Proteomics

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Global Analyses of Selective Insulin Resitance in Hepatocytes due to Palmitate Lipotoxicity


ABSTRACT: Obesity is tightly linked to hepatic steatosis and insulin resistance. One feature of this association is the paradox of selective insulin resistance: insulin fails to suppress hepatic gluconeogenesis but activates lipid synthesis in the liver. How lipid accumulation interferes selectively with some branches of hepatic insulin signaling is not well understood. Here we provide a resource, based on unbiased approaches and established in a simple cell culture system, to enable investigations of the phenomenon of selective insulin resistance. We analyzed the phosphoproteome of insulin-treated human hepatoma cells and identified sites in which palmitate selectively impairs insulin signaling. As an example, we show that palmitate interferes with insulin signaling to FoxO1, a key transcription factor regulating gluconeogenesis, and identify a possible mechanism. This model system, together with our comprehensive characterization of the proteome, phosphoproteome, and lipidome changes in response to palmitate treatment, provides a novel and useful resource for unraveling the mechanisms underlying selective insulin resistance.

OTHER RELATED OMICS DATASETS IN: MTBLS582

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Hepatocyte, Cell Culture

SUBMITTER: Zon Weng Lai  

LAB HEAD: Tobias Walther

PROVIDER: PXD006395 | Pride | 2018-02-14

REPOSITORIES: Pride

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Publications

Global Analyses of Selective Insulin Resistance in Hepatocytes Caused by Palmitate Lipotoxicity.

Li Zhihuan Z   Lai Zon Weng ZW   Christiano Romain R   Gazos-Lopes Felipe F   Walther Tobias C TC   Farese Robert V RV  

Molecular & cellular proteomics : MCP 20180205 5


Obesity is tightly linked to hepatic steatosis and insulin resistance. One feature of this association is the paradox of selective insulin resistance: insulin fails to suppress hepatic gluconeogenesis but activates lipid synthesis in the liver. How lipid accumulation interferes selectively with some branches of hepatic insulin signaling is not well understood. Here we provide a resource, based on unbiased approaches and established in a simple cell culture system, to enable investigations of the  ...[more]

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