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Pancreas islets in metabolic signaling - focus on the &946;-cell
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  • Published: 27 March 2008

Pancreas islets in metabolic signaling - focus on the &946;-cell

  • Jakob Suckale1 &
  • Michele Solimena2 

Nature Precedings (2008)Cite this article

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Abstract

Taken together the Islets of Langerhans form a nutrient sensing network spread throughout the pancreas. They are tightly connected to the source organ - the intestine - and the target organs - liver, muscle, and fat cells. The expression of a unique set of proteins enables [beta] cells, the most frequent islet cell type, to detect elevated blood glucose levels and secrete insulin accordingly. Neighbouring [beta]-cells achieve tighter regulation of glucose-induced insulin secretion by coordination through cell surface proteins. They also adjust their secretory pathway capacity and flow to avoid being damaged. The immediate reaction of the [beta] cell to nutrients is regulated by translational mechanisms, while longer term adaptations involve changes in transcription. Glucose increases protein synthesis in the [beta] cell overall and especially that of some secretory proteins including insulin. This effect may be mediated through recognition of RNA motifs in the untranslated regions of those messengers. Failure of essential molecular components of the nutrient sensing system due to mutation or weakness paired with cellular stress can lead to dysfunctions, which on a larger scale manifest as diseases like diabetes mellitus.

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Authors and Affiliations

  1. Dresden University of Technology, Int’l Max Planck Research School https://www.nature.com/nature

    Jakob Suckale

  2. Experimental Diabetology, Department of Medicine III, Dresden University of Technology & MPI-CBG https://www.nature.com/nature

    Michele Solimena

Authors
  1. Jakob Suckale
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  2. Michele Solimena
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Correspondence to Jakob Suckale or Michele Solimena.

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Suckale, J., Solimena, M. Pancreas islets in metabolic signaling - focus on the &946;-cell. Nat Prec (2008). https://doi.org/10.1038/npre.2008.1724.1

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  • Received: 26 March 2008

  • Accepted: 27 March 2008

  • Published: 27 March 2008

  • DOI: https://doi.org/10.1038/npre.2008.1724.1

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Keywords

  • insulin
  • metabolism
  • diabetes
  • pancreas islets
  • beta cell
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