scholarly journals Role of AMPK in mammals reproduction: Specific controls and whole-body energy sensing

2019 ◽  
Vol 342 (1-2) ◽  
pp. 1-6 ◽  
Author(s):  
Thi Mong Diep Nguyen
Keyword(s):  
Whole Body ◽  
Energy Sensing ◽  
Body Energy

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 Uncoupling of sarcoendoplasmic reticulum calcium ATPase pump activity by sarcolipin as the basis for muscle non-shivering thermogenesis

2020 ◽  
Vol 375 (1793) ◽  
pp. 20190135 ◽  
Author(s):  
Naresh C. Bal ◽  
Muthu Periasamy
Keyword(s):  
Energy Homeostasis ◽  
Atp Hydrolysis ◽  
Calcium Atpase ◽  
Whole Body ◽  
Signalling Molecule ◽  
Brown Adipose ◽  
Pump Activity ◽  
Body Energy ◽  
Shivering Thermogenesis

Thermogenesis in endotherms relies on both shivering and non-shivering thermogenesis (NST). The role of brown adipose tissue (BAT) in NST is well recognized, but the role of muscle-based NST has been contested. However, recent studies have provided substantial evidence for the importance of muscle-based NST in mammals. This review focuses primarily on the role of sarcoplasmic reticulum (SR) Ca 2+ -cycling in muscle NST; specifically, it will discuss recent data showing how uncoupling of sarcoendoplasmic reticulum calcium ATPase (SERCA) (inhibition of Ca 2+ transport but not ATP hydrolysis) by sarcolipin (SLN) results in futile SERCA pump activity, increased ATP hydrolysis and heat production contributing to muscle NST. It will also critically examine how activation of muscle NST can be an important factor in regulating metabolic rate and whole-body energy homeostasis. In this regard, SLN has emerged as a powerful signalling molecule to promote mitochondrial biogenesis and oxidative metabolism in muscle. Furthermore, we will discuss the functional interplay between BAT and muscle, especially with respect to how reduced BAT function in mammals could be compensated by muscle-based NST. Based on the existing data, we argue that SLN-mediated thermogenesis is an integral part of muscle NST and that muscle NST potentially contributed to the evolution of endothermy within the vertebrate clade. This article is part of the theme issue ‘Vertebrate palaeophysiology’.

scholarly journals TLR4-interactor with leucine-rich repeats (TRIL) is involved in diet-induced hypothalamic inflammation

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Alexandre Moura-Assis ◽  
Pedro A. S. Nogueira ◽  
Jose C. de-Lima-Junior ◽  
Fernando M. Simabuco ◽  
Joana M. Gaspar ◽  
...  
Keyword(s):  
Dietary Fats ◽  
Whole Body ◽  
Metabolic Dysfunction ◽  
Diet Induced Obesity ◽  
Hypothalamic Inflammation ◽  
Novel Target ◽  
Tlr4 Activation ◽  
Leucine Rich Repeats ◽  
Body Energy

AbstractObesity and high-fat diet (HFD) consumption result in hypothalamic inflammation and metabolic dysfunction. While the TLR4 activation by dietary fats is a well-characterized pathway involved in the neuronal and glial inflammation, the role of its accessory proteins in diet-induced hypothalamic inflammation remains unknown. Here, we demonstrate that the knockdown of TLR4-interactor with leucine-rich repeats (Tril), a functional component of TLR4, resulted in reduced hypothalamic inflammation, increased whole-body energy expenditure, improved the systemic glucose tolerance and protection from diet-induced obesity. The POMC-specific knockdown of Tril resulted in decreased body fat, decreased white adipose tissue inflammation and a trend toward increased leptin signaling in POMC neurons. Thus, Tril was identified as a new component of the complex mechanisms that promote hypothalamic dysfunction in experimental obesity and its inhibition in the hypothalamus may represent a novel target for obesity treatment.

2006-P: The Role of Adipose Tissue-Resident Eosinophils in Adipocyte Metabolism and Whole-Body Energy Homeostasis

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 2006-P ◽  
Author(s):  
TING LI ◽  
WILLIAM LESUER ◽  
ABHILASHA SINGH ◽  
JAMES D. HERNANDEZ ◽  
XIAODONG ZHANG ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Energy Homeostasis ◽  
Whole Body ◽  
Body Energy

Role of alpha- and beta-adrenoceptors in sympathetically mediated thermogenesis

1993 ◽  
Vol 264 (1) ◽  
pp. E11-E17 ◽  
Author(s):  
E. E. Blaak ◽  
M. A. van Baak ◽  
K. P. Kempen ◽  
W. H. Saris
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Energy Expenditure ◽  
Whole Body ◽  
Healthy Male ◽  
Beta Adrenoceptor ◽  
Beta 2 ◽  
Body Energy ◽  
Stimulation Of

