The DOI matches its Crossref record; 67 of the 67 references it cites were found in a registry or an index.
Attenuated mTOR Signaling and Enhanced Autophagy in Adipocytes from Obese Patients with Type 2 Diabetes
Open accessAbstract
Type 2 diabetes (T2D) is strongly linked to obesity and an adipose tissue unresponsive to insulin. The insulin resistance is due to defective insulin signaling, but details remain largely unknown. We examined insulin signaling in adipocytes from T2D patients, and contrary to findings in animal studies, we observed attenuation of insulin activation of mammalian target of rapamycin (mTOR) in complex with raptor (mTORC1). As a consequence, mTORC1 downstream effects were also affected in T2D: feedback signaling by insulin to signal-mediator insulin receptor substrate-1 (IRS1) was attenuated, mitochondria were impaired and autophagy was strongly upregulated. There was concomitant autophagic destruction of mitochondria and lipofuscin particles, and a dependence on autophagy for ATP production. Conversely, mitochondrial dysfunction attenuated insulin activation of mTORC1, enhanced autophagy and attenuated feedback to IRS1. The overactive autophagy was associated with large numbers of cytosolic lipid droplets, a subset with colocalization of perlipin and the autophagy protein LC3/atg8, which can contribute to excessive fatty acid release. Patients with diagnoses of T2D and overweight were consecutively recruited from elective surgery, whereas controls did not have T2D. Results were validated in a cohort of patients without diabetes who exhibited a wide range of insulin sensitivities. Because mitochondrial dysfunction, inflammation, endoplasmic-reticulum stress and hypoxia all inactivate mTORC1, our results may suggest a unifying mechanism for the pathogenesis of insulin resistance in T2D, although the underlying causes might differ.
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Cites
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TOR signaling in growth and metabolism
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Parkin is recruited selectively to impaired mitochondria and promotes their autophagy
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Autophagy regulates lipid metabolism
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Dysfunction of Mitochondria in Human Skeletal Muscle in Type 2 Diabetes
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Impaired Mitochondrial Activity in the Insulin-Resistant Offspring of Patients with Type 2 Diabetes
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Serum retinol binding protein 4 contributes to insulin resistance in obesity and type 2 diabetes
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Cited by
Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition).
Klionsky, D. J., Abdelmohsen, K., Abe, A., Abedin, M. J., Abeliovich, H., Acevedo Arozena, A., Adachi, H., Adams, C. M., Adams, P. D., Adeli, K., et al. (2016) · Autophagy · doi:10.1080/15548627.2015.1100356 · Cited by 5,894
Guidelines for the use and interpretation of assays for monitoring autophagy
Klionsky, D. J., Abdalla, F. C., Abeliovich, H., Abraham, R. T., Acevedo-Arozena, A., Adeli, K., Agholme, L., Agnello, M., Agostinis, P., Aguirre-Ghiso, J. A., et al. (2012) · Autophagy · doi:10.4161/auto.19496 · Cited by 3,996
Self-citationGuidelines for the use and interpretation of assays for monitoring autophagy (4th edition) 1
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“upstream insulin resistance), the implication is that mTORC1 activity is reduced in insulinresistant human adipocytes in vivo [116].”
BackgroundLipophagy: Connecting Autophagy and Lipid Metabolism
Singh, R., & Cuervo, A. M. (2012) · International Journal of Cell Biology · doi:10.1155/2012/282041 · Cited by 497
Metadata
- Authors
- Öst, A., Svensson, K., Ruishalme, I., Brännmark, C., Franck, N., Krook, H., Sandström, P., Kjolhede, P., & Strålfors, P.
- Venue
- Molecular Medicine
- Published
- 2010-03-26
- Volume
- 16
- Issue
- 7-8
- Pages
- 235-246
- ISSN
- 1076-1551 (ISSN-L)
- 1528-3658
- OpenAlex
- W1525943215
- Cited by
- 270
- References
- 67
- FWCI
- 11.11
- Type
- journal article
- Language
- en
- Open access
- gold
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- Öst, A., Svensson, K., Ruishalme, I., Brännmark, C., Franck, N., Krook, H., Sandström, P., Kjolhede, P., & Strålfors, P. (2010). Attenuated mTOR Signaling and Enhanced Autophagy in Adipocytes from Obese Patients with Type 2 Diabetes. Molecular Medicine. https://doi.org/10.2119/molmed.2010.00023
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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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