scholarly journals Brown adipose tissue and type 2 diabetes

2020 ◽  
Vol 2020 (1) ◽  
pp. 70-71
Author(s):  
Stephanie B Levy
Keyword(s):  
Blood Pressure ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Type Ii Diabetes ◽  
Whole Body ◽  
Future Research ◽  
Protective Effects ◽  
Type Ii ◽  
Negative Consequences ◽  
Brown Adipose

Abstract Recent work proposes that a regimen of repeated mild cold exposure may have protective effects against the development of type II diabetes mellitus (T2D) by activating brown adipose tissue (BAT) metabolism. BAT may protect against by increasing whole-body energy expenditure and insulin sensitivity. An evolutionary perspective, however, highlights several limitations of this hypothesis. Some individuals adapt to acute cold stress by constricting their blood vessels, which leads to high blood pressure. Thus, a regimen of repeated mild cooling may have beneficial health effects for some individuals and negative consequences for others. Future research should examine the relationships between low temperature exposure, BAT metabolism, blood pressure, and type II diabetes risk.

Contribution of brown adipose tissue to central PGE1-evoked hyperthermia in rats

1991 ◽  
Vol 260 (1) ◽  
pp. R59-R66 ◽  
Author(s):  
D. M. Fyda ◽  
K. E. Cooper ◽  
W. L. Veale
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Adipose Tissue ◽  
Systolic Blood Pressure ◽  
Brown Adipose Tissue ◽  
Core Temperature ◽  
Tissue Temperature ◽  
Whole Body ◽  
Central Administration ◽  
Brown Adipose

The relative contribution of several effector systems to a prostaglandin E1-(PGE1) evoked hyperthermia was examined. Infusion of 150 ng of PGE1 into a lateral cerebral ventricle increased core temperature and whole body metabolic rate, brown adipose tissue temperature, systolic blood pressure, and heart rate. Pretreating the animals with a nonselective beta-antagonist propranolol (1 mg/kg iv in 0.3 ml followed by 3 mg.kg-1.h-1 in 0.3 ml/h) not only attenuated the rise in metabolism observed after the central administration of 150 ng PGE1 but also diminished the elevation in both core and brown fat tissue temperatures as well as the increase in heart rate. Pretreating the animals with the alpha-antagonist prazosin (2 mg/kg im followed by 50 micrograms.kg-1.h-1 iv in 0.3 ml/h) somewhat reduced the rise in whole body metabolism, suppressed the elevation in core temperature, but failed to alter the rise in brown adipose tissue temperature normally seen after the central administration of PGE1. Moreover, both the rise in systolic blood pressure and heart rate were attenuated when the PGE1 administration was preceded by prazosin. These results suggest that brown adipose tissue is an important effector organ responsible for mediating the hyperthermic response observed after the intracerebral injection of PGE1. In addition, the results indicate that alterations in vasomotor tone may also be important in producing or sustaining the elevated core temperature found after a pyrogen administration.

scholarly journals Intestinal AMPK modulation of microbiota mediates cross-talk with brown fat to control thermogenesis

2021 ◽  
Author(s):  
Wendong Huang ◽  
Eryun Zhang ◽  
Lihua JIN ◽  
Yangmeng Wang ◽  
Jui Tu ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Type Ii Diabetes ◽  
Therapeutic Effects ◽  
Type Ii ◽  
Energy Status ◽  
Cellular Energy ◽  
Nutrient Processing ◽  
Brown Adipose ◽  
Amp Activated Protein Kinase

Abstract The energy-dissipating capacity of brown adipose tissue through thermogenesis can be targeted to improve energy balance. Mammalian 5′-AMP-activated protein kinase (AMPK), a key nutrient sensor for maintaining cellular energy status, is a known therapeutic target for glucose control in Type II diabetes (T2D). Despite current understandings of its well-established roles in regulating glucose metabolism in various tissues, the functions of AMPK in the intestine, an organ for nutrient processing, remain largely unexplored. Using an intestinal epithelium-specific AMPK-null (AMPK-IKO) mouse model, we demonstrated that AMPK in the intestine communicated with brown adipose tissue (BAT) to promote thermogenesis. Mechanistically, we uncovered a novel link between intestinal AMPK activation and BAT thermogenic regulation through modulating the anti-microbial peptide (AMP)-controlled gut microbiota and the metabolites. Our findings identified a new AMPK-mediated mechanism of intestine-BAT communication that may partially underlie the therapeutic effects of AMPK activator metformin (N, N-dimethylbiguanide).

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.

KCTD10 regulates brown adipose tissue thermogenesis and metabolic function via Notch Signaling

2021 ◽  
Author(s):  
Mingsheng Ye ◽  
Liping Luo ◽  
Qi Guo ◽  
Guanghua Lei ◽  
Chao Zeng ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Notch Signaling ◽  
Molecular Mechanisms ◽  
Uncoupling Protein ◽  
Notch Signaling Pathway ◽  
Whole Body ◽  
Brown Adipocyte ◽  
Metabolic Function ◽  
Brown Adipose

Brown adipose tissue (BAT) is emerging as a target to beat obesity through the dissipation of chemical energy to heat. However, the molecular mechanisms of brown adipocyte thermogenesis remain to be further elucidated. Here, we show that KCTD10, a member of the polymerase delta-interacting protein 1 (PDIP1) family, was reduced in BAT by cold stress and a β3 adrenoceptor agonist. Moreover, KCTD10 level increased in the BAT of obese mice, and KCTD10 overexpression attenuates uncoupling protein 1 (UCP1) expression in primary brown adipocytes. BAT-specific KCTD10 knockdown mice had increased thermogenesis and cold tolerance protecting from high fat diet (HFD)-induced obesity. Conversely, overexpression of KCTD10 in BAT caused reduced thermogenesis, cold intolerance, and obesity. Mechanistically, inhibiting Notch signaling restored the KCTD10 overexpression suppressed thermogenesis. Our study presents that KCTD10 serves as an upstream regulator of notch signaling pathway to regulate BAT thermogenesis and whole-body metabolic function.

