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Cited by 215

The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.

Deletion of the Mammalian INDY Homolog Mimics Aspects of Dietary Restriction and Protects against Adiposity and Insulin Resistance in Mice

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Birkenfeld, Andreas L., Lee, Hui-Young, Guebre-Egziabher, Fitsum, Alves, Tiago C., Jurczak, Michael J., Jornayvaz, Francois R., Zhang, Dongyang, Hsiao, Jennifer J., Martin-Montalvo, Alejandro, Fischer-Rosinsky, Antje, Spranger, Joachim, Pfeiffer, Andreas F., Jordan, Jens, Fromm, Martin F., König, Jörg, Lieske, Stefanie, Carmean, Christopher M., Frederick, David W., Weismann, Dirk, Knauf, Felix, Irusta, Pablo M., De Cabo, Rafael, Helfand, Stephen L., Samuel, Varman T., Shulman, Gerald I.·2011·Cell Metabolism

Abstract

SUMMARY Reduced expression of the Indy (= I am Not Dead, Yet) gene in D. melanogaster and C. elegans prolongs life span, and in D. melanogaster augments mitochondrial biogenesis in a manner akin to caloric restriction. However, the cellular mechanism by which Indy does this is unknown. Here, we report on the knockout-mouse model of the mammalian Indy (mIndy) homologue, SLC13A5. Deletion of mIndy in mice (mINDY−/− mice) reduces hepatocellular ATP/ADP ratio, activates hepatic AMPK, induces PGC-1α, inhibits ACC-2, and reduces SREBP-1c levels. This signaling network promotes hepatic mitochondrial biogenesis, lipid oxidation, and energy expenditure and attenuates hepatic de novo lipogenesis. Together, these traits protect mINDY−/− mice from the adiposity and insulin resistance that evolve with high-fat feeding and aging. Our studies demonstrate a profound effect of mIndy on mammalian energy metabolism and suggest that mINDY might be a therapeutic target for the treatment of obesity and type 2 diabetes.

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Metadata

Authors
Birkenfeld, A. L., Lee, H.-Y., Guebre-Egziabher, F., Alves, T. C., Jurczak, M. J., Jornayvaz, F. R., Zhang, D., Hsiao, J. J., Martin-Montalvo, A., Fischer-Rosinsky, A., Spranger, J., Pfeiffer, A. F., Jordan, J., Fromm, M. F., König, J., Lieske, S., Carmean, C. M., Frederick, D. W., Weismann, D., Knauf, F., Irusta, P. M., De Cabo, R., Helfand, S. L., Samuel, V. T., & Shulman, G. I.
Venue
Cell Metabolism
Publisher
Elsevier BV
Published
2011-08
Volume
14
Issue
2
Pages
184-195
ISSN
1550-4131 (ISSN-L)
OpenAlex
W2065261177
Cited by
215
References
11
FWCI
4.82
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Deletion of the Mammalian INDY Homolog Mimics Aspects of Dietary Restriction and Protects against Adiposity and Insulin Resistance in Mice. https://app.cochat.ai/papers/10.1016/j.cmet.2011.06.009
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Birkenfeld, A. L., Lee, H.-Y., Guebre-Egziabher, F., Alves, T. C., Jurczak, M. J., Jornayvaz, F. R., Zhang, D., Hsiao, J. J., Martin-Montalvo, A., Fischer-Rosinsky, A., Spranger, J., Pfeiffer, A. F., Jordan, J., Fromm, M. F., König, J., Lieske, S., Carmean, C. M., Frederick, D. W., Weismann, D., . . . Shulman, G. I. (2011). Deletion of the Mammalian INDY Homolog Mimics Aspects of Dietary Restriction and Protects against Adiposity and Insulin Resistance in Mice. Cell Metabolism. https://doi.org/10.1016/j.cmet.2011.06.009

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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.