The DOI matches its Crossref record; 12 of the 12 references it cites were found in a registry or an index.
Liver-Specific Inhibition of ChREBP Improves Hepatic Steatosis and Insulin Resistance in ob/ob Mice
Open accessAbstract
Obesity is a metabolic disorder often associated with type 2 diabetes, insulin resistance, and hepatic steatosis. Leptin-deficient (ob/ob) mice are a well-characterized mouse model of obesity in which increased hepatic lipogenesis is thought to be responsible for the phenotype of insulin resistance. We have recently demonstrated that carbohydrate responsive element–binding protein (ChREBP) plays a key role in the control of lipogenesis through the transcriptional regulation of lipogenic genes, including acetyl-CoA carboxylase and fatty acid synthase. The present study reveals that ChREBP gene expression and ChREBP nuclear protein content are significantly increased in liver of ob/ob mice. To explore the involvement of ChREBP in the physiopathology of hepatic steatosis and insulin resistance, we have developed an adenovirus-mediated RNA interference technique in which short hairpin RNAs (shRNAs) were used to inhibit ChREBP expression in vivo. Liver-specific inhibition of ChREBP in ob/ob mice markedly improved hepatic steatosis by specifically decreasing lipogenic rates. Correction of hepatic steatosis also led to decreased levels of plasma triglycerides and nonesterified fatty acids. As a consequence, insulin signaling was improved in liver, skeletal muscles, and white adipose tissue, and overall glucose tolerance and insulin sensitivity were restored in ob/ob mice after a 7-day treatment with the recombinant adenovirus expressing shRNA against ChREBP. Taken together, our results demonstrate that ChREBP is central for the regulation of lipogenesis in vivo and plays a determinant role in the development of the hepatic steatosis and of insulin resistance in ob/ob mice.
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Cites
Nonalcoholic Fatty Liver Disease
Angulo, P. (2002) · New England Journal of Medicine · doi:10.1056/nejmra011775 · Cited by 5,228
Donnelly, K. L., Smith, C. I., Schwarzenberg, S. J., Jessurun, J., Boldt, M. D., & Parks, E. J. (2005) · Journal of Clinical Investigation · doi:10.1172/jci23621 · Cited by 3,604
Nonalcoholic Fatty Liver Disease
Marchesini, G., Brizi, M., Bianchi, G., Tomassetti, S., Bugianesi, E., Lenzi, M., McCullough, A. J., Natale, S., Forlani, G., & Melchionda, N. (2001) · Diabetes · doi:10.2337/diabetes.50.8.1844 · Cited by 2,581
Insulin-regulated hepatic gluconeogenesis through FOXO1–PGC-1α interaction
Puigserver, P., Rhee, J., Donovan, J., Walkey, C. J., Yoon, J. C., Oriente, F., Kitamura, Y., Altomonte, J., Dong, H., Accili, D., et al. (2003) · Nature · doi:10.1038/nature01667 · Cited by 1,487
Regulation of hepatic fatty acid oxidation and ketone body production
McGarry, J. D., & Foster, D. W. (1980) · Annual Review of Biochemistry · doi:10.1146/annurev.bi.49.070180.002143 · Cited by 1,460 · cited 1×
“Lipogenesis and -oxidation are correlated since malonyl-CoA, synthesized by ACC, is the allosteric inhibitor of L-CPT-1, the rate-limiting enzyme of -oxidation (27).”
BackgroundMechanism of hepatic insulin resistance in non-alcoholic fatty liver disease
Samuel, V. T., Liu, Z.-X., Qu, X., Elder, B. D., Bilz, S., Befroy, D., Romanelli, A. J., & Shulman, G. I. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.m313478200 · Cited by 1,322
Petersen, K. F., Dufour, S., Befroy, D., Lehrke, M., Hendler, R. E., & Shulman, G. I. (2005) · Diabetes · doi:10.2337/diabetes.54.3.603 · Cited by 911
A possible role for malonyl-CoA in the regulation of hepatic fatty acid oxidation and ketogenesis.
McGarry, J. D., Mannaerts, G. P., & Foster, D. W. (1977) · Journal of Clinical Investigation · doi:10.1172/jci108764 · Cited by 736
Mayerson, 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
Schwarz, J.-M., Linfoot, P., Dare, D., & Aghajanian, K. (2003) · The American Journal of Clinical Nutrition · doi:10.1093/ajcn/77.1.43 · Cited by 496
Abu-Elheiga, L., Oh, W., Kordari, P., & Wakil, S. J. (2003) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1733877100 · Cited by 389
Dentin, R. (2005) · Journal of Clinical Investigation · doi:10.1172/jci25256 · Cited by 315
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Cited by
Molecular mechanisms of hepatic lipid accumulation in non-alcoholic fatty liver disease
Ipsen, D. H., Lykkesfeldt, J., & Tveden-Nyborg, P. (2018) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-018-2860-6 · Cited by 1,471
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
Regulation of glucose metabolism from a liver-centric perspective
Han, H.-S., Kang, G., Kim, J. S., Choi, B. H., & Koo, S.-H. (2016) · Experimental & Molecular Medicine · doi:10.1038/emm.2015.122 · Cited by 835
The role of fructose in the pathogenesis of NAFLD and the metabolic syndrome
Lim, J. S., Mietus-Snyder, M., Valente, A., Schwarz, J.-M., & Lustig, R. H. (2010) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/nrgastro.2010.41 · Cited by 771
Fatty acid metabolism: Target for metabolic syndrome
Wakil, S. J., & Abu-Elheiga, L. A. (2009) · Journal of Lipid Research · doi:10.1194/jlr.r800079-jlr200 · Cited by 731
Metadata
- Authors
- Dentin, R., Benhamed, F., Hainault, I., Fauveau, V., Foufelle, F., Dyck, J. R. B., Girard, J., & Postic, C.
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2006-08-01
- Volume
- 55
- Issue
- 8
- Pages
- 2159-2170
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2160870282
- Cited by
- 433
- References
- 12
- FWCI
- 13.72
- Type
- journal article
- Language
- en
- Open access
- bronze
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