scholarly journals Brown Adipose Tissue Activation by Cold Treatment Ameliorates Polycystic Ovary Syndrome in Rat

2021 ◽  
Vol 12 ◽  
Author(s):  
Rongcai Ye ◽  
Chunlong Yan ◽  
Huiqiao Zhou ◽  
Yuanyuan Huang ◽  
Meng Dong ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Polycystic Ovary Syndrome ◽  
Brown Adipose Tissue ◽  
Therapeutic Strategy ◽  
Polycystic Ovary ◽  
Cold Treatment ◽  
Whole Body ◽  
Ovary Syndrome ◽  
Bat Activity ◽  
Brown Adipose

Polycystic ovary syndrome (PCOS) is a common endocrine disease accompanied by energetic metabolic imbalance. Because the etiology of PCOS is complex and remains unclear, there is no effective and specific treatment for PCOS. It is often accompanied by various metabolic disorders such as obesity, insulin resistances, and others. Activated brown adipose tissue (BAT) consumes excess energy via thermogenesis, which has positive effects on energy metabolism. Our previous research and that of others indicates that BAT activity is decreased in PCOS patients, and exogenous BAT transplantation can improve PCOS rodents. Notably however, it is difficult to apply this therapeutic strategy in clinical practice. Therapeutic strategies of enhancing endogenous BAT activity and restoring whole-body endocrine homeostasis may be more meaningful for PCOS treatment. In the current study, the dehydroepiandrosterone-induced PCOS rat was exposed to low temperature for 20 days. The results show that cold treatment could reverse acyclicity of the estrous cycle and reduce circulating testosterone and luteinizing hormone in PCOS rats by activating endogenous BAT. It also significantly reduced the expression of steroidogenic enzymes as well as inflammatory factors in the ovaries of PCOS rats. Histological investigations revealed that cold treatment could significantly reduce ovary cystic follicles and increase corpus luteum, indicating that ovulation was recovered to a normal level. Concordant with these results, cold treatment also improved fertility in PCOS rats. Collectively, these findings suggest that cold treatment could be a novel therapeutic strategy for PCOS.

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.

Rapid changes in metabolic cold defense and GDP binding to brown adipose tissue mitochondria of rat pups

1993 ◽  
Vol 264 (5) ◽  
pp. R1017-R1023 ◽  
Author(s):  
G. Kortner ◽  
K. Schildhauer ◽  
O. Petrova ◽  
I. Schmidt
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Time Course ◽  
Developmental Changes ◽  
Whole Body ◽  
Rat Pups ◽  
Brown Adipose ◽  
Rapid Changes ◽  
Whole Body Metabolism

To determine developmental changes of brown adipose tissue (BAT) thermogenic activity at defined circadian and thermal states, we evaluated the time course of cold-induced increases of in vitro guanosine 5'-diphosphate (GDP) binding in parallel with whole body metabolism (oxygen consumption, VO2) and core temperature (Tc) in 1- to 11-day-old rat pups. During the maximum phase of the juvenile diurnal cycle, Tc of littermates was recorded continuously and VO2 alternately until 2 min before animals were killed for removal of interscapular BAT. GDP binding after 1.5 h at thermoneutrality and its increase during physiologically comparable cold loads were significantly lower in 1-day-old pups than in 5- and 11-day-old pups. Cold defense was activated more rapidly in the older pups, but GDP binding in even the 1-day-old pups was significantly increased during the second 10-min period of cold exposure. We conclude that rapid changes in thermogenic activity, in connection with the known developmental changes in the dependence of the suckling rat's metabolic cold defense on maternal and sibling contact and circadian phase, will distort longitudinal studies of any fast-changing BAT parameter when the conditions immediately before tissue removal are not thoroughly controlled.

Central stimulatory effect of leptin on T3production is mediated by brown adipose tissue type II deiodinase

2002 ◽  
Vol 283 (5) ◽  
pp. E980-E987 ◽  
Author(s):  
Philippe Cettour-Rose ◽  
Albert G. Burger ◽  
Christoph A. Meier ◽  
Theo J. Visser ◽  
Françoise Rohner-Jeanrenaud
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Mrna Expression ◽  
Uncoupling Protein ◽  
Tissue Type ◽  
Type I ◽  
Type Ii ◽  
Brown Adipose ◽  
Small Doses ◽  
Food Consumed

To assess whether intracerebroventricular leptin administration affects monodeiodinase type II (D2) activity in the tissues where it is expressed [cerebral cortex, hypothalamus, pituitary, and brown adipose tissue (BAT)], hepatic monodeiodinase type I (D1) activity was inhibited with propylthiouracil (PTU), and small doses of thyroxine (T4; 0.6 nmol · 100 g body wt−1 · day−1) were supplemented to compensate for the PTU-induced hypothyroidism. Two groups of rats were infused with leptin for 6 days, one of them being additionally treated with reverse triiodothyronine (rT3), an inhibitor of D2. Control rats were infused with vehicle and pair-fed the amount of food consumed by leptin-infused animals. Central leptin administration produced marked increases in D2 mRNA expression and activity in BAT, changes that were likely responsible for increased plasma T3 and decreased plasma T4 levels. Indeed, plasma T3 and T4 concentrations were unaltered by central leptin administration in the presence of rT3. The additional observation of a leptin-induced increased mRNA expression of BAT uncoupling protein-1 suggested that the effect on BAT D2 may be mediated by the sympathetic nervous system.

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