The endoplasmic reticulum in pancreatic beta cells of type 2 diabetes patients
Open accessAbstract
Aims/hypothesis Pancreatic beta cells have highly developed endoplasmic reticulum (ER) due to their role in insulin secretion. Since ER stress has been associated with beta cell dysfunction, we studied several features of beta cell ER in human type 2 diabetes.Methods Pancreatic samples and/or isolated islets from non-diabetic controls (ND) and type 2 diabetes patients were evaluated for insulin secretion, apoptosis (electron microscopy and ELISA), morphometric ER assessment (electron microscopy), and expression of ER stress markers in beta cell prepared by laser capture microdissection and in isolated islets.Results Insulin release was lower and beta cell apoptosis higher in type 2 diabetes than ND islets. ER density volume was significantly increased in type 2 diabetes beta cells. Expression of alpha-mannosidase (also known as mannosidase, alpha, class 1A, member 1) and UDP-glucose glycoprotein glucosyl transferase like 2 (UGCGL2), assessed by microarray and/or real-time reverse transcriptase polymerase chain reaction (RT-PCR), differed between ND and type 2 diabetes beta cells. Expression of immunoglobulin heavy chain binding protein (BiP, also known as heat shock 70 kDa protein 5 [glucose-regulated protein, 78 kDa] [HSPA5]), X-box binding protein 1 (XBP-1, also known as XBP1) and C/EBP homologous protein (CHOP, also known as damage-inducible transcript 3 [DDIT3]) was not higher in type 2 diabetes beta cell or isolated islets cultured at 5.5 mmol/l glucose (microarray and real-time RT-PCR) than in ND samples. When islets were cultured for 24 h at 11.1 mmol/l glucose, there was induction of BiP and XBP-1 in type 2 diabetes islets but not in ND islets.Conclusions/interpretation Beta cell in type 2 diabetes showed modest signs of ER stress when studied in pancreatic samples or isolated islets maintained at physiological glucose concentration. However, exposure to increased glucose levels induced ER stress markers in type 2 diabetes islet cells, which therefore may be more susceptible to ER stress induced by metabolic perturbations.
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In flies and humans, changes in expression and activity levels of α-mannosidases have been linked to impairments in insulin signaling and glucose metabolism.
“In both flies and humans, changes in expression and activity levels of α-mannosidases have been linked to impairments in insulin signaling and glucose metabolism (66–70).”
From Corazonin signaling integrates energy homeostasis and lunar phase to regulate aspects of growth and sexual maturation in <i>Platynereis</i> (2020) · cites this paper as [70]
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“Signals of endoplasmic reticulum (ER) stress are present in beta cells of individuals with type 1 [5] and type 2 diabetes [6, 7], and several monogenic forms of diabetes are caused by mutations in genes involved in the response to ER stress (also known as the unfolded protein response) [8].”
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- Authors
- Marchetti, P., Bugliani, M., Lupi, R., Marselli, L., Masini, M., Boggi, U., Filipponi, F., Weir, G. C., Eizirik, D. L., & Cnop, M.
- Affiliations
- University of Pisa (IT)
- Joslin Diabetes Center (US)
- Université Libre de Bruxelles (BE)
- Corresponding author
- Marchetti, P.
- ORCID
- Venue
- Diabetologia
- Published
- 2007-09-30
- Volume
- 50
- Issue
- 12
- Pages
- 2486-2494
- ISSN
- 0012-186X (ISSN-L)
- 1432-0428
- OpenAlex
- W2074549465
- Cited by
- 413
- References
- 49
- Citations by year
- 2026: 7 · 2025: 9 · 2024: 20 · 2023: 14 · 2022: 29 · 2021: 24 · 2020: 19 · 2019: 20 · 2018: 14 · 2017: 16 · 2016: 16 · 2015: 29 · 2014: 24 · 2013: 20 · 2012: 31
- FWCI
- 12.42
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Diabetologia (publishedVersion)
- PubMed (publishedVersion)
- Dépôt institutionnel de l'Université libre de Bruxelles (Université Libre de Bruxelles) (submittedVersion)
- CINECA IRIS Institutial research information system (University of Pisa) (submittedVersion)
- INFM-OAR (INFN Catania) (submittedVersion, other-oa)
- Funders
- Pfizer
- European Commission (LSHM-CT-2006-518153)
- European Foundation for the Study of Diabetes
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Endoplasmic Reticulum Stress and Disease
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
- Keywords
- endoplasmic reticulum, pancreatic beta cells, type 2 diabetes, endoplasmic reticulum stress, insulin secretion, beta-cell apoptosis, alpha-mannosidase, BiP, XBP1, CHOP, pancreatic islets
- MeSH terms
- Regulatory Factor X Transcription Factors, X-Box Binding Protein 1, Insulin Secretion, Endoplasmic Reticulum Chaperone BiP, Aged, Cells, Cultured, Diabetes Mellitus, Type 2, DNA-Binding Proteins, Endoplasmic Reticulum, Female, Glucose, Heat-Shock Proteins, Humans, Insulin, Islets of Langerhans, Male, Middle Aged, Nuclear Proteins, Transcription Factors, Gene Expression, Apoptosis, Molecular Chaperones, Oligonucleotide Array Sequence Analysis, Gene Expression Profiling, Insulin-Secreting Cells, Transcription Factor CHOP
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