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Autophagy-nutrient sensing pathways in diabetic complications.
Urvi M Parmar1, Manjiri P Jalgaonkar1, Yogesh A Kulkarni2
1SVKM's Dr. Bhanuben Nanavati College of Pharmacy, Vile Parle (W), Mumbai 400056, India.
Pharmacological Research
|August 21, 2022
Summary
Autophagy, regulated by nutrient-sensing pathways like SIRT1, mTOR, and AMPK, shows promise in combating diabetes complications. Targeting these pathways could offer new therapeutic strategies for metabolic disorders.
Area of Science:
- Metabolic disorders
- Cellular homeostasis
- Molecular biology
Background:
- Diabetes incidence is rising globally, leading to severe micro and macrovascular complications.
- Hyperglycemia in diabetes causes oxidative stress, protein misfolding, and cellular dysfunction.
- Insulin resistance, linked to redox alterations and inflammation, is central to obesity and diabetes development.
Purpose of the Study:
- To review the role of autophagy in metabolic homeostasis.
- To explore the function of nutrient-sensing pathways (SIRT1, mTOR, AMPK) in regulating autophagy.
- To identify autophagy and these pathways as potential therapeutic targets for diabetic complications.
Main Methods:
- Literature review of studies on autophagy, nutrient-sensing pathways, and diabetes.
- Analysis of the molecular mechanisms linking cellular stress, insulin resistance, and autophagy.
- Synthesis of current research on SIRT1, mTOR, and AMPK in regulating autophagy.
Main Results:
- Disrupted autophagy is implicated in the pathogenesis of obesity and diabetes.
- Autophagy acts as a cellular cleansing mechanism, crucial for restoring homeostasis.
- SIRT1, mTOR, and AMPK are key regulators of autophagy in response to nutrient availability.
Conclusions:
- Autophagy regulation is beneficial in metabolic disorders like diabetes.
- Targeting autophagy and nutrient-sensing pathways (SIRT1, mTOR, AMPK) offers potential therapeutic avenues.
- Modulating these pathways may help reduce the progression of diabetic complications.
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