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Mitochondrial Ultrastructure and Glucose Signaling Pathways Attributed to the Kv1.3 Ion Channel
Christopher P Kovach1, Dolly Al Koborssy2, Zhenbo Huang2
1Program in Neuroscience, Florida State UniversityTallahassee, FL, USA; Department of Biological Science, Florida State UniversityTallahassee, FL, USA.
Frontiers in Physiology
|June 1, 2016
Summary
Deleting the Kv1.3 channel in mice enhances their sense of smell and metabolism. This knockout improves glucose uptake and alters mitochondrial structure, potentially driving whole-body metabolic changes.
Area of Science:
- Neuroscience
- Metabolic Research
- Molecular Biology
Background:
- The potassium channel Kv1.3 plays a role in cellular excitability and energy metabolism.
- Kv1.3 knockout (Kv1.3(-∕-)) mice exhibit enhanced olfactory abilities and metabolic benefits, including resistance to obesity.
- The olfactory bulb (OB) is energy-intensive, requiring efficient glucose utilization and mitochondrial function.
Purpose of the Study:
- To investigate the cellular mechanisms by which Kv1.3 deletion in the OB influences glucose utilization and metabolic rate.
- To explore the relationship between Kv1.3, glucose transporter type 4 (GLUT4), and mitochondrial structure in the OB.
- To understand how Kv1.3 channel function impacts energy expenditure and metabolic homeostasis.
Main Methods:
- In situ hybridization to assess co-localization of Kv1.3 and GLUT4 in the OB.
- HEK 293 cell experiments to evaluate the effect of Kv1.3 pore mutations on GLUT4 translocation.
- Transmission electron microscopy to examine OB mitochondrial ultrastructure in wildtype (WT) and Kv1.3(-∕-) mice fed a high-fat diet.
- Metabolic phenotyping of WT and Kv1.3(-∕-) mice, including body weight, adiposity, and total energy expenditure (TEE).
Main Results:
- Kv1.3 and GLUT4 are co-localized in the mitral cell layer of the OB.
- Disruption of Kv1.3 channel function promotes GLUT4 translocation to the plasma membrane.
- Kv1.3(-∕-) mice exhibit smaller mitochondria and resistance to diet-induced mitochondrial changes compared to WT mice.
- Kv1.3(-∕-) mice display reduced adiposity, increased TEE, and resistance to obesity.
Conclusions:
- Kv1.3 channel deletion in the OB regulates mitochondrial structure and alters glucose utilization.
- These cellular changes in the OB may contribute to the observed whole-body metabolic benefits, including increased energy expenditure and obesity resistance.
- Targeted disruption of Kv1.3 in the OB represents a potential mechanism for modulating systemic metabolism.
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