Abstract Title

Central melanocortin receptor-induced skeletal muscle thermogenesis: Effect of inhibition of beta-adrenergic receptors

Abstract

One strategy to counter obesity focuses on increasing kilocalories burned through heat production, or thermogenesis. Compared to white and brown adipose tissue thermogenesis, there has been relatively little effort to exploit thermogenic mechanisms in skeletal muscle. We previously showed muscle thermogenic induction by injecting the mixed melanocortin agonist, Melanotan II (MTII), into the ventromedial hypothalamus (VMH). MTII also activates sympathetic nervous system (SNS) outflow to skeletal muscle which leads us to hypothesize that the centrally induced muscle thermogenesis was mediated by SNS activation of skeletal muscle thermogenesis via beta-adrenergic receptor activation. Using the peripherally acting mixed beta antagonist, nadolol, we investigated the contribution of beta 1 and 2 receptors to muscle thermogenesis. Stereotaxic surgeries were performed on adult male rats (n=12) implanting a guide cannulae aimed at the VMH. Temperature transponders were also implanted in both hind limb gastrocnemius muscles. Rats were given intra-VMH microinjections of MTII or its vehicle (artificial cerebrospinal fluid) in combination with peripheral injections of either nadolol or its vehicle; muscle temperatures were measured before injection and each 30-minute interval after injection for 4 hours. Activation of brain melanocortin receptors significantly increased muscle temperature over 4 hours. Surprisingly, blocking beta-adrenergic receptors did not significantly change MTII-induced muscle thermogenesis. This contrasts with evidence from our laboratory that blocking peripheral beta adrenergic receptors diminishes the induction of muscle thermogenesis in alternative settings. The differential involvement of beta adrenergic receptors may help explain the distinct pattern and magnitude of muscle thermogenesis in other contexts.

Modified Abstract

One strategy to counter obesity focuses on increasing kilocalories burned through skeletal muscle thermogenesis. We previously showed that injecting the mixed melanocortin agonist, Melanotan II (MTII), into the ventromedial hypothalamus (VMH) activated both muscle thermogenesis and sympathetic nervous system (SNS) outflow to skeletal muscle. Using the peripherally acting mixed beta antagonist, nadolol, we investigated the contribution of beta-adrenergic receptors to muscle thermogenesis. Activation of brain melanocortin receptors significantly increased muscle temperature over 4 hours. Surprisingly, blocking beta-adrenergic receptors with the antagonist nadolol did not significantly change MTII-induced muscle thermogenesis. This contrasts with evidence from our laboratory that nadolol diminishes muscle thermogenesis induced by predator odor, suggesting differential involvement of beta-adrenergic receptors by other stimuli that activate muscle thermogenesis.

Research Category

Biology/Ecology

Primary Author's Major

Zoology

Mentor #1 Information

Dr. Colleen M. Novak

Mentor #2 Information

Erin E. Gorrell

Presentation Format

Poster

Start Date

5-4-2018 1:00 PM

Research Area

Other Neuroscience and Neurobiology

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Apr 5th, 1:00 PM

Central melanocortin receptor-induced skeletal muscle thermogenesis: Effect of inhibition of beta-adrenergic receptors

One strategy to counter obesity focuses on increasing kilocalories burned through heat production, or thermogenesis. Compared to white and brown adipose tissue thermogenesis, there has been relatively little effort to exploit thermogenic mechanisms in skeletal muscle. We previously showed muscle thermogenic induction by injecting the mixed melanocortin agonist, Melanotan II (MTII), into the ventromedial hypothalamus (VMH). MTII also activates sympathetic nervous system (SNS) outflow to skeletal muscle which leads us to hypothesize that the centrally induced muscle thermogenesis was mediated by SNS activation of skeletal muscle thermogenesis via beta-adrenergic receptor activation. Using the peripherally acting mixed beta antagonist, nadolol, we investigated the contribution of beta 1 and 2 receptors to muscle thermogenesis. Stereotaxic surgeries were performed on adult male rats (n=12) implanting a guide cannulae aimed at the VMH. Temperature transponders were also implanted in both hind limb gastrocnemius muscles. Rats were given intra-VMH microinjections of MTII or its vehicle (artificial cerebrospinal fluid) in combination with peripheral injections of either nadolol or its vehicle; muscle temperatures were measured before injection and each 30-minute interval after injection for 4 hours. Activation of brain melanocortin receptors significantly increased muscle temperature over 4 hours. Surprisingly, blocking beta-adrenergic receptors did not significantly change MTII-induced muscle thermogenesis. This contrasts with evidence from our laboratory that blocking peripheral beta adrenergic receptors diminishes the induction of muscle thermogenesis in alternative settings. The differential involvement of beta adrenergic receptors may help explain the distinct pattern and magnitude of muscle thermogenesis in other contexts.