Pancreas islets in metabolic signaling - Focus on the beta-cell
Research output: Contribution to journal › Research article › Contributed › peer-review
Contributors
Abstract
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. Clustered beta-cells achieve tighter regulation of glucose-induced insulin secretion by coordination through cell surface proteins. They also adjust their secretory 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 overall protein synthesis in beta-cells but selectively boosts translation of some secretory proteins including insulin. This may be mediated through recognition of RNA motifs in the untranslated regions of those messengers. If essential molecular components of this nutrient sensing system are broken or fail due to repeated stress, beta cells malfunction, which on a larger scale manifest as diseases like diabetes mellitus.
Details
Original language | English |
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Pages (from-to) | 7156-7171 |
Number of pages | 16 |
Journal | Frontiers in bioscience |
Volume | 13 |
Issue number | 18 |
Publication status | Published - 1 May 2008 |
Peer-reviewed | Yes |
External IDs
PubMed | 18508724 |
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Keywords
Sustainable Development Goals
ASJC Scopus subject areas
Keywords
- Adrenergic neurons, Alpha cells, AMP-activated protein kinase, AMPK, Beta cells, Blood glucose, Calpain, Contact signaling, Cooperativity, CORI cycle, Delta cells, Diabetes mellitus, Dorsal pancreas, Eif2a, Endoplasmic reticulum stress response, EphA, Ephrin A, ER stress response, Eukaryotic initiation factor 2a, FANCONI-Bickel syndrome, GAPDH, Ghrelin, GIP, GLP1, Glucagon, Glucagon-like peptide 1, Glucokinase, Glucose homeostasis, Glucose transporter 2, Glucose-dependent insulinotropic polypeptide, GLUT2, Glyceraldehyde dehydrogenase, Hyperglycaemia, Hyperglycemia, Hypoglycaemia, Hypoglycemia, ICA512, Insulin, Internal ribosome entry site, IRE1a, IRES, Islet size, ISLETS of Langerhans, Katp channel, KCNJ11, Kir6.2, Lactate, Metabolism, Mody, Mrna stability, Pancreas, Pancreatic islets, Pancreatic polypeptide, Parasympathetic, PERK, Post-translational control, Review, Somatostatin, STAT5, SUMO, Sumoylation, SUR1, Sympathetic, Translational control, Unfolded protein response, Untranslated region, UPR, Utr, Vascularisation, VEGF-A, Ventral pancreas, WFS1, Wolcott-Rallison syndrome, Wolfram syndrome, XBP1