The DOI matches its Crossref record; 18 of the 18 references it cites were found in a registry or an index.
The “Metabolic Memory”: Is More Than Just Tight Glucose Control Necessary to Prevent Diabetic Complications?
Abstract
CONTEXT: The concept of a "metabolic memory," that is of diabetic vascular stresses persisting after glucose normalization, has been supported both in the laboratory and in the clinic and in both type 1 and type 2 diabetes. EVIDENCE ACQUISITION: Using PubMed, we searched for publications on diabetic micro- and macrovascular complications using terms such as persistence, prolongation, sustained, and "memory" and focusing on the mechanistic basis behind this metabolic memory. EVIDENCE SYNTHESIS: We found that as early as the mid-1980s this memory phenomenon was described in diabetic animals and isolated cells exposed to high glucose followed by normalized glucose and then, beginning around 2002, in results from large clinical trials such as the Diabetes Complications and Control Trial-Epidemiology of Diabetes Interventions and Complications and the United Kingdom Prospective Diabetes Study. Furthermore, mechanisms for propagating this memory appear focused on the nonenzymatic glycation of cellular proteins and lipids and on an excess of cellular reactive oxygen and nitrogen species, in particular originating at the level of glycated mitochondrial proteins and perhaps acting in concert with one another to maintain stress signaling independent of glucose levels. CONCLUSIONS: The emergence of this metabolic memory suggests the need for early aggressive treatment aiming to "normalize" metabolic control together perhaps with the addition of agents which reduce cellular reactive species and glycation in order to minimize long-term diabetic complications.
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Citations
Cites
Effects of Intensive Glucose Lowering in Type 2 Diabetes
(2008) · New England Journal of Medicine · doi:10.1056/nejmoa0802743 · Cited by 7,888
10-year follow-up of intensive glucose control in type 2 diabetes
Holman, R. R., Paul, S. K., Bethel, M. A., Matthews, D. R., & Neil, H. A. W. (2008) · New England Journal of Medicine · doi:10.1056/nejmoa0806470 · Cited by 7,751
Intensive blood glucose control and vascular outcomes in patients with type 2 diabetes
(2008) · New England Journal of Medicine · doi:10.1056/nejmoa0802987 · Cited by 7,397
Intensive diabetes treatment and cardiovascular disease in patients with type 1 diabetes
(2005) · New England Journal of Medicine · doi:10.1056/nejmoa052187 · Cited by 5,138
Normalizing mitochondrial superoxide production blocks three pathways of hyperglycaemic damage
Nishikawa, T., Edelstein, D., Du, X. L., Yamagishi, S.-I., Matsumura, T., Kaneda, Y., Yorek, M. A., Beebe, D., Oates, P. J., Hammes, H.-P., et al. (2000) · Nature · doi:10.1038/35008121 · Cited by 4,277
Advanced Glycation End Products: Sparking the Development of Diabetic Vascular Injury
Goldin, A., Beckman, J. A., Schmidt, A. M., & Creager, M. A. (2006) · Circulation · doi:10.1161/circulationaha.106.621854 · Cited by 2,261
Ceriello, A., Esposito, K., Piconi, L., Ihnat, M. A., Thorpe, J. E., Testa, R., Boemi, M., & Giugliano, D. (2008) · Diabetes · doi:10.2337/db08-0063 · Cited by 1,310
Self-citationEl-Osta, A., Brasacchio, D., Yao, D., Pocai, A., Jones, P. L., Roeder, R. G., Cooper, M. E., & Brownlee, M. (2008) · The Journal of Experimental Medicine · doi:10.1084/jem.20081188 · Cited by 1,115
Intensive Diabetes Therapy and Carotid Intima–Media Thickness in Type 1 Diabetes Mellitus
(2003) · New England Journal of Medicine · doi:10.1056/nejmoa022314 · Cited by 815
Cited by
Cosentino, F., Grant, P. J., Aboyans, V., Bailey, C. J., Ceriello, A., Delgado, V., Federici, M., Filippatos, G., Grobbee, D. E., Hansen, T. B., et al. (2020) · European Heart Journal · doi:10.1093/eurheartj/ehz486 · Cited by 4,763
Self-citationPathophysiology of type 2 diabetes mellitus
Galicia-Garcia, U., Benito-Vicente, A., Jebari, S., Larrea-Sebal, A., Siddiqi, H., Uribe, K. B., Ostolaza, H., & Martín, C. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21176275 · Cited by 3,360
“The increase in O2− production activates the five major pathways involved in the pathogenesis of diabetes complications: enhancement of the polyol pathway, increased formation of advanced glycation end products (AGEs), increased expression of AGEs receptor and its activating ligands, activation of protein kinase C (PK…”
BackgroundInfluentialReactive oxygen species (ROS) in macrophage activation and function in diabetes
Rendra, E., Riabov, V., Mossel, D. M., Sevastyanova, T., Harmsen, M. C., & Kzhyshkowska, J. (2019) · Immunobiology · doi:10.1016/j.imbio.2018.11.010 · Cited by 636
Laiteerapong, N., Ham, S. A., Gao, Y., Moffet, H. H., Liu, J. Y., Huang, E. S., & Karter, A. J. (2019) · Diabetes Care · doi:10.2337/dc17-1144 · Cited by 574
Impact of diabetes on cardiovascular disease: an update
Matheus, A. S. D. M., Tannus, L. R. M., Cobas, R. A., Palma, C. C. S., Negrato, C. A., & Gomes, M. D. B. (2013) · International Journal of Hypertension · doi:10.1155/2013/653789 · Cited by 547
Metadata
- Authors
- Ceriello, A., Ihnat, M. A., & Thorpe, J. E.
- Venue
- The Journal of Clinical Endocrinology & Metabolism
- Publisher
- The Endocrine Society
- Published
- 2009-02-01
- Volume
- 94
- Issue
- 2
- Pages
- 410-415
- ISSN
- 0021-972X (ISSN-L)
- 1945-7197
- OpenAlex
- W2103254817
- Cited by
- 413
- References
- 18
- FWCI
- 12.33
- Type
- journal article
- Language
- en
- Open access
- closed
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