biology, Cincinnati Children's Hospital Medical Center, 3333 Burnet Ave, Cincinnati, OH 45229-3039, USA.

Development (Cambridge, England)
|June 4, 2017
PubMed

Insights

Nutrient sensing via mechanistic target of rapamycin (mTOR) is crucial for postnatal islet development. mTORC1 regulates beta-cell function and maturation, while mTORC2 impacts islet mass and architecture.

Area of Science:

  • Endocrinology
  • Developmental Biology
  • Molecular Biology

Background:

  • Embryonic development and adult homeostasis of the endocrine pancreas are well-understood.
  • Regulation of early postnatal islet development and maturation remains largely unknown.
  • Postnatal life involves the first exposure to enteral nutrition, suggesting nutrient-regulated pathways are key.

Purpose of the Study:

  • Investigate the role of nutrient-sensing pathways in postnatal islet development.
  • Examine the impact of mechanistic target of rapamycin (mTOR) signaling on islet maturation and function in mice.
  • Delineate the distinct roles of mTORC1 and mTORC2 in postnatal islet development.

Main Methods:

  • Conducted loss-of-function studies of mTOR in pancreatic endocrine cells of mice.
  • Utilized genetic deletion of Mtor to assess its impact on embryonic and postnatal islet development.
  • Analyzed islet morphology, beta-cell function, maturation, and overall islet mass.

Main Results:

  • Mtor deletion did not affect embryonic islet development.
  • Postnatal mTOR deficiency led to dysmorphic islets, impaired beta-cell maturation and function, and reduced islet mass.
  • mTORC1 primarily mediates islet maturation and function, while mTORC2 influences islet mass and architecture.

Conclusions:

  • Nutrient sensing through mTOR signaling is essential for triggering postnatal beta-cell maturation and islet development.
  • Distinct mTOR complexes (mTORC1 and mTORC2) play specific roles in regulating different aspects of postnatal islet growth and function.
  • Findings highlight the critical link between nutrition and endocrine pancreas development after birth.

Keywords:
DiabetesIsletMouseMtorPancreasPostnatal

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