scholarly journals Brown Adipose Tissue, Whole-Body Energy Expenditure, and Thermogenesis in Healthy Adult Men

Obesity ◽  
2011 ◽  
Vol 19 (1) ◽  
pp. 13-16 ◽  
Author(s):  
Takeshi Yoneshiro ◽  
Sayuri Aita ◽  
Mami Matsushita ◽  
Toshimitsu Kameya ◽  
Kunihiro Nakada ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Energy Expenditure ◽  
Brown Adipose Tissue ◽  
Healthy Adult ◽  
Whole Body ◽  
Adult Men ◽  
Brown Adipose ◽  
Body Energy

scholarly journals Kaempferia parviflora Extract Increases Whole-Body Energy Expenditure in Humans: Roles of Brown Adipose Tissue

2015 ◽  
Vol 61 (1) ◽  
pp. 79-83 ◽  
Author(s):  
Mami MATSUSHITA ◽  
Takeshi YONESHIRO ◽  
Sayuri AITA ◽  
Tomoyasu KAMIYA ◽  
Nobutaka KUSABA ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Energy Expenditure ◽  
Brown Adipose Tissue ◽  
Whole Body ◽  
Kaempferia Parviflora ◽  
Brown Adipose ◽  
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.

Nesfatin-1 Acts Centrally to Induce Sympathetic Activation of Brown Adipose Tissue and Non-Shivering Thermogenesis

2019 ◽  
Vol 51 (10) ◽  
pp. 678-685 ◽  
Author(s):  
Luka Levata ◽  
Riccardo Dore ◽  
Olaf Jöhren ◽  
Markus Schwaninger ◽  
Carla Schulz ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Energy Expenditure ◽  
Brown Adipose Tissue ◽  
Body Weight Loss ◽  
Whole Body ◽  
Central Administration ◽  
Adrenergic Stimulation ◽  
Interscapular Brown Adipose Tissue ◽  
Adrenoceptor Antagonist ◽  
Brown Adipose

AbstractNesfatin-1 has originally been established as a bioactive peptide interacting with key hypothalamic nuclei and neural circuitries in control of feeding behavior, while its effect on energy expenditure has only recently been investigated. Hence, the aim of this study was to examine whether centrally acting nesfatin-1 can induce β3-adrenergic stimulation, which is a prerequisite for the activation of thermogenic genes and heat release from interscapular brown adipose tissue, key physiological features that underlie increased energy expenditure. This question was addressed in non-fasted mice stereotactically cannulated to receive nesfatin-1 intracerebroventricularly together with peripheral injection of the β3-adrenoceptor antagonist SR 59230 A, to assess whole-body energy metabolism. Using a minimally invasive thermography technique, we now demonstrate that the thermogenic effect of an anorectic nesfatin-1 dose critically depends on β3 adrenergic stimulation, as the co-administration with SR 59230 A completely abolished heat production from interscapular brown adipose tissue and rise in ocular surface temperature, thus preventing body weight loss. Moreover, through indirect calorimetry it could be shown that the anorectic concentration of nesfatin-1 augments overall caloric expenditure. Plausibly, central administration of nesfatin-1 also enhanced the expression of DIO2 and CIDEA mRNA in brown adipose tissue critically involved in the regulation of thermogenesis.

scholarly journals Front cover: Cyanidin-3-glucoside increases whole body energy metabolism by upregulating brown adipose tissue mitochondrial function

2017 ◽  
Vol 61 (11) ◽  
pp. 1770111
Author(s):  
Yilin You ◽  
Xiaoxue Yuan ◽  
Xiaomeng Liu ◽  
Chen Liang ◽  
Minghui Meng ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Energy Metabolism ◽  
Brown Adipose Tissue ◽  
Mitochondrial Function ◽  
Whole Body ◽  
Front Cover ◽  
Brown Adipose ◽  
Body Energy

Fat feeding causes widespread in vivo insulin resistance, decreased energy expenditure, and obesity in rats

1986 ◽  
Vol 251 (5) ◽  
pp. E576-E583 ◽  
Author(s):  
L. H. Storlien ◽  
D. E. James ◽  
K. M. Burleigh ◽  
D. J. Chisholm ◽  
E. W. Kraegen
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Energy Expenditure ◽  
Metabolic Rate ◽  
Brown Adipose Tissue ◽  
Whole Body ◽  
Brown Adipose ◽  
Glucose Output ◽  
Fat Feeding

