The DOI matches its Crossref record; 20 of the 20 references it cites were found in a registry or an index.
beta-cell dysfunction and failure in type 2 diabetes: potential mechanisms.
Open accessAbstract
Type 2 diabetes is characterized by a progressive loss of beta-cell function throughout the course of the disease. The pattern of loss is an initial defect in early or first-phase insulin secretion, followed by a decreasing maximal capacity of glucose to potentiate all nonglucose signals. Last, a defective steady-state and basal insulin secretion develops, leading to complete beta-cell failure requiring insulin treatment. This functional loss exceeds the expected impact of a 20-50% loss of beta-cells reported at autopsy, which has been associated with amyloid deposits. This review summarizes the nature of the amyloid deposition process and its association with disproportionate hyperproinsulinemia. It reviews recent studies in IAPP (islet-amyloid polypeptide, or amylin) transgenic mice developing islet amyloid deposits and hyperglycemia to suggest that the process of amyloid fibril formation impairs function early and leads to beta-cell failure and eventual death. Based on the known association of amyloid deposits and relative hyperproinsulinemia, it is hypothesized that fibril formation begins during impaired glucose tolerance after other factors cause the initial defects in early insulin secretion and insulin action. Thus, the process that leads to beta-cell loss is implicated in the deposition of amyloid and the late unrelenting progressive hyperglycemia now found in all patients despite current therapies.
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Cites
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Pancreatic islet cell toxicity of amylin associated with type-2 diabetes mellitus
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Insulin secretion in diabetes mellitus
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Self-citationThe influence of amyloid deposits on the islet volume in maturity onset diabetes mellitus
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Assessing the potential for α-glucosidase inhibitors in prediabetic states
Holman, R. R. (1998) · Diabetes Research and Clinical Practice · doi:10.1016/s0168-8227(98)00038-2 · Cited by 197
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Proinsulin as a marker for the development of NIDDM in Japanese-American men
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Cited by
Prevalence of impaired glucose tolerance among children and adolescents with marked obesity
Sinha, R., Fisch, G., Teague, B., Tamborlane, W. V., Banyas, B., Allen, K., Savoye, M., Rieger, V., Taksali, S., Barbetta, G., et al. (2002) · New England Journal of Medicine · doi:10.1056/nejmoa012578 · Cited by 1,709
Ectopic Fat in Insulin Resistance, Dyslipidemia, and Cardiometabolic Disease
Shulman, G. I. (2014) · New England Journal of Medicine · doi:10.1056/nejmra1011035 · Cited by 1,126
Molecular Mechanisms Linking Oxidative Stress and Diabetes Mellitus
Yaribeygi, H., Sathyapalan, T., Atkin, S. L., & Sahebkar, A. (2020) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2020/8609213 · Cited by 685
Metabolic Signaling in Fuel-Induced Insulin Secretion
Prentki, M., Matschinsky, F. M., & Madiraju, S. R. M. (2013) · Cell Metabolism · doi:10.1016/j.cmet.2013.05.018 · Cited by 548
Burgert, T. S., Taksali, S. E., Dziura, J., Goodman, T. R., Yeckel, C. W., Papademetris, X., Constable, R. T., Weiss, R., Tamborlane, W. V., Savoye, M., et al. (2006) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2006-1010 · Cited by 369
Metadata
- Authors
- Porte, D., & Kahn, S. E.
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2001-02-01
- Volume
- 50
- Issue
- suppl_1
- Pages
- S160
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2139698840
- Cited by
- 332
- References
- 20
- Type
- conference abstract
- Language
- en
- Open access
- bronze
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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