Interactive Effects of Zinc and Zilpaterol Hydrochloride on Bovine &amp;lt;i&amp;gt;β&amp;lt;/i&amp;gt;-Adrenergic Receptors

J E Hergenreder,B J Johnson,A D Hosford,M Branine,T L Harris,J O Baggerman

doi:10.4236/ojas.2020.103025

Abstract

The objective of this study was to determine if the addition of zinc (Zn) in combination with zilpaterol HCL (ZH) affected the interaction of ZH with the beta2-adrenergic receptor (β-AR) by altering cAMP production, gene expression, and protein abundance in cultured skeletal muscle cells. Cultures of muscle bovine satellite cells were established and treated at 120 h with: 1) 0 μM Zn/zilpaterol hydrochloride (ZH; CON); 2) 0 μM Zn/10 μM ZH (ZH); 3) 1 μM Zn from Zn chloride/0 μM ZH (Zn); 4) 1 μM Zn from Zn chloride/10 μM ZH (ZN/ZH) in differentiation media for an additional 0, 6, 24, 48 and 96 h. Protein and mRNA were isolated and quantified at 24 and 96 h, and cAMP was measured at 0, 6, 24, 48 and 96 h. At 0, 24, 48 and 96 h, no differences (P > 0.05) were detected in cAMP production. At 6 h, Zn cells had the greatest concentration of cAMP (P P > 0.05) were detected in mRNA abundance at 24 h. At 96 h, 0 μM Zn/10 μM ZH cells had an increased abundance of myosin heavy chain (MHC)-I mRNA (P P P P > 0.05) were detected in the protein abundance of β1AR and the β2AR. These results indicated Zn and ZH in combination did not have an additive effect on β2-AR function as indicated by cAMP concentrations.

Highlights

The objective of this study was to determine if the addition of zinc (Zn) in combination with zilpaterol HCL (ZH) affected the interaction of Zilpaterol HCl (ZH) with the beta2-adrenergic receptor (β-AR) by altering cyclic adenosine monophosphate (cAMP) production, gene expression, and protein abundance in cultured skeletal muscle cells
No differences (P > 0.05) were detected in the protein abundance of β1AR and the β2AR. These results indicated Zn and ZH in combination did not have an additive effect on β2-AR function as indicated by cAMP concentrations
This is in contrast to that reported by [16], who reported no difference in cAMP concentration at 6 h between bovine satellite cells treated with Zn and ractopamine HCl (RH)

Summary

Introduction

Beta-adrenergic agonists have been reported to increase lipolysis and decrease lipogenesis in adipose tissue [1] [2] [3]. These β-AA work through an interaction with the beta-adrenergic receptors (β-AR) [4] [5]. Overstimulation of the β-ARs by β-AA has been reported to result in receptor desensitization [6] [7]. Receptor desensitization results in a down regulation of adenylate cyclase catalytic activity resulting in a reduction of cAMP synthesis [8]. When the β-ARs become desensitized, they are sequestered within an intracellular vesicle, losing the ability to induce signal transduction [6] [7]

Objectives

Methods

Results