High levels of dietary fat may contribute to both insulin resistance and obesity in humans but evidence is limited. The euglycemic clamp technique combined with tracer administration was used to study insulin action in vivo in liver and individual peripheral tissues after fat feeding. Basal and nutrient-stimulated metabolic rate was assessed by open-circuit respirometry. Adult male rats were pair-fed isocaloric diets high in either carbohydrate (69% of calories; HiCHO) or fat (59% of calories; HiFAT) for 24 +/- 1 days. Feeding of the HiFAT diet resulted in a greater than 50% reduction in net whole-body glucose utilization at midphysiological insulin levels (90-100 mU/l) due to both reduced glucose disposal and, to a lesser extent, failure to suppress liver glucose output. Major suppressive effects of the HiFAT diet on glucose uptake were found in oxidative skeletal muscles (29-61%) and in brown adipose tissue (BAT; 78-90%), the latter accounting for over 20% of the whole-body effect. There was no difference in basal metabolic rate but thermogenesis in response to glucose ingestion was higher in the HiCHO group. In contrast to their reduced BAT weight, the HiFAT group accumulated more white adipose tissue, consistent with reduced energy expenditure. HiFAT feeding also resulted in major decreases in basal and insulin-stimulated conversion of glucose to lipid in liver (26-60%) and brown adipose tissue (88-90%) with relatively less effect in white adipose (0-43%). We conclude that high-fat feeding results in insulin resistance due mainly to effects in oxidative skeletal muscle and BAT.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Brown Adipose Tissue - role in metabolic disorders

2019 ◽  
Vol 13 (1) ◽  
pp. 002
Author(s):  
Tahniyah Haq ◽  
Frank Joseph Ong ◽  
Sarah Kanji
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Metabolic Diseases ◽  
Uncoupling Protein ◽  
Whole Body ◽  
Positron Emission ◽  
Brown Adipose ◽  
Magnetic Resonance Imaging Mri ◽  
Fdg Pet Ct ◽  
Body Energy

Brown adipose tissue, a thermogenic organ, previously thought to be present in only small mammals and children has recently been identified in adult humans. Located primarily in the supraclavicular and cervical area, it produces heat by uncoupling oxidative phosphorylation due to the unique presence of uncoupling protein 1 by a process called nonshivering thermogenesis. BAT activity depends on many factors including age, sex, adiposity and outdoor temperature. Positron-emission tomography using 18F-fluorodeoxyglucose and computed tomography (18F-FDG PET–CT), magnetic resonance imaging (MRI) and thermal imaging (IRT) are among several methods used to detect BAT in humans. The importance of BAT is due to its role in whole body energy expenditure and fuel metabolism. Thus it is postulated that it may be useful in the treatment of metabolic diseases. However, there are still many unanswered questions to the clinical usefulness of this novel tissue. IMC J Med Sci 2019; 13(1): 002

scholarly journals Brown adipose tissue transplantation improves whole-body energy metabolism

Cell Research ◽  
2013 ◽  
Vol 23 (6) ◽  
pp. 851-854 ◽  
Author(s):  
Xiaomeng Liu ◽  
Zongji Zheng ◽  
Xiaoming Zhu ◽  
Minghui Meng ◽  
Lan Li ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Energy Metabolism ◽  
Brown Adipose Tissue ◽  
Tissue Transplantation ◽  
Whole Body ◽  
Brown Adipose ◽  
Body Energy

Cyanidin-3-glucoside increases whole body energy metabolism by upregulating brown adipose tissue mitochondrial function

2017 ◽  
Vol 61 (11) ◽  
pp. 1700261 ◽  
Author(s):  
Yilin You ◽  
Xiaoxue Yuan ◽  
Xiaomeng Liu ◽  
Chen Liang ◽  
Minghui Meng ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Energy Metabolism ◽  
Brown Adipose Tissue ◽  
Mitochondrial Function ◽  
Whole Body ◽  
Brown Adipose ◽  
Body Energy

scholarly journals Grains of paradise (Aframomum melegueta) extract activates brown adipose tissue and increases whole-body energy expenditure in men

