Diet-Induced Obesity Resistance of Kv1.3-/- Mice is Olfactory Bulb Dependent

Kristal Raylone Tucker, J. M. Overton, D. A. Fadool

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

Gene-targeted deletion of the voltage-gated potassium channel, Kv1.3 (Kv1.3-/-), increases olfactory sensitivity and discriminatory ability, and causes resistance to diet-induced obesity (DIO) in mice. The present study aimed to determine whether the enhanced olfactory ability of the Kv1.3-/- mouse contributes to the resistance to DIO. Kv1.3+/+ and Kv1.3-/- mice were subject to bilateral olfactory bulbectomy (OBX) or sham surgery at 9weeks of age and placed on either a control chow diet or a 32% moderately high-fat diet (MHF). Caloric and water intake, locomotor activity and oxygen consumption were monitored after 5weeks of diet treatment. At the end of 26weeks of diet treatment, fat pad weight and blood chemistry were evaluated. Kv1.3+/+ mice exhibited a significant increase in weight, adiposity, fasting glucose and fasting leptin in response to the MHF-diet, with or without OBX. When treated with a MHF-diet, Kv1.3-/- mice gained significantly less weight than Kv1.3+/+ mice and exhibited a significant increase in light phase metabolism. OBX of Kv1.3-/- mice prevented the resistance to DIO and concomitant up-regulation of light phase metabolism at the same time as decreasing dark phase metabolism and total energy expenditure. These findings suggest that pathways activated in Kv1.3-/- that increased energy expenditure and led to resistance to DIO are olfactory bulb dependent. Thus, these findings add to a growing body of evidence suggesting that the olfactory system can modulate the pathways involved in the regulation of energy balance.

Original languageEnglish (US)
Pages (from-to)1087-1095
Number of pages9
JournalJournal of Neuroendocrinology
Volume24
Issue number8
DOIs
StatePublished - Aug 1 2012

Fingerprint

Olfactory Bulb
Obesity
Diet
High Fat Diet
Aptitude
Weights and Measures
Energy Metabolism
Fasting
Voltage-Gated Potassium Channels
Light
Gene Deletion
Adiposity
Locomotion
Leptin
Energy Intake
Oxygen Consumption
Drinking
Adipose Tissue
Up-Regulation
Glucose

All Science Journal Classification (ASJC) codes

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism
  • Endocrine and Autonomic Systems
  • Cellular and Molecular Neuroscience

Cite this

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abstract = "Gene-targeted deletion of the voltage-gated potassium channel, Kv1.3 (Kv1.3-/-), increases olfactory sensitivity and discriminatory ability, and causes resistance to diet-induced obesity (DIO) in mice. The present study aimed to determine whether the enhanced olfactory ability of the Kv1.3-/- mouse contributes to the resistance to DIO. Kv1.3+/+ and Kv1.3-/- mice were subject to bilateral olfactory bulbectomy (OBX) or sham surgery at 9weeks of age and placed on either a control chow diet or a 32{\%} moderately high-fat diet (MHF). Caloric and water intake, locomotor activity and oxygen consumption were monitored after 5weeks of diet treatment. At the end of 26weeks of diet treatment, fat pad weight and blood chemistry were evaluated. Kv1.3+/+ mice exhibited a significant increase in weight, adiposity, fasting glucose and fasting leptin in response to the MHF-diet, with or without OBX. When treated with a MHF-diet, Kv1.3-/- mice gained significantly less weight than Kv1.3+/+ mice and exhibited a significant increase in light phase metabolism. OBX of Kv1.3-/- mice prevented the resistance to DIO and concomitant up-regulation of light phase metabolism at the same time as decreasing dark phase metabolism and total energy expenditure. These findings suggest that pathways activated in Kv1.3-/- that increased energy expenditure and led to resistance to DIO are olfactory bulb dependent. Thus, these findings add to a growing body of evidence suggesting that the olfactory system can modulate the pathways involved in the regulation of energy balance.",
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Diet-Induced Obesity Resistance of Kv1.3-/- Mice is Olfactory Bulb Dependent. / Tucker, Kristal Raylone; Overton, J. M.; Fadool, D. A.

In: Journal of Neuroendocrinology, Vol. 24, No. 8, 01.08.2012, p. 1087-1095.

Research output: Contribution to journalArticle

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