Functional and morphological alterations of mitochondria in pancreatic beta cells from type 2 diabetic patients
Open accessAbstract
Aims/hypothesis Little information is available on the insulin release properties of pancreatic islets isolated from type 2 diabetic subjects. Since mitochondria represent the site where important metabolites that regulate insulin secretion are generated, we studied insulin release as well as mitochondrial function and morphology directly in pancreatic islets isolated from type 2 diabetic patients.Methods Islets were prepared by collagenase digestion and density gradient purification, and insulin secretion in response to glucose and arginine was assessed by the batch incubation method. Adenine nucleotides, mitochondrial membrane potential, the expression of UCP-2, complex I and complex V of the respiratory chain, and nitrotyrosine levels were evaluated and correlated with insulin secretion.Results Compared to control islets, diabetic islets showed reduced insulin secretion in response to glucose, and this defect was associated with lower ATP levels, a lower ATP/ADP ratio and impaired hyperpolarization of the mitochondrial membrane. Increased protein expression of UCP-2, complex I and complex V of the respiratory chain, and a higher level of nitrotyrosine were also found in type 2 diabetic islets. Morphology studies showed that control and diabetic beta cells had a similar number of mitochondria; however, mitochondrial density volume was significantly higher in type 2 diabetic beta cells.Conclusions/interpretation In pancreatic beta cells from type 2 diabetic subjects, the impaired secretory response to glucose is associated with a marked alteration of mitochondrial function and morphology. In particular, UCP-2 expression is increased (probably due to a condition of fuel overload), which leads to lower ATP, decreased ATP/ADP ratio, with consequent reduction of insulin release.
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Impaired β-cell metabolism in type 2 diabetes donor islets and in hyperglycaemic mouse neonatal diabetes β-cells supports the idea that inhibition of mitochondrial metabolism is central to β-cell dysfunction.
“Impairment in β-cell metabolism observed in islets from donors with T2DM and in β-cells from a mouse model of human neonatal diabetes upon exposure to hyperglycaemia support the notion that inhibition of mitochondrial metabolism is central to β-cell dysfunction143,144.”
From Mitochondrial and metabolic dysfunction in ageing and age-related diseases (2022) · cites this paper as [143]
Islets from people with type 2 diabetes have increased expression of UCP2, complex I, and ATP synthase.
“Moreover, increased expression of uncoupling protein 2 (UCP2), complex I and ATP synthase have been observed in islets from patients with T2DM143.”
From Mitochondrial and metabolic dysfunction in ageing and age-related diseases (2022) · cites this paper as [143]
Islets from people with type 2 diabetes have higher mitochondrial density volume than islets from people without type 2 diabetes, along with morphological and functional abnormalities not seen in control β-cells.
“While there is no evidence for mitochondrial depletion in β-cells from patients with T2DM, the mitochondrial density volume is considerably higher in islets from patients with T2DM than in islets from those without T2DM, with both morphological and functional abnormalities that have not been observed in β-cells from control individuals143.”
From Mitochondrial and metabolic dysfunction in ageing and age-related diseases (2022) · cites this paper as [143]
There is no evidence for mitochondrial depletion in β-cells from people with type 2 diabetes.
“While there is no evidence for mitochondrial depletion in β-cells from patients with T2DM, the mitochondrial density volume is considerably higher in islets from patients with T2DM than in islets from those without T2DM, with both morphological and functional abnormalities that have not been observed in β-cells from control individuals143.”
From Mitochondrial and metabolic dysfunction in ageing and age-related diseases (2022) · cites this paper as [143]
In islets from people with type 2 diabetes, ATP content and the glucose-stimulated ATP-to-ADP ratio are lower than in control islets.
“In islets from patients with T2DM, the ATP content, and the increase in the ATP to ADP ratio stimulated by glucose, was lower than in islets from control individuals143.”
From Mitochondrial and metabolic dysfunction in ageing and age-related diseases (2022) · cites this paper as [143]
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References 65 · Cited by 385
- Authors
- Anello, M., Lupi, R., Spampinato, D., Piro, S., Masini, M., Boggi, U., Del Prato, S., Rabuazzo, A. M., Purrello, F., & Marchetti, P.
- Affiliations
- University of Catania (IT)
- University of Pisa (IT)
- Corresponding author
- Purrello, F.
- Venue
- Diabetologia
- Published
- 2005-01-15
- Volume
- 48
- Issue
- 2
- Pages
- 282-289
- ISSN
- 0012-186X (ISSN-L)
- 1432-0428
- OpenAlex
- W2055791664
- Cited by
- 385
- References
- 65
- Citations by year
- 2026: 15 · 2025: 15 · 2024: 21 · 2023: 19 · 2022: 29 · 2021: 23 · 2020: 28 · 2019: 14 · 2018: 19 · 2017: 14 · 2016: 23 · 2015: 15 · 2014: 19 · 2013: 16 · 2012: 26
- FWCI
- 15.22
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Diabetologia (publishedVersion)
- PubMed (publishedVersion)
- CINECA IRIS Institutial research information system (University of Pisa) (submittedVersion)
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Keywords
- type 2 diabetes, pancreatic beta cells, mitochondrial function, mitochondrial morphology, insulin secretion, glucose-stimulated insulin secretion, mitochondrial membrane potential, ATP/ADP ratio, UCP2, respiratory chain complexes, nitrotyrosine, islets
- MeSH terms
- Insulin Secretion, Adenine Nucleotides, Arginine, Cell Separation, Diabetes Mellitus, Type 2, Glucose, Humans, Insulin, Islets of Langerhans, Mitochondria, Reference Values
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