Targeting skeletal muscle mitochondrial health in obesity

Pileggi, Chantal; Hooks, Breana G.; McPherson, Ruth; Dent, Robert; Harper, Mary‐Ellen

doi:10.1042/cs20210506

Cited by 6 publications

(4 citation statements)

References 385 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…While it is not clear whether the alteration in fiber type distribution in the muscle of obese individuals is a cause or a consequence of obesity [ 11 ], recent studies with human models have reported a reduction of type I fibers in obese individuals. This phenomenon is linked to the metabolic environment associated with obesity, particularly concerning the content and function of mitochondria [ 10 , 11 ].…”

Section: Discussionmentioning

confidence: 99%

“…For instance, reduced activity of citrate synthase, an important enzyme in the mitochondrial energy system, has been reported in subjects affected by obesity and insulin resistance [ 9 ]. Considering the impact of mitochondrial content in oxidative muscle fibers, alterations of the mitochondrial systems have been identified as a factor contributing to the loss of type I fibers in obese individuals [ 10 , 11 , 12 ]. However, whether the alteration in muscle fiber composition is a cause or consequence of obesity remains elusive.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Moderate-Intensity Exercise Enhances Mitochondrial Biogenesis Markers in the Skeletal Muscle of a Mouse Model Affected by Diet-Induced Obesity

Jun,

Knight,

Broderick

et al. 2024

Nutrients

View full text Add to dashboard Cite

Skeletal muscle is composed of bundles of muscle fibers with distinctive characteristics. Oxidative muscle fiber types contain higher mitochondrial content, relying primarily on oxidative phosphorylation for ATP generation. Notably, as a result of obesity, or following prolonged exposure to a high-fat diet, skeletal muscle undergoes a shift in fiber type toward a glycolytic type. Mitochondria are highly dynamic organelles, constantly undergoing mitochondrial biogenesis and dynamic processes. Our study aims to explore the impact of obesity on skeletal muscle mitochondrial biogenesis and dynamics and also ascertain whether the skeletal muscle fiber type shift occurs from the aberrant mitochondrial machinery. Furthermore, we investigated the impact of exercise in preserving the oxidative muscle fiber types despite obesity. Mice were subjected to a normal standard chow and water or high-fat diet with sugar water (HFS) with or without exercise training. After 12 weeks of treatment, the HFS diet resulted in a noteworthy reduction in the markers of mitochondrial content, which was recovered by exercise training. Furthermore, higher mitochondrial biogenesis markers were observed in the exercised group with a subsequent increase in the mitochondrial fission marker. In conclusion, these findings imply a beneficial impact of moderate-intensity exercise on the preservation of oxidative capacity in the muscle of obese mouse models.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Moderate-Intensity Exercise Enhances Mitochondrial Biogenesis Markers in the Skeletal Muscle of a Mouse Model Affected by Diet-Induced Obesity

Jun,

Knight,

Broderick

et al. 2024

Nutrients

View full text Add to dashboard Cite

show abstract

“…Moreover, PGC-1 α overexpression ameliorates angiotensin II-induced hypertension via the regulation of eNOS [ 41 ]. SDH is one of the molecules that are stimulated by PGC-1 α and is an essential component in both the citric acid cycle and the electron transport system in mitochondria, and the elevations of the mitochondrial fraction and oxidative phosphorylation in skeletal muscle are intimately correlated with weight loss [ 42 , 43 ]. In this study, buspirone increased the protein levels of PPAR δ , AMPK, and PGC-1 α in skeletal muscle and abdominal fat tissues from SHRs and elevated the SDH activity in the skeletal muscle.…”

Section: Discussionmentioning

confidence: 99%

Buspirone Induces Weight Loss and Normalization of Blood Pressure via the Stimulation of PPARδ Dependent Energy Producing Pathway in Spontaneously Hypertensive Rats

