Fed state (vs Fasting state):
- Anabolism or Catabolism?
- mTOR activation or deactivation?
- Protein synthesis or autophagy?
- Insulin sensitization or resistance?
- Lipogenesis or Lipolysis?
- Glycogenesis of glycolysis (glucose utilisation)
- Anabolism
- mTOR activation
- Protein synthesis
- Insulin resistance
- Lipogenesis
- Glycogenesis
Fasting state:
What is the ratio
NAD+:NADH
What are the implications?
HIGH (there is more NAD+)
- Increase in Longevity genes
- Activation in SIRT (Sirtuines)
- Activation in FOX
What are FOX proteins?
FOX (Forkhead box) proteins
- family of transcription factors
- regulate expression of genes involved in
- cell growth
- proliferation
- differentiation
- longevity
mTOR Complex 1 (mTORC1)
What does it do?
In order to grow and divide, cells must
- ??????? production of proteins, lipids, and nucleotides
- ??????? catabolic pathways such as autophagy
controls the balance between anabolism and catabolism in response to environmental conditions
In order to grow and divide, cells must:
- increase production of proteins, lipids, and nucleotides
- suppress catabolic pathways such as autophagy
is mTORC1 activated following feeding?
Hell yes!
The mTORC1-dependent shift towards increased anabolism should only occur in the presence of pro-growth endocrine signals as well as sufficient energy and chemical building blocks for macromolecular synthesis. In mammals, these inputs are largely dependent on diet, such that mTORC1 is activated following feeding to promote growth and energy storage in tissues such as the liver and muscle, but inhibited during fasting conserve limited resources.
Does a postprandial increase of insulin and glucose acutely activate mTOR?
Yes
Does mTOR play an important role in glucose and lipid metabolism?
Yes
Can obesity and nutrient overload (hyperglycemia and hyperinsulinemia) cause Hyperactive mTORC1 or 2?
Hyperactive mTORC1
Is mTOR activated by growth factors?
Yes