This study was intended to investigate the role of alpha- and beta-adrenoceptor populations in the sympathetically mediated thermogenesis in healthy lean males. In the first study, the beta 1-, beta 2-, and beta 3-agonist isoprenaline was infused in increasing doses with and without simultaneous infusion of the beta 1-blocker atenolol (Iso and Iso+AT, respectively). There was an increase in whole body energy expenditure (EE) after infusing Iso+AT (P < 0.001) and an almost twofold higher increase after infusion of Iso only (P < 0.001). Stimulation of the beta 2-adrenoceptors by a specific agonist (salbutamol) resulted in a significant increase in EE (P < 0.001). The effect of stimulation of alpha 1-adrenoceptors on EE was measured by infusing increasing doses of the alpha 1-agonist phenylephrine. EE did not change, whereas blood pressure (BP) increased (P < 0.001) and heart rate decreased (P < 0.01). In addition to this study, the alpha 1-, alpha 2-, beta 1-, beta 2-, and beta 3-agonists norepinephrine and epinephrine were infused with simultaneous infusion of the beta 1- and beta 2-blocker propranolol. In both studies, there was no effect on EE, whereas BP increased (P < 0.01). In conclusion, in healthy male lean volunteers both beta 1- and beta 2-adrenoceptors are involved in the sympathetically mediated thermogenesis, whereas the alpha 1-, alpha 2-, and beta 3-adrenoceptors do not play a role.

scholarly journals Paracrine role for endothelial IGF-1 receptor in white adipocyte beiging

2021 ◽  
Author(s):  
Natalie J Haywood ◽  
Katherine I Bridge ◽  
Cheukyau Luk ◽  
Nele Warmke ◽  
Katie J Simmons ◽  
...  
Keyword(s):  
Potential Role ◽  
Whole Body ◽  
Environmental Cues ◽  
Brown Adipocytes ◽  
White Adipocyte ◽  
Beige Adipocytes ◽  
Close Proximity ◽  
Body Energy ◽  
Existing Form

SummaryThere are at least two distinct types of thermogenic adipocyte in mammals: a pre-existing form established during development, termed classical brown adipocytes and an inducible form, ‘beige’ adipocytes1–3. Various environmental cues can stimulate a process frequently referred to as ‘beiging’ of white adipose tissue (WAT), leading to enhanced thermogenesis and obesity resistance 4, 5. Whilst beiging of WAT as a therapeutic goal for obesity and obesity-related complications has attracted much attention6–9; therapeutics stimulating beiging without deleterious side-effects remain elusive10. The endothelium lines all blood vessels and is therefore in close proximity to all cells. Many studies support the possibility that the endothelium acts as a paracrine organ11–14. We explored the potential role of endothelial insulin-like growth factor-1 receptor (IGF-1R) as a paracrine modulator of WAT phenotype. Here we show that a reduction in endothelial IGF-1R expression in the presence of nutrient excess leads to white adipocyte beiging, increases whole-body energy expenditure and enhances insulin sensitivity via a non-cell autonomous paracrine mechanism. We demonstrate that this is mediated by endothelial release of malonic acid, which we show, using prodrug analogues, has potentially therapeutically-relevant properties in the treatment of metabolic disease.

scholarly journals The two faces of reactive oxygen species (ROS) in adipocyte function and dysfunction

2016 ◽  
Vol 397 (8) ◽  
pp. 709-724 ◽  
Author(s):  
José Pedro Castro ◽  
Tilman Grune ◽  
Bodo Speckmann
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Animal Studies ◽  
Energy Homeostasis ◽  
Reactive Oxygen ◽  
Whole Body ◽  
Oxygen Species ◽  
Body Energy

Abstract White adipose tissue (WAT) is actively involved in the regulation of whole-body energy homeostasis via storage/release of lipids and adipokine secretion. Current research links WAT dysfunction to the development of metabolic syndrome (MetS) and type 2 diabetes (T2D). The expansion of WAT during oversupply of nutrients prevents ectopic fat accumulation and requires proper preadipocyte-to-adipocyte differentiation. An assumed link between excess levels of reactive oxygen species (ROS), WAT dysfunction and T2D has been discussed controversially. While oxidative stress conditions have conclusively been detected in WAT of T2D patients and related animal models, clinical trials with antioxidants failed to prevent T2D or to improve glucose homeostasis. Furthermore, animal studies yielded inconsistent results regarding the role of oxidative stress in the development of diabetes. Here, we discuss the contribution of ROS to the (patho)physiology of adipocyte function and differentiation, with particular emphasis on sources and nutritional modulators of adipocyte ROS and their functions in signaling mechanisms controlling adipogenesis and functions of mature fat cells. We propose a concept of ROS balance that is required for normal functioning of WAT. We explain how both excessive and diminished levels of ROS, e.g. resulting from over supplementation with antioxidants, contribute to WAT dysfunction and subsequently insulin resistance.

Role of hypothalamic autophagy in the control of whole body energy balance

2013 ◽  
Vol 14 (4) ◽  
pp. 377-386 ◽  
Author(s):  
Min-Seon Kim ◽  
Wenying Quan ◽  
Myung-Shik Lee
Keyword(s):  
Energy Balance ◽  
Whole Body ◽  
Body Energy

scholarly journals The Endocrine Role of Adipose Tissue and Its Management of Obesity-Related Diseases.

2020 ◽  
pp. 1-2
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid Esters ◽  
Whole Body ◽  
Low Grade ◽  
Endocrine Organ ◽  
Hydroxyl Fatty Acids ◽  
Body Energy ◽  
Low Grade Inflammation ◽  
Acid Esters

Adipose tissue plays a central role in regulating whole-body energy. Moreover, adipose tissue acts as an endocrine organ and produces numerous bioactive factors called adipokines which communicate with other organs and modulate a range of metabolic pathways: proteins (adiponectin, angiopoietins, chemerin, etc.), lipids (fatty acid esters of hydroxyl fatty acids, lysophosphatidic acids and sphingolipids), metabolites (uric acid and uridine) and microRNAs. However, excessive adipose tissue is associated with a chronic state of low-grade inflammation, caused by unbalanced production or secretion of these adipokines and can contribute to the development of obesity [1].

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