Abstract Title

Genetically Altered Endocannabinoid Receptors: Relationship to Non-Shivering Muscle Thermogenesis

Abstract

Multiple regulatory pathways contribute to obesity and energy expenditure, including thermogenesis. Our research program has that muscle thermogenesis is rapidly induced in rats and mice after exposure to predator odor. Of the many systems contributing to energy balance, we focus on the endocannabinoid system and CB1 receptors, which regulate appetite and thermogenesis. Because endocannabinoids promote weight gain, we hypothesized that mice deficient in CB1 receptor would show an increase in muscle thermogenesis. To test this hypothesis, temperature transponders were implanted into mouse gastrocnemius muscle of three CB1 genotypes (wild-type, heterozygote, knockout); mice were habituated to the experimental environment, and a Biomedical Data System Reader recorded muscle temperatures. After measuring initial baseline temperature in the housing facility, mice were moved to a testing room, all enrichments were removed from the cages, and cages were placed onto elevated stands. Then, a microisolator lid and sheet were placed over the cages and mice were acclimated for 3 hours. A second baseline was recorded before whiffle balls containing predator or control towels were placed into the cages. Subsequently, temperatures were recorded over 4 hours. Against expectations, I found significant suppression of thermogenic induction in mice with genetically altered CB1 receptors relative to wild-type controls. These results led us to develop an alternative hypothesis wherein CB1 receptor suppresses baseline thermogenesis; suppression is relieved upon predator threat. Further studies will test the ability of CB1 receptor agonists and antagonists to alter predator-odor induced thermogenesis, and to replicate the suppression of thermogenesis in a larger group.

Modified Abstract

Inducing thermogenesis can be used to combat weight gain. Energy expenditure is regulated by multiple pathways. One of these is the endocannabinoid system. This includes the primary brain receptor, CB1 receptor. I sought to determine if this receptor was part of the brain pathway regulating the induction of muscle thermogenesis. To do this, I used genetically altered CB1 mice. We have found that a reliable inducer of thermogenesis in mice is the odor of a predator. Temperatures were measured using transponders implanted into the muscle and a transponder reader. I found that predator odor induced muscle thermogenesis in wild-type mice but not in CB1 deficient mice. This supports the hypothesis that CB1 plays a role in suppressing baseline thermogenesis rather than in inhibiting its induction.

Research Category

Biomedical Sciences

Primary Author's Major

Biology

Mentor #1 Information

Dr. Colleen

Novak

Presentation Format

Poster

Start Date

April 2019

Research Area

Musculoskeletal, Neural, and Ocular Physiology | Neuroscience and Neurobiology | Physiology

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Apr 9th, 1:00 PM

Genetically Altered Endocannabinoid Receptors: Relationship to Non-Shivering Muscle Thermogenesis

Multiple regulatory pathways contribute to obesity and energy expenditure, including thermogenesis. Our research program has that muscle thermogenesis is rapidly induced in rats and mice after exposure to predator odor. Of the many systems contributing to energy balance, we focus on the endocannabinoid system and CB1 receptors, which regulate appetite and thermogenesis. Because endocannabinoids promote weight gain, we hypothesized that mice deficient in CB1 receptor would show an increase in muscle thermogenesis. To test this hypothesis, temperature transponders were implanted into mouse gastrocnemius muscle of three CB1 genotypes (wild-type, heterozygote, knockout); mice were habituated to the experimental environment, and a Biomedical Data System Reader recorded muscle temperatures. After measuring initial baseline temperature in the housing facility, mice were moved to a testing room, all enrichments were removed from the cages, and cages were placed onto elevated stands. Then, a microisolator lid and sheet were placed over the cages and mice were acclimated for 3 hours. A second baseline was recorded before whiffle balls containing predator or control towels were placed into the cages. Subsequently, temperatures were recorded over 4 hours. Against expectations, I found significant suppression of thermogenic induction in mice with genetically altered CB1 receptors relative to wild-type controls. These results led us to develop an alternative hypothesis wherein CB1 receptor suppresses baseline thermogenesis; suppression is relieved upon predator threat. Further studies will test the ability of CB1 receptor agonists and antagonists to alter predator-odor induced thermogenesis, and to replicate the suppression of thermogenesis in a larger group.