scholarly journals Management of Oxidative Stress: Crosstalk Between Brown/Beige Adipose Tissues and Skeletal Muscles

2021 ◽  
Vol 12 ◽  
Author(s):  
Ruping Pan ◽  
Yong Chen
Keyword(s):  
Oxidative Stress ◽  
Adipose Tissue ◽  
Skeletal Muscles ◽  
Strenuous Exercise ◽  
Pathological State ◽  
Adipose Tissues ◽  
Brown Adipose ◽  
Exercise Induced ◽  
Shivering Thermogenesis

Exercise plays an important role in the physiology, often depending on its intensity, duration, and frequency. It increases the production of reactive oxygen species (ROS). Meanwhile, it also increases antioxidant enzymes involved in the oxidative damage defense. Prolonged, acute, or strenuous exercise often leads to an increased radical production and a subsequent oxidative stress in the skeletal muscles, while chronic regular or moderate exercise results in a decrease in oxidative stress. Notably, under pathological state, such as obesity, aging, etc., ROS levels could be elevated in humans, which could be attenuated by proper exercise. Significantly, exercise stimulates the development of beige adipose tissue and potentially influence the function of brown adipose tissue (BAT), which is known to be conducive to a metabolic balance through non-shivering thermogenesis (NST) and may protect from oxidative stress. Exercise-related balance of the ROS levels is associated with a healthy metabolism in humans. In this review, we summarize the integrated effects of exercise on oxidative metabolism, and especially focus on the role of brown and beige adipose tissues in this process, providing more evidence and knowledge for a better management of exercise-induced oxidative stress.

scholarly journals Role of Ubiquilins for Brown Adipocyte Proteostasis and Thermogenesis

2021 ◽  
Vol 12 ◽  
Author(s):  
Carolin Muley ◽  
Stefan Kotschi ◽  
Alexander Bartelt
Keyword(s):  
Gene Expression ◽  
Quality Control ◽  
Adipose Tissue ◽  
Cold Exposure ◽  
Protein Quality ◽  
Brown Adipocyte ◽  
Brown Adipocytes ◽  
Brown Adipose ◽  
Shivering Thermogenesis

The acclimatization of brown adipose tissue (BAT) to sustained cold exposure requires an adaptive increase in proteasomal protein quality control. Ubiquilins represent a recently identified family of shuttle proteins with versatile functions in protein degradation, such as facilitating substrate targeting and proteasomal degradation. However, whether ubiquilins participate in brown adipocyte function has not been investigated so far. Here, we determine the role of ubiquilins for proteostasis and non-shivering thermogenesis in brown adipocytes. We found that Ubqln1, 2 and 4 are highly expressed in BAT and their expression was induced by cold and proteasomal inhibition. Surprisingly, silencing of ubiquilin gene expression (one or multiple in combinations) did not lead to aggravated ER stress or inflammation. Moreover, ubiquitin level and proteasomal activity under basal conditions were not impacted by loss of ubiquilins. Also, non-shivering thermogenesis measured by norepinephrine-induced respiration remained intact after loss of ubiquilins. In conclusion, ubiquilin proteins are highly abundant in BAT and regulated by cold, but they are dispensable for brown adipocyte proteostasis and thermogenesis.

scholarly journals Effect of Quercetin on Non-shivering Thermogenesis and Intestinal Microbial Populations (P06-037-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Dammah Otieno ◽  
Ya Pei ◽  
Inah Gu ◽  
Sun-Ok Lee ◽  
Hye Won Kang
Keyword(s):  
Adipose Tissue ◽  
Energy Metabolism ◽  
Relative Abundance ◽  
Intestinal Microbiome ◽  
Microbial Populations ◽  
Fibroblast Growth Factor 21 ◽  
Adipose Tissues ◽  
Brown Adipose ◽  
Beige Adipocytes ◽  
Shivering Thermogenesis

