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Glucose availability regulates nicotinamide N-methyltransferase expression in adipocytes
Franziska Ehebauer1, Sharang Ghavampour1, Daniel Kraus1
1Universitätsklinikum Würzburg, Medizinische Klinik und Poliklinik I, Oberdürrbacher Str. 6, 97080 Würzburg, Germany.
Life Sciences
|March 1, 2020
Summary
Glucose availability impacts Nicotinamide N-methyltransferase (NNMT) levels in fat cells. Low glucose increases NNMT, regulated by the mTOR pathway, offering insights into obesity and diabetes.
Area of Science:
- Metabolic regulation in adipocytes
- Cellular energy homeostasis
- Obesity and diabetes research
Background:
- Nicotinamide N-methyltransferase (NNMT) is a key regulator of energy balance in fat cells.
- Elevated NNMT in adipose tissue is linked to obesity and diabetes.
- NNMT's role in insulin resistance and glucose transporter 4 (GLUT4) expression is established.
Purpose of the Study:
- To investigate the regulatory mechanisms controlling NNMT expression in adipocytes.
- To understand how glucose availability influences NNMT levels.
- To elucidate the signaling pathways involved in NNMT regulation.
Main Methods:
- 3T3-L1 adipocytes were treated with varying glucose concentrations.
- Intracellular pathways were modulated using activators and inhibitors.
- NNMT mRNA and protein levels were quantified using qPCR and Western blotting.
Main Results:
- Glucose deprivation significantly increased NNMT mRNA and protein expression.
- Inhibition of glucose transport and glycolysis mimicked the effect of glucose deprivation.
- AMP-activated protein kinase (AMPK) activation and mammalian target of rapamycin (mTOR) inhibition increased NNMT.
- mTOR activation blocked the glucose deprivation-induced NNMT upregulation.
- NNMT upregulation was dependent on autophagy and protein translation.
Conclusions:
- Adipocyte NNMT expression is regulated by glucose availability.
- The mTOR signaling pathway is a critical mediator of this regulation.
- Findings provide mechanistic insights into NNMT's role in metabolic diseases.
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