2013 ◽  
Vol 110 (4) ◽  
pp. 733-738 ◽  
Author(s):  
Jun Sugita ◽  
Takeshi Yoneshiro ◽  
Takuya Hatano ◽  
Sayuri Aita ◽  
Takeshi Ikemoto ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Energy Expenditure ◽  
Human Subjects ◽  
Whole Body ◽  
Negative Group ◽  
Oral Ingestion ◽  
Positive Group ◽  
Bat Activity ◽  
Brown Adipose ◽  
Body Energy

Brown adipose tissue (BAT) is responsible for cold- and diet-induced thermogenesis, and thereby contributes to the control of whole-body energy expenditure (EE) and body fat content. BAT activity can be assessed by fluoro-2-deoxyglucose (FDG)-positron emission tomography (PET) in human subjects. Grains of paradise (GP, Aframomum melegueta), a species of the ginger family, contain pungent, aromatic ketones such as 6-paradol, 6-gingerol and 6-shogaol. An alcohol extract of GP seeds and 6-paradol are known to activate BAT thermogenesis in small rodents. The present study aimed to examine the effects of the GP extract on whole-body EE and to analyse its relation to BAT activity in men. A total of nineteen healthy male volunteers aged 20–32 years underwent FDG-PET after 2 h of exposure to cold at 19°C with light clothing. A total of twelve subjects showed marked FDG uptake into the adipose tissue of the supraclavicular and paraspinal regions (BAT positive). The remaining seven showed no detectable uptake (BAT negative). Within 4 weeks after the FDG-PET examination, whole-body EE was measured at 27°C before and after oral ingestion of GP extract (40 mg) in a single-blind, randomised, placebo-controlled, crossover design. The resting EE of the BAT-positive group did not differ from that of the BAT-negative group. After GP extract ingestion, the EE of the BAT-positive group increased within 2 h to a significantly greater (P< 0·01) level than that of the BAT-negative group. Placebo ingestion produced no significant change in EE. These results suggest that oral ingestion of GP extract increases whole-body EE through the activation of BAT in human subjects.

Adipocyte-specific mTORC2 deficiency impairs BAT and iWAT thermogenic capacity without affecting glucose uptake and energy expenditure in cold-acclimated mice

2021 ◽  
Author(s):  
Erique Castro ◽  
Thayna S Vieira ◽  
Tiago E. Oliveira ◽  
Milene Ortiz-Silva ◽  
Maynara L Andrade ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Energy Expenditure ◽  
Glucose Uptake ◽  
Residual Activity ◽  
De Novo Lipogenesis ◽  
Whole Body ◽  
Mrna Levels ◽  
Brown Adipose ◽  
Body Energy ◽  
Thermogenic Capacity

Deletion of mTORC2 essential component Rictor by a Cre recombinase under control of the broad, non-adipocyte specific aP2/FABP4 promoter impairs thermoregulation and brown adipose tissue (BAT) glucose uptake upon acute cold exposure. We investigated herein whether adipocyte-specific mTORC2 deficiency affects BAT and inguinal white adipose tissue (iWAT) signaling, metabolism and thermogenesis in cold-acclimated mice. For this, 8-weeks old male mice bearing Rictor deletion and therefore mTORC2 deficiency in adipocytes (adiponectin-Cre) and littermates controls were either kept at thermoneutrality (30 ± 1ºC) or cold-acclimated (10 ± 1ºC) for 14 days and evaluated for BAT and iWAT signaling, metabolism and thermogenesis. Cold acclimation inhibited mTORC2 in BAT and iWAT, but its residual activity is still required for the cold-induced increases in BAT adipocyte number, total UCP-1 content and mRNA levels of proliferation markers Ki67 and cyclin 1D and de novo lipogenesis enzymes ATP-citrate lyase and acetyl-CoA carboxylase. In iWAT, mTORC2 residual activity is partially required for the cold-induced increases in multilocular adipocytes, mitochondrial mass and UCP-1 content. Conversely, BAT mTORC1 activity and BAT and iWAT glucose uptake were upregulated by cold independently of mTORC2. Noteworthy, the impairment in BAT and iWAT total UCP-1 content and thermogenic capacity induced by adipocyte mTORC2 deficiency had no major impact on whole-body energy expenditure in cold-acclimated mice due to a compensatory activation of muscle shivering. In conclusion, adipocyte mTORC2 deficiency impairs, through different mechanisms, BAT and iWAT total UCP-1 content and thermogenic capacity in cold-acclimated mice, without affecting glucose uptake and whole-body energy expenditure.

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