BST Stimulation Induces Atrophy and Changes in Aerobic Energy Metabolism in Rat Skeletal Muscles—The Biphasic Action of Endogenous Glucocorticoids

Abstract

(1) The primary involvement in stress-induced disturbances in skeletal muscles is assigned to the release of glucocorticoids (GCs). The current study aims to investigate the impact of the biphasic action of the chronic stress response (CSR) induced by the electrical stimulation of the bed nucleus of the stria terminalis (BST) effects on muscle atrophy and aerobic energy metabolism in soleus (SOL) and extensor digitorum longus (EDL) muscles. (2) Male Wistar rats (n = 17) were used. The rats were divided randomly into three groups: the BST two weeks (ST2), four weeks (ST4), and the sham (SHM) electrically stimulated group. The plasma corticosterone (CORT) and irisin concentration were measured. Glucocorticoid and mineralocorticoid receptors (GR and MR), 11β-hydroxysteroid dehydrogenase type 1 and 2 (HSD11B1 and HSD11B2), atrogin-1, and insulin-like growth factor-1 (IGF-1) level were determined in SOL and EDL muscles. Citrate synthase (CS) activity was measured in both muscles. (3) We found elevated plasma concentration of CORT and irisin, raised the level of GR in SOL muscle, and the higher level of MR in both muscles in the ST4 group. The level of HSD11B1 was also higher in the ST4 group compared to the SHM group. Moreover, we observed increased activity of CS in SOL. (4) We suggest that biphasic action of the glucocorticoid induced by the CSR occurs and causes dysregulation of proteins involved in muscle atrophy and aerobic energy metabolism. Our findings potentially contribute to a better understanding of the mechanisms by which GCs and the CSR may regulate muscle atrophy and energy preservation of the red muscle.

The Positive Impact of Vitamin D on Glucocorticoid-Dependent Skeletal Muscle Atrophy

“…Interestingly, in an experiment conducted by Nishida and coworkers, no changes in SOL and EDL muscle mass were observed even during DEX treatment (5 days, dose 600 µg/kg) [ 29 ]. Our recent work [ 25 , 26 ] showed that the CSR and increased CORT level do not have to accompany changes in body and muscle weight (data not shown); nevertheless, an increased level of atrogin-1 was observed. Furthermore, we assume that to explain this phenomenon in these particular conditions, it is necessary to consider intramuscular fat stores in rats from groups exposed to the chronic cold water immersion [ 30 , 31 ].…”

“…Our results indicate that DEX-induced muscle loss is abolished in rats supplemented with vitamin D 3 but only in SOL muscle. Based on previously published data [ 25 ], we assumed that a similar effect should be observed in the CSR conditions. However, instead of HPA axis activation and CORT surge, we did not note any changes in the body and muscle weight.…”

Exercise Training Enhances Myocardial Mitophagy and Improves Cardiac Function via Irisin/FNDC5-PINK1/Parkin Pathway in MI Mice

“…Irisin is a novel myokine and adipokine in various body tissues, including skeletal muscle, myocardium and adipose tissue, which can be effectively induced by several kinds of stimulation such as exercise training [ 9 , 14 ]. Some research showed that many different types of exercise can significantly increase the myocardial Irisin expression [ 26 , 27 , 28 , 29 ]. This study found that the expression of myocardium irisin/FNDC5 was significantly up-regulated in different exercise intervention and skeletal muscle electrical stimulation models, among which the resistance exercise had the significant effects.…”

The ‘Jekyll and Hyde’ of Gluconeogenesis: Early Life Adversity, Later Life Stress, and Metabolic Disturbances

“…Moreover, GC signalling through the GR is a trigger of insulin resistance in muscles, supressing GLUT 4 translocation to the cell surface, as well as downregulating glycogen synthesis [ 66 ]. It would appear that the GR interacts directly with both the insulin and insulin-like growth factor 1 (IGF-1) pathways [ 67 ], although detailed mechanistic studies of GC effects in muscle carbohydrate metabolism are severely lacking [ 3 ].…”