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Isolation of Primary Mouse Hepatocytes for Nascent Protein Synthesis Analysis by Non-radioactive L-azidohomoalanine Labeling Method
Published on: October 23, 2018
Critical role for hypothalamic mTOR activity in energy balance
Hiroyuki Mori1, Ken Inoki, Heike Münzberg
1Life Sciences Institute, University of Michigan, Ann Arbor, MI 48109, USA.
Cell Metabolism
|April 10, 2009
Summary
Disabling Tsc1 in Pomc neurons activates mTOR signaling, causing hyperphagia and obesity. Inhibiting mTOR with rapamycin reverses these effects, highlighting mTOR
Area of Science:
- Neuroscience
- Metabolic Signaling
- Obesity Research
Background:
- Mammalian target of rapamycin (mTOR) regulates anabolic processes.
- TSC1 and TSC2 tumor suppressors inhibit mTOR signaling.
- Hypothalamic disruption can affect feeding circuits.
Purpose of the Study:
- To investigate the role of Tsc1 deletion in hypothalamic Pomc neurons.
- To determine the impact of mTOR activation on feeding behavior and obesity.
- To assess the therapeutic potential of mTOR inhibition.
Main Methods:
- Utilized Rip2/Cre and Pomc/Cre mouse models for Tsc1 deletion.
- Analyzed mTOR signaling pathways and neuronal morphology.
- Administered rapamycin to evaluate treatment effects.
Main Results:
- Tsc1 deletion in Pomc neurons led to hyperphagia and obesity.
- Increased mTOR signaling and enlarged Pomc neurons were observed.
- Rapamycin treatment ameliorated obesity and normalized Pomc neuron morphology.
Conclusions:
- Ongoing mTOR activation in Pomc neurons promotes nutrient intake and adiposity.
- Targeting mTOR signaling in Pomc neurons is a potential strategy for obesity treatment.
- Tsc1 loss in Pomc neurons dysregulates feeding circuits via mTOR activation.
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