Suppression of the mTORC1/STAT3/Notch1 pathway by activated AMPK prevents hepatic insulin resistance induced by excess amino acids

Nutrient overload is associated with the development of obesity, insulin resistance, and type 2 diabetes. However, the underlying mechanisms for developing insulin resistance in the presence of excess nutrients are incompletely understood. We investigated whether activation of AMP-activated protein...

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Veröffentlicht in:	American journal of physiology: endocrinology and metabolism 2014-01, Vol.306 (2), p.E197-E209
Hauptverfasser:	Li, Hongliang, Lee, Jiyeon, He, Chaoyong, Zou, Ming-Hui, Xie, Zhonglin
Format:	Artikel
Sprache:	eng
Schlagworte:	Amino acids Amino Acids - metabolism Amino Acids - pharmacology AMP-Activated Protein Kinases - physiology Animals Diabetes Down-Regulation - drug effects Enzyme Activation Hep G2 Cells Humans Insulin Resistance Kinases Liver - drug effects Liver - metabolism Male Mechanistic Target of Rapamycin Complex 1 Mice Mice, Inbred C57BL Multiprotein Complexes - antagonists & inhibitors Obesity Phosphorylation Receptor, Notch1 - antagonists & inhibitors Signal Transduction - drug effects Signal Transduction - physiology STAT3 Transcription Factor - antagonists & inhibitors TOR Serine-Threonine Kinases - antagonists & inhibitors
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