et al. 2023

View full text Add to dashboard Cite

Introduction. Buspirone, as a partial agonist for a 5-hydroxytryptamine (serotonin) receptor 1A (5-HT1A), has been prescribed as an anxiolytic drug for patients. In addition, the lowering effect of serotonin on blood pressure was reported in hypertensive animal model. We investigated the therapeutic mechanism of buspirone against lipid metabolism disturbed by hypertension of early stage via hypertensive and obese animal model. Methods. The levels of various biomarkers related to lipid metabolism and hypertension were estimated through the measurement of body weight and fat weight, blood analysis, western blotting, immunohistochemistry, and staining methods. Results. The lipid accumulation was lowered in differentiated 3T3-L1 cells by buspirone treatments of 50 and 100 μM compared with untreated differentiated control. Body weight and abdominal fat weight were lowered in spontaneously hypertensive rats (SHRs) administered with buspirone of 10 mg/kg/day for 4 weeks than 8-week untreated group. Triglyceride (TG) level was decreased in SHRs administered with buspirone of 5 and 10 mg/kg/day compared to 8-week untreated group. High-density lipoprotein (HDL)-cholesterol concentration was elevated by buspirone 10 mg/kg/day treatment compared to 8-week untreated group. Blood pressures in SHRs were lowered by buspirone treatments of 5 and 10 mg/kg/day compared with 8-week untreated group. Protein levels for peroxisome proliferator-activated receptor δ (PPARδ), 5 ′ adenosine monophosphate-activated protein kinase (AMPK), and PPARγ coactivator-1 alpha (PGC-1α) were increased both in C2C12 cells treated by buspirone of 100 μM and in SHRs administered by buspirone of 1, 5, and 10 mg/kg/day compared to untreated control cells and 8-week untreated group. Fat cell numbers decreased in 8-week untreated group were increased in SHRs administered by buspirone treats of 1, 5, and 10 mg/kg/day. Protein expression levels for angiotensin II type 1 receptor (AT1R) and vascular cell adhesion molecule 1 (VCAM1) were increased in 8-week untreated group compared to 4-week group, however, they were decreased by buspirone treatments of 1, 5, and 10 mg/kg/day. Conclusion. Buspirone may induce the losses of body weight and abdominal fat weight through the activation of PPARδ dependent catabolic metabolism producing energy, and eventually, the ameliorated lipid metabolism could normalize high blood pressure.

show abstract

“…Increasing evidence suggests that an inability to adapt to metabolic stimuli, such as insulin signaling or fatty acid exposure, may lead to the decrease in muscle oxidative capacity characteristic of obesity [ 67 , 68 , 69 ]. In their study including 28 juvenile Iberian pigs fed either a control or a high-fructose, high-fat (HFF) diet for 10 weeks, H.C. Spooner et al [ 70 ] demonstrated that the HFF diet resulted in decreased IMCL fat content and in the formation of less oxidative skeletal muscle phenotype, reflecting the disturbed ability of skeletal muscles to use lipids as a fuel.…”

Section: Skeletal Muscles In Obesitymentioning

confidence: 99%

Possible Mechanisms Linking Obesity, Steroidogenesis, and Skeletal Muscle Dysfunction

Sheptulina,

Antyukh,

Kiselev

et al. 2023

Life

View full text Add to dashboard Cite

Increasing evidence suggests that skeletal muscles may play a role in the pathogenesis of obesity and associated conditions due to their impact on insulin resistance and systemic inflammation. Skeletal muscles, as well as adipose tissue, are largely recognized as endocrine organs, producing biologically active substances, such as myokines and adipokines. They may have either beneficial or harmful effects on the organism and its functions, acting through the endocrine, paracrine, and autocrine pathways. Moreover, the collocation of adipose tissue and skeletal muscles, i.e., the amount of intramuscular, intermuscular, and visceral adipose depots, may be of major importance for metabolic health. Traditionally, the generalized and progressive loss of skeletal muscle mass and strength or physical function, named sarcopenia, has been thought to be associated with age. That is why most recently published papers are focused on the investigation of the effect of obesity on skeletal muscle function in older adults. However, accumulated data indicate that sarcopenia may arise in individuals with obesity at any age, so it seems important to clarify the possible mechanisms linking obesity and skeletal muscle dysfunction regardless of age. Since steroids, namely, glucocorticoids (GCs) and sex steroids, have a major impact on the amount and function of both adipose tissue and skeletal muscles, and are involved in the pathogenesis of obesity, in this review, we will also discuss the role of steroids in the interaction of these two metabolically active tissues in the course of obesity.

show abstract

Targeting skeletal muscle mitochondrial health in obesity

Cited by 6 publications

References 385 publications

Moderate-Intensity Exercise Enhances Mitochondrial Biogenesis Markers in the Skeletal Muscle of a Mouse Model Affected by Diet-Induced Obesity

Moderate-Intensity Exercise Enhances Mitochondrial Biogenesis Markers in the Skeletal Muscle of a Mouse Model Affected by Diet-Induced Obesity

Buspirone Induces Weight Loss and Normalization of Blood Pressure via the Stimulation of PPARδ Dependent Energy Producing Pathway in Spontaneously Hypertensive Rats

Possible Mechanisms Linking Obesity, Steroidogenesis, and Skeletal Muscle Dysfunction

Contact Info

Product

Resources

About