The DOI matches its Crossref record; 12 of the 12 references it cites were found in a registry or an index.
Ectopic Fat in Insulin Resistance, Dyslipidemia, and Cardiometabolic Disease
Abstract
To the Editor: Shulman (Sept. 18 issue)1 theorized that ectopic fat plays a major role in the development of insulin resistance. We speculate, however, that insulin resistance may be caused by another major pathway, in which glucose itself, at high levels, plays a critical role. Reasonable evidence has shown that when glucose levels are elevated, glucose molecules may randomly bind to proteins similar to the insulin receptor on the plasma membrane of the cell and in time become advanced glycation end products.2 Circulating insulin levels would easily fail to dock properly with the advanced glycation end product deposited on the insulin receptor and would therefore fail to initiate the glucose-transport process, effectively causing insulin resistance.3 This pathway for glycation-induced insulin resistance would explain why insulin resistance often develops in persons who are not obese and who probably do not have substantial ectopic fat.
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Randle, P. J., Garland, P. B., Hales, C. N., & Newsholme, E. A. (1963) · The Lancet · doi:10.1016/s0140-6736(63)91500-9 · Cited by 5,093
Genetic variation in PNPLA3 confers susceptibility to nonalcoholic fatty liver disease
Romeo, S., Kozlitina, J., Xing, C., Pertsemlidis, A., Cox, D., Pennacchio, L. A., Boerwinkle, E., Cohen, J. C., & Hobbs, H. H. (2008) · Nature Genetics · doi:10.1038/ng.257 · Cited by 3,416
Mechanisms for Insulin Resistance: Common Threads and Missing Links
Samuel, V. T., & Shulman, G. I. (2012) · Cell · doi:10.1016/j.cell.2012.02.017 · Cited by 2,294
Impaired Mitochondrial Activity in the Insulin-Resistant Offspring of Patients with Type 2 Diabetes
Petersen, K. F., Dufour, S., Befroy, D., Garcia, R., & Shulman, G. I. (2004) · New England Journal of Medicine · doi:10.1056/nejmoa031314 · Cited by 2,193
Dresner, A., Laurent, D., Marcucci, M., Griffin, M. E., Dufour, S., Cline, G. W., Slezak, L. A., Andersen, D. K., Hundal, R. S., Rothman, D. L., et al. (1999) · Journal of Clinical Investigation · doi:10.1172/jci5001 · Cited by 1,311
Krssak, M., Falk Petersen, K., Dresner, A., DiPietro, L., Vogel, S. M., Rothman, D. L., Shulman, G. I., & Roden, M. (1999) · Diabetologia · doi:10.1007/s001250051123 · Cited by 1,264
Shulman, G. I., Rothman, D. L., Jue, T., Stein, P., DeFronzo, R. A., & Shulman, R. G. (1990) · New England Journal of Medicine · doi:10.1056/nejm199001253220403 · Cited by 1,248
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
Identification and characterization of metabolically benign obesity in humans
Stefan, N. (2008) · Archives of Internal Medicine · doi:10.1001/archinte.168.15.1609 · Cited by 1,049
Self-citationMayerson, A. B., Hundal, R. S., Dufour, S., Lebon, V., Befroy, D., Cline, G. W., Enocksson, S., Inzucchi, S. E., Shulman, G. I., & Petersen, K. F. (2002) · Diabetes · doi:10.2337/diabetes.51.3.797 · Cited by 647
Research works printed but not linked: 7
- 10.1055/s-0028-1082085 · DOI
- 10.2174/138161208784139747 · DOI · Paper page
- 10.1016/j.tibs.2003.12.004 · DOI · Paper page
- 10.1016/j.cmet.2007.08.013 · DOI · Paper page
- 10.2337/diacare.22.9.1462 · DOI · Paper page
- 10.1016/j.metabol.2008.04.019 · DOI
- 10.1073/pnas.0608537103 · DOI · Paper page
Cited by
Tilg, H., Moschen, A. R., & Roden, M. (2017) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/nrgastro.2016.147 · Cited by 1,002
Trends in insulin resistance: insights into mechanisms and therapeutic strategy
Li, M., Chi, X., Wang, Y., Setrerrahmane, S., Xie, W., & Xu, H. (2022) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-022-01073-0 · Cited by 939
Obesity and type 2 diabetes mellitus: connections in epidemiology, pathogenesis, and treatments
Ruze, R., Liu, T., Zou, X., Song, J., Chen, Y., Xu, R., Yin, X., & Xu, Q. (2023) · Frontiers in Endocrinology · doi:10.3389/fendo.2023.1161521 · Cited by 799
“suppressing insulin action (will be discussed later), which in turn, increases hepatic gluconeogenic enzymes transcription through the activation of nuclear factor kB (NF-kB), Jun N-terminal kinase (JNK), and ceramide biosynthetic pathways (39) (Figure 3).”
BackgroundInfluentialPathogenesis of sarcopenia and the relationship with fat mass: descriptive review
Li, C., Yu, K., Shyh‐Chang, N., Jiang, Z., Liu, T., Ma, S., Luo, L., Guang, L., Liang, K., Ma, W., et al. (2022) · Journal of Cachexia, Sarcopenia and Muscle · doi:10.1002/jcsm.12901 · Cited by 626
The impact of insulin resistance on the kidney and vasculature
Artunc, F., Schleicher, E., Weigert, C., Fritsche, A., Stefan, N., & Häring, H.-U. (2016) · Nature Reviews Nephrology · doi:10.1038/nrneph.2016.145 · Cited by 462
Metadata
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 2014-12-04
- Volume
- 371
- Issue
- 23
- Pages
- 2236-2238
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- OpenAlex
- W2288447626
- Cited by
- 228
- References
- 12
- FWCI
- 11.01
- Type
- journal article
- Language
- en
- Open access
- closed
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