Abstract Objectives Activation of non-shivering thermogenesis in adipose tissues and alteration in intestinal microbiome have been linked with improved obese condition. With emerging evidences of dietary compounds to prevent obesity, the objective of this study was to examine whether quercetin activates non-shivering thermogenesis in adipose tissues and influences intestinal microbiome, which eventually improves obese condition. Methods Four-week-old C57BL/6 male mice were fed either a low-fat diet (LFD) or a high-fat diet (HFD) with or without 1% quercetin (Q) for 16 weeks. On the completion of the feeding study, brown adipose tissue (BAT), white adipose tissue (WAT), and cecum were collected. Total RNA was extracted from BAT and WAT, and then cDNA was synthesized. The expression of genes that are involved in the regulation of non-shivering thermogenesis such as uncoupling protein 1 (ucp1), cell death-inducing DFFA-like effector A (cidea), peroxisome proliferator-activated receptor gamma (pparγ), pparγ-coactivator 1 alpha (pgc1α), fibroblast growth factor 21 (fgf21), positive regulatory domain containing 16 (prdm16), and T-box protein 1 (tbx1) were determined by a real-time PCR. The expression of the proteins such as UCP1 and AMP-activated protein kinase (AMPK) was assessed by western blot analysis. Microbial populations in cecum were analyzed via the Illumnia MiSeq sequencing platform and QIIME (Quantitative Insights Into Microbial Ecology) Software. Results Mice fed HFDQ showed reduced body weight and retroperitoneal (R) WAT weight compared to mice fed HFD. Quercetin supplementation increased the expression of ucp1, prdm16, pgc1α, cidea, and tbx1 genes in BAT and RWAT of mice fed HFD. The expression of UCP1 protein and phosphorylation of AMPK were increased. However, browning effect was not observed in other WATs. Mice fed LFDQ and HFDQ exhibited higher relative abundance of Bacteroidetes than mice fed LFD and HFD whereas the relative abundance of Firmicutes was decreased. Conclusions Quercetin may be a potential dietary compound that increases energy metabolism by activating BAT and attracting beige adipocytes in RWAT. In addition, quercetin-induced energy metabolism may have a correlation with changes of microbial populations in intestine. Funding Sources The work was supported by USDA.

scholarly journals The Role of Adipose Tissue Mitochondria: Regulation of Mitochondrial Function for the Treatment of Metabolic Diseases

2019 ◽  
Vol 20 (19) ◽  
pp. 4924 ◽  
Author(s):  
Lee ◽  
Park ◽  
Oh ◽  
Lee ◽  
Kim ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Mitochondrial Function ◽  
Energy Homeostasis ◽  
Metabolic Diseases ◽  
Oxidative Capacity ◽  
Adipose Tissues ◽  
Adaptive Thermogenesis ◽  
Brown Adipose

: Mitochondria play a key role in maintaining energy homeostasis in metabolic tissues, including adipose tissues. The two main types of adipose tissues are the white adipose tissue (WAT) and the brown adipose tissue (BAT). WAT primarily stores excess energy, whereas BAT is predominantly responsible for energy expenditure by non-shivering thermogenesis through the mitochondria. WAT in response to appropriate stimuli such as cold exposure and β-adrenergic agonist undergoes browning wherein it acts as BAT, which is characterized by the presence of a higher number of mitochondria. Mitochondrial dysfunction in adipocytes has been reported to have strong correlation with metabolic diseases, including obesity and type 2 diabetes. Dysfunction of mitochondria results in detrimental effects on adipocyte differentiation, lipid metabolism, insulin sensitivity, oxidative capacity, and thermogenesis, which consequently lead to metabolic diseases. Recent studies have shown that mitochondrial function can be improved by using thiazolidinedione, mitochondria-targeted antioxidants, and dietary natural compounds; by performing exercise; and by controlling caloric restriction, thereby maintaining the metabolic homeostasis by inducing adaptive thermogenesis of BAT and browning of WAT. In this review, we focus on and summarize the molecular regulation involved in the improvement of mitochondrial function in adipose tissues so that strategies can be developed to treat metabolic diseases.

scholarly journals The Interplay Between Adipose Tissue and Vasculature: Role of Oxidative Stress in Obesity

