scholarly journals Direct Control of Brown Adipose Tissue Thermogenesis by Central Nervous System Glucagon-Like Peptide-1 Receptor Signaling

Diabetes ◽  
2012 ◽  
Vol 61 (11) ◽  
pp. 2753-2762 ◽  
Author(s):  
S. H. Lockie ◽  
K. M. Heppner ◽  
N. Chaudhary ◽  
J. R. Chabenne ◽  
D. A. Morgan ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Receptor Signaling ◽  
Direct Control ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

scholarly journals Glucagon-like peptide-1 regulates brown adipose tissue thermogenesis via the gut-brain axis in rats

2018 ◽  
Vol 315 (4) ◽  
pp. R708-R720 ◽  
Author(s):  
Jean-Philippe Krieger ◽  
Ellen Paula Santos da Conceição ◽  
Graciela Sanchez-Watts ◽  
Myrtha Arnold ◽  
Klaus G. Pettersen ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Energy Balance ◽  
Brown Adipose Tissue ◽  
Body Weight Gain ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis ◽  
Sympathetic Regulation ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Endogenous intestinal glucagon-like peptide-1 (GLP-1) controls satiation and glucose metabolism via vagal afferent neurons (VANs). Recently, VANs have received increasing attention for their role in brown adipose tissue (BAT) thermogenesis. It is, however, unclear whether VAN GLP-1 receptor (GLP-1R) signaling affects BAT thermogenesis and energy expenditure (EE) and whether this VAN mechanism contributes to energy balance. First, we tested the effect of the GLP-1R agonist exendin-4 (Ex4, 0.3 μg/kg ip) on EE and BAT thermogenesis and whether these effects require VAN GLP-1R signaling using a rat model with a selective Glp1r knockdown (kd) in VANs. Second, we examined the role of VAN GLP-1R in energy balance during chronic high-fat diet (HFD) feeding in VAN Glp1r kd rats. Finally, we used viral transsynaptic tracers to identify the possible neuronal substrates of such a gut-BAT interaction. VAN Glp1r kd attenuated the acute suppressive effects of Ex4 on EE and BAT thermogenesis. Consistent with this finding, the VAN Glp1r kd increased EE and BAT activity, diminished body weight gain, and improved insulin sensitivity compared with HFD-fed controls. Anterograde transsynaptic viral tracing of VANs infected major hypothalamic and hindbrain areas involved in BAT sympathetic regulation. Moreover, retrograde tracing from BAT combined with laser capture microdissection revealed that a population of VANs expressing Glp1r is synaptically connected to the BAT. Our findings reveal a novel role of VAN GLP-1R signaling in the regulation of EE and BAT thermogenesis and imply that through this gut-brain-BAT connection, intestinal GLP-1 plays a role in HFD-induced metabolic syndrome.

scholarly journals Nicotine Improves Obesity and Hepatic Steatosis and ER Stress in Diet-Induced Obese Male Rats

Endocrinology ◽  
2014 ◽  
Vol 155 (5) ◽  
pp. 1679-1689 ◽  
Author(s):  
Patricia Seoane-Collazo ◽  
Pablo B. Martínez de Morentin ◽  
Johan Fernø ◽  
Carlos Diéguez ◽  
Rubén Nogueiras ◽  
...  
Keyword(s):  
Nervous System ◽  
Body Weight ◽  
Adipose Tissue ◽  
Energy Balance ◽  
Protein Kinase ◽  
Brown Adipose Tissue ◽  
Male Rats ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis ◽  
Amp Activated Protein Kinase

Nicotine, the main addictive component of tobacco, promotes body weight reduction in humans and rodents. Recent evidence has suggested that nicotine acts in the central nervous system to modulate energy balance. Specifically, nicotine modulates hypothalamic AMP-activated protein kinase to decrease feeding and to increase brown adipose tissue thermogenesis through the sympathetic nervous system, leading to weight loss. Of note, most of this evidence has been obtained in animal models fed with normal diet or low-fat diet (LFD). However, its effectiveness in obese models remains elusive. Because obesity causes resistance towards many factors involved in energy homeostasis, the aim of this study has been to compare the effect of nicotine in a diet-induced obese (DIO) model, namely rats fed a high-fat diet, with rats fed a LFD. Our data show that chronic peripheral nicotine treatment reduced body weight by decreasing food intake and increasing brown adipose tissue thermogenesis in both LFD and DIO rats. This overall negative energy balance was associated to decreased activation of hypothalamic AMP-activated protein kinase in both models. Furthermore, nicotine improved serum lipid profile, decreased insulin serum levels, as well as reduced steatosis, inflammation, and endoplasmic reticulum stress in the liver of DIO rats but not in LFD rats. Overall, this evidence suggests that nicotine diminishes body weight and improves metabolic disorders linked to DIO and might offer a clear-cut strategy to develop new therapeutic approaches against obesity and its metabolic complications.

scholarly journals Brown Adipose Crosstalk in Tissue Plasticity and Human Metabolism

2019 ◽  
Vol 41 (1) ◽  
pp. 53-65 ◽  
Author(s):  
Camilla Scheele ◽  
Christian Wolfrum
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Metabolic Regulation ◽  
Immune Cell ◽  
Primary Source ◽  
Whole Body ◽  
Brown Adipose ◽  
The Central Nervous System

Abstract Infants rely on brown adipose tissue (BAT) as a primary source of thermogenesis. In some adult humans, residuals of brown adipose tissue are adjacent to the central nervous system and acute activation increases metabolic rate. Brown adipose tissue (BAT) recruitment occurs during cold acclimation and includes secretion of factors, known as batokines, which target several different cell types within BAT, and promote adipogenesis, angiogenesis, immune cell interactions, and neurite outgrowth. All these processes seem to act in concert to promote an adapted BAT. Recent studies have also provided exciting data on whole body metabolic regulation with a broad spectrum of mechanisms involving BAT crosstalk with liver, skeletal muscle, and gut as well as the central nervous system. These widespread interactions might reflect the property of BAT of switching between an active thermogenic state where energy is highly consumed and drained from the circulation, and the passive thermoneutral state, where energy consumption is turned off. (Endocrine Reviews 41: XXX – XXX, 2020)

Central GLP-1 receptor signaling directly controls brown adipose tissue thermogenesis

Appetite ◽  
2011 ◽  
Vol 57 ◽  
pp. S27
Author(s):  
S.H. Lockie ◽  
N. Chaudhary ◽  
K. Heppner ◽  
D. Smiley ◽  
D. Morgan ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Receptor Signaling ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis

scholarly journals Central Nervous System Regulation of Brown Adipose Tissue

2014 ◽  
pp. 1677-1713 ◽  
Author(s):  
Shaun F. Morrison ◽  
Christopher J. Madden
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Brown Adipose

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
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