Role of UCP homologues in skeletal muscles and brown adipose tissue: mediators of thermogenesis or regulators of lipids as fuel substrate?

1998 ◽  
Vol 12 (9) ◽  
pp. 715-724 ◽  
Author(s):  
S. Samec ◽  
J. Seydoux ◽  
A. G. Dulloo
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Skeletal Muscles ◽  
Brown Adipose

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.

142-OR: Unique Role of the a4 Component for S6-Kinase Activity in Metabolic Regulation and Anti-apoptotic Effect in Brown Adipose Tissue

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 142-OR
Author(s):  
MASAJI SAKAGUCHI ◽  
SHOTA OKAGAWA ◽  
SAYAKA KITANO ◽  
TATSUYA KONDO ◽  
EIICHI ARAKI
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Metabolic Regulation ◽  
Kinase Activity ◽  
S6 Kinase ◽  
Unique Role ◽  
Brown Adipose ◽  
Apoptotic Effect

The endocrine role of brown adipose tissue: An update on actors and actions

2021 ◽  
Author(s):  
Aleix Gavaldà-Navarro ◽  
Joan Villarroya ◽  
Rubén Cereijo ◽  
Marta Giralt ◽  
Francesc Villarroya
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Brown Adipose

scholarly journals The Role of AMPK Signaling in Brown Adipose Tissue Activation

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1122
Author(s):  
Jamie I. van der van der Vaart ◽  
Mariëtte R. Boon ◽  
Riekelt H. Houtkooper
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Whole Body ◽  
Ampk Signaling ◽  
Mitochondrial Homeostasis ◽  
Brown Adipose ◽  
Metabolic Stresses ◽  
Amp Activated Protein Kinase ◽  
Body Energy

Obesity is becoming a pandemic, and its prevalence is still increasing. Considering that obesity increases the risk of developing cardiometabolic diseases, research efforts are focusing on new ways to combat obesity. Brown adipose tissue (BAT) has emerged as a possible target to achieve this for its functional role in energy expenditure by means of increasing thermogenesis. An important metabolic sensor and regulator of whole-body energy balance is AMP-activated protein kinase (AMPK), and its role in energy metabolism is evident. This review highlights the mechanisms of BAT activation and investigates how AMPK can be used as a target for BAT activation. We review compounds and other factors that are able to activate AMPK and further discuss the therapeutic use of AMPK in BAT activation. Extensive research shows that AMPK can be activated by a number of different kinases, such as LKB1, CaMKK, but also small molecules, hormones, and metabolic stresses. AMPK is able to activate BAT by inducing adipogenesis, maintaining mitochondrial homeostasis and inducing browning in white adipose tissue. We conclude that, despite encouraging results, many uncertainties should be clarified before AMPK can be posed as a target for anti-obesity treatment via BAT activation.

scholarly journals The role of active brown adipose tissue (aBAT) in lipid metabolism in healthy Chinese adults

2016 ◽  
Vol 15 (1) ◽  
Author(s):  
Xiaoliang Shao ◽  
Wei Yang ◽  
Xiaonan Shao ◽  
Chun Qiu ◽  
Xiaosong Wang ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Brown Adipose Tissue ◽  
Chinese Adults ◽  
Brown Adipose ◽  
Healthy Chinese

Neural influences on trophic changes in brown adipose tissue during cold acclimation

1988 ◽  
Vol 255 (6) ◽  
pp. R874-R881 ◽  
Author(s):  
I. R. Park ◽  
J. Himms-Hagen
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Acclimation ◽  
Elevated Level ◽  
Uncoupling Protein ◽  
Sympathetic Innervation ◽  
Intact Tissue ◽  
Brown Adipose ◽  
Neural Influences

We studied the role of the sympathetic innervation in development and maintenance of increased levels of uncoupling protein (UCP) and of thyroxine 5'-deiodinase (TD) during cold-induced growth of brown adipose tissue (BAT). Interscapular BAT was unilaterally (and in some experiments, bilaterally) denervated either before acclimation to cold (4 degrees C) for 12 days or after 14 days of a total 28-day period of acclimation to cold. BAT norepinephrine was reduced to 3-7% of the normal level in denervated BAT for up to 26 days. Denervation slowed, but did not prevent, cold-induced increases in total protein, in mitochondrial GDP binding, and in mitochondrial UCP concentration, which all reached 50% or more of the elevated level in intact tissue. In contrast, TD activity did not exceed 10% of the elevated level in intact tissue at any time. Denervation after cold acclimation resulted in a very rapid loss of TD activity, a slower and selective loss (after a lag of 1 day) of UCP, and a much slower loss of tissue protein. We conclude that the sympathetic innervation is required for an optimal trophic response of BAT to cold acclimation and for maintenance in the hypertrophied state but that other factors are also involved. Induction and maintenance of TD in BAT does need the sympathetic innervation.

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