2021 ◽  
Vol 8 ◽  
Author(s):  
Yawen Zhou ◽  
Huige Li ◽  
Ning Xia
Keyword(s):  
Oxidative Stress ◽  
Adipose Tissue ◽  
Cardiovascular Health ◽  
Vascular Endothelial ◽  
Adipose Tissues ◽  
Pathophysiological Role ◽  
The Impact ◽  
Vascular Oxidative Stress ◽  
The Relationship

Cardiovascular diseases (CVDs) rank the leading cause of morbidity and mortality globally. Obesity and its related metabolic syndrome are well-established risk factors for CVDs. Therefore, understanding the pathophysiological role of adipose tissues is of great importance in maintaining cardiovascular health. Oxidative stress, characterized by excessive formation of reactive oxygen species, is a common cellular stress shared by obesity and CVDs. While plenty of literatures have illustrated the vascular oxidative stress, very few have discussed the impact of oxidative stress in adipose tissues. Adipose tissues can communicate with vascular systems, in an endocrine and paracrine manner, through secreting several adipocytokines, which is largely dysregulated in obesity. The aim of this review is to summarize current understanding of the relationship between oxidative stress in obesity and vascular endothelial dysfunction. In this review, we briefly describe the possible causes of oxidative stress in obesity, and the impact of obesity-induced oxidative stress on adipose tissue function. We also summarize the crosstalk between adipose tissue and vasculature mediated by adipocytokines in vascular oxidative stress. In addition, we highlight the potential target mediating adipose tissue oxidative stress.

Stimulatory effects of cold exposure and cold acclimation on glucose uptake in rat peripheral tissues

1990 ◽  
Vol 259 (5) ◽  
pp. R1043-R1049 ◽  
Author(s):  
A. L. Vallerand ◽  
F. Perusse ◽  
L. J. Bukowiecki
Keyword(s):  
Adipose Tissue ◽  
Glucose Uptake ◽  
Cold Acclimation ◽  
Cold Exposure ◽  
Skeletal Muscles ◽  
Contractile Activity ◽  
Peripheral Tissues ◽  
Brown Adipose ◽  
Shivering Thermogenesis ◽  
Stimulation Of

The effects of cold exposure on the net rates of 2-[3H]deoxy-D-glucose uptake (Ki) in rat peripheral tissues were investigated comparatively in warm- and cold-acclimated animals to determine whether cold acclimation induces regulatory alterations in glucose metabolism. Acute exposure of warm-acclimated (25 degrees C) rats to cold (48 h at 5 degrees C) markedly increased the Ki values in red and white skeletal muscles (2-5 times), in the heart (8 times), in several white adipose tissue (WAT) depots (4-20 times), and in brown adipose tissue (BAT) (110 times). After cold acclimation (3 wk at 5 degrees C), the Ki values further increased in the heart (15 times) and WAT (up to 29 times) but decreased in BAT (36 times). Remarkably, glucose uptake was still increased in muscles of cold-exposed/cold-acclimated animals (that do not shiver), demonstrating that enhanced glucose uptake may occur in muscles in the absence of shivering thermogenesis (or contractile activity). When cold-acclimated rats were returned to the warm for 18 h, the Ki values of all tissues, except WAT, returned to control levels. Cold exposure synergistically potentiated the stimulation of tissue glucose uptake induced by a maximal effective dose of insulin (0.5 U/kg iv) in warm- as well as in cold-acclimated animals.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Increased Reliance on Muscle-based Thermogenesis upon Acute Minimization of Brown Adipose Tissue Function

2016 ◽  
Vol 291 (33) ◽  
pp. 17247-17257 ◽  
Author(s):  
Naresh C. Bal ◽  
Santosh K. Maurya ◽  
Sushant Singh ◽  
Xander H. T. Wehrens ◽  
Muthu Periasamy
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Skeletal Muscles ◽  
Dominant Role ◽  
Major Site ◽  
Bat Activity ◽  
Brown Adipose ◽  
A Site

