mTORC1 Activates SREBP-1c and Uncouples Lipogenesis From Gluconeogenesis
Insulin resistance, which is defined as the inability of insulin to promote efficient glucose uptake by peripheral tissues, is a metabolic condition associated with obesity, type 2 diabetes, dyslipidemia, and cardiovascular diseases. Although important advances in our understanding of the molecular...
| Main Authors: | , |
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| Other Authors: | |
| Format: | Article |
| Language: | en_US |
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National Academy of Sciences
2011
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| Online Access: | http://hdl.handle.net/1721.1/61405 https://orcid.org/0000-0002-1446-7256 |
| Summary: | Insulin resistance, which is defined as the inability of insulin to promote efficient glucose uptake by peripheral tissues, is a metabolic condition associated with obesity, type 2 diabetes, dyslipidemia, and cardiovascular diseases. Although important advances in our understanding of the molecular mechanisms involved in the development of insulin resistance have been made during the last decades ( 1), many questions remain. One of these questions relates to the fact that, in the liver of many insulin-resistant mouse models, insulin fails to suppress glucose production (gluconeogenesis) but continues to promote lipid synthesis (lipogenesis) ( 2). This selective hepatic insulin resistance contributes to hyperglycemia and hyperlipidemia and suggests that the insulin-signaling pathway must bifurcate upstream of lipogenesis and gluconeogenesis. In this issue of PNAS, Li et al. ( 3) identify a bifurcation point in the insulin-signaling pathway that could help resolve this important paradox. |
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