scholarly journals Inhibiting peripheral serotonin synthesis reduces obesity and metabolic dysfunction by promoting brown adipose tissue thermogenesis

2014 ◽  
Vol 21 (2) ◽  
pp. 166-172 ◽  
Author(s):  
Justin D Crane ◽  
Rengasamy Palanivel ◽  
Emilio P Mottillo ◽  
Adam L Bujak ◽  
Huaqing Wang ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Metabolic Dysfunction ◽  
Serotonin Synthesis ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis

scholarly journals Leptin Improves Parameters of Brown Adipose Tissue Thermogenesis in Lipodystrophic Mice

Nutrients ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 2499
Author(s):  
Annett Hoffmann ◽  
Thomas Ebert ◽  
Mohammed K. Hankir ◽  
Gesine Flehmig ◽  
Nora Klöting ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Uncoupling Protein ◽  
Regulatory Element ◽  
Subcutaneous Administration ◽  
Sympathetic Nerves ◽  
Metabolic Dysfunction ◽  
Brown Adipose ◽  
Element Binding Protein ◽  
Brown Adipose Tissue Thermogenesis

Lipodystrophy syndromes (LD) are a heterogeneous group of very rare congenital or acquired disorders characterized by a generalized or partial lack of adipose tissue. They are strongly associated with severe metabolic dysfunction due to ectopic fat accumulation in the liver and other organs and the dysregulation of several key adipokines, including leptin. Treatment with leptin or its analogues is therefore sufficient to reverse some of the metabolic symptoms of LD in patients and in mouse models through distinct mechanisms. Brown adipose tissue (BAT) thermogenesis has emerged as an important regulator of systemic metabolism in rodents and in humans, but it is poorly understood how leptin impacts BAT in LD. Here, we show in transgenic C57Bl/6 mice overexpressing sterol regulatory element-binding protein 1c in adipose tissue (Tg (aP2-nSREBP1c)), an established model of congenital LD, that daily subcutaneous administration of 3 mg/kg leptin for 6 to 8 weeks increases body temperature without affecting food intake or body weight. This is associated with increased protein expression of the thermogenic molecule uncoupling protein 1 (UCP1) and the sympathetic nerve marker tyrosine hydroxylase (TH) in BAT. These findings suggest that leptin treatment in LD stimulates BAT thermogenesis through sympathetic nerves, which might contribute to some of its metabolic benefits by providing a healthy reservoir for excess circulating nutrients.

Brown adipose tissue thermogenesis in women with polycystic ovary syndrome

2017 ◽  
Author(s):  
Soulmaz Shorakae ◽  
Eveline Jona ◽  
Courten Barbora de ◽  
Gavin Lambert ◽  
Elisabeth Lambert ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Polycystic Ovary Syndrome ◽  
Brown Adipose Tissue ◽  
Polycystic Ovary ◽  
Ovary Syndrome ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis

scholarly journals Stimulatory, but not anxiogenic, doses of caffeine act centrally to activate interscapular brown adipose tissue thermogenesis in anesthetized male rats

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
L. Van Schaik ◽  
C. Kettle ◽  
R. Green ◽  
W. Sievers ◽  
M. W. Hale ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Basolateral Amygdala ◽  
Free Breathing ◽  
Male Rats ◽  
Central Administration ◽  
Hypothalamic Area ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis

AbstractThe role of central orexin in the sympathetic control of interscapular brown adipose tissue (iBAT) thermogenesis has been established in rodents. Stimulatory doses of caffeine activate orexin positive neurons in the lateral hypothalamus, a region of the brain implicated in stimulating BAT thermogenesis. This study tests the hypothesis that central administration of caffeine is sufficient to activate BAT. Low doses of caffeine administered either systemically (intravenous [IV]; 10 mg/kg) and centrally (intracerebroventricular [ICV]; 5–10 μg) increases BAT thermogenesis, in anaesthetised (1.5 g/kg urethane, IV) free breathing male rats. Cardiovascular function was monitored via an indwelling intra-arterial cannula and exhibited no response to the caffeine. Core temperature did not significantly differ after administration of caffeine via either route of administration. Caffeine administered both IV and ICV increased neuronal activity, as measured by c-Fos-immunoreactivity within subregions of the hypothalamic area, previously implicated in regulating BAT thermogenesis. Significantly, there appears to be no neural anxiety response to the low dose of caffeine as indicated by no change in activity in the basolateral amygdala. Having measured the physiological correlate of thermogenesis (heat production) we have not measured indirect molecular correlates of BAT activation. Nevertheless, our results demonstrate that caffeine, at stimulatory doses, acting via the central nervous system can increase thermogenesis, without adverse cardio-dynamic impact.

Dopaminergic Input from the Posterior Hypothalamus to the Raphe Pallidus Area Inhibits Brown Adipose Tissue Thermogenesis

2021 ◽  
Author(s):  
Ellen Paula Santos da Conceição Furber ◽  
Clarissa M.D. Mota ◽  
Edward Veytsman ◽  
Shaun F. Morrison ◽  
Christopher J. Madden
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Posterior Hypothalamus ◽  
Brown Adipose ◽  
Premotor Neurons ◽  
Brown Adipose Tissue Thermogenesis ◽  
Pre Treatment ◽  
Type 3 ◽  
Raphe Pallidus

Systemic administration of dopamine (DA) receptor agonists leads to falls in body temperature. However, the central thermoregulatory pathways modulated by DA have not been fully elucidated. Here we identified a source and site of action contributing to DA's hypothermic action by inhibition of brown adipose tissue (BAT) thermogenesis. Nanoinjection of the type 2 and type 3 DA receptor (D2R/D3R) agonist, 7-OH-DPAT, in the rostral raphe pallidus area (rRPa) inhibits the sympathetic activation of BAT evoked by cold exposure or by direct activation of NMDA receptors in the rRPa. Blockade of D2R/D3R in the rRPa with nanoinjection of SB-277011A increases BAT thermogenesis, consistent with a tonic release of DA in the rRPa contributing to inhibition of BAT thermogenesis. Accordingly, D2R are expressed in cold-activated and serotonergic neurons in the rRPa and anatomical tracing studies revealed that neurons in the posterior hypothalamus (PH) are a source of dopaminergic input to the rRPa. Disinhibitory activation of PH neurons with nanoinjection of gabazine inhibits BAT thermogenesis, which is reduced by pre-treatment of the rRPa with SB-277011A. In conclusion, the rRPa, the site of sympathetic premotor neurons for BAT, receives a tonically-active, dopaminergic input from the PH that suppresses BAT thermogenesis.

scholarly journals Brown adipose tissue thermogenesis in polycystic ovary syndrome

2018 ◽  
Author(s):  
Soulmaz Shorakae ◽  
Eveline Jona ◽  
Barbora de Courten ◽  
Gavin W. Lambert ◽  
Elisabeth A. Lambert ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Polycystic Ovary Syndrome ◽  
Brown Adipose Tissue ◽  
Polycystic Ovary ◽  
Ovary Syndrome ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis

Brown Adipose Tissue Thermogenesis

2013 ◽  
Vol 21 (6) ◽  
pp. 265-269 ◽  
Author(s):  
Ross A. Mund ◽  
William H. Frishman
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis
Sign in / Sign up

Export Citation Format

Share Document