Skeletal muscle has been suggested as a site of nonshivering thermogenesis (NST) besides brown adipose tissue (BAT). Studies in birds, which do not contain BAT, have demonstrated the importance of skeletal muscle-based NST. However, muscle-based NST in mammals remains poorly characterized. We recently reported that sarco/endoplasmic reticulum Ca2+ cycling and that its regulation by SLN can be the basis for muscle NST. Because of the dominant role of BAT-mediated thermogenesis in rodents, the role of muscle-based NST is less obvious. In this study, we investigated whether muscle will become an important site of NST when BAT function is conditionally minimized in mice. We surgically removed interscapular BAT (iBAT, which constitutes ∼70% of total BAT) and exposed the mice to prolonged cold (4 °C) for 9 days. The iBAT-ablated mice were able to maintain optimal body temperature (∼35–37 °C) during the entire period of cold exposure. After 4 days in the cold, both sham controls and iBAT-ablated mice stopped shivering and resumed routine physical activity, indicating that they are cold-adapted. The iBAT-ablated mice showed higher oxygen consumption and decreased body weight and fat mass, suggesting an increased energy cost of cold adaptation. The skeletal muscles in these mice underwent extensive remodeling of both the sarcoplasmic reticulum and mitochondria, including alteration in the expression of key components of Ca2+ handling and mitochondrial metabolism. These changes, along with increased sarcolipin expression, provide evidence for the recruitment of NST in skeletal muscle. These studies collectively suggest that skeletal muscle becomes the major site of NST when BAT activity is minimized.

scholarly journals Differential Role of Adipose Tissues in Obesity and Related Metabolic and Vascular Complications

2016 ◽  
Vol 2016 ◽  
pp. 1-15 ◽  
Author(s):  
Almudena Gómez-Hernández ◽  
Nuria Beneit ◽  
Sabela Díaz-Castroverde ◽  
Óscar Escribano
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Vascular Complications ◽  
New Drugs ◽  
Adipose Tissues ◽  
Brown Adipose ◽  
Brown Adipose Tissue Activity ◽  
Atherosclerotic Process ◽  
New Treatments

This review focuses on the contribution of white, brown, and perivascular adipose tissues to the pathophysiology of obesity and its associated metabolic and vascular complications. Weight gain in obesity generates excess of fat, usually visceral fat, and activates the inflammatory response in the adipocytes and then in other tissues such as liver. Therefore, low systemic inflammation responsible for insulin resistance contributes to atherosclerotic process. Furthermore, an inverse relationship between body mass index and brown adipose tissue activity has been described. For these reasons, in recent years, in order to combat obesity and its related complications, as a complement to conventional treatments, a new insight is focusing on the role of the thermogenic function of brown and perivascular adipose tissues as a promising therapy in humans. These lines of knowledge are focused on the design of new drugs, or other approaches, in order to increase the mass and/or activity of brown adipose tissue or the browning process of beige cells from white adipose tissue. These new treatments may contribute not only to reduce obesity but also to prevent highly prevalent complications such as type 2 diabetes and other vascular alterations, such as hypertension or atherosclerosis.

scholarly journals Orexin modulates brown adipose tissue thermogenesis

2012 ◽  
Vol 3 (4) ◽  
pp. 381-386 ◽  
Author(s):  
Christopher J. Madden ◽  
Domenico Tupone ◽  
Shaun F. Morrison
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Energy Homeostasis ◽  
Pathological Conditions ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis ◽  
The Central Nervous System ◽  
Conceptual Overview ◽  
Shivering Thermogenesis

AbstractNon-shivering thermogenesis in brown adipose tissue (BAT) plays an important role in thermoregulation. In addition, activations of BAT have important implications for energy homeostasis due to the metabolic consumption of energy reserves entailed in the production of heat in this tissue. In this conceptual overview, we describe the role of orexins/hypocretins within the central nervous system in the modulation of thermogenesis in BAT under several physiological conditions. Within this framework, we consider potential neural mechanisms underlying the pathological conditions associated with the absence of the central orexinergic modulation of BAT thermogenesis and energy expenditure. Overall, the experimental basis for our understanding of the role of central orexin in regulating body temperature and energy homeostasis provides an illustrative example that highlights several general principles and caveats that should help guide future investigations of the neurochemical regulation of thermogenesis and metabolism.

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