scholarly journals In vivoassessment of cold stimulation effects on the fat fraction of brown adipose tissue using DIXON MRI

2016 ◽  
Vol 45 (2) ◽  
pp. 369-380 ◽  
Author(s):  
Vanessa Stahl ◽  
Florian Maier ◽  
Martin T. Freitag ◽  
Ralf O. Floca ◽  
Moritz C. Berger ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Stimulation ◽  
Brown Adipose ◽  
Fat Fraction

scholarly journals Multimodal Imaging for the Detection of Brown Adipose Tissue Activation in Women: A Pilot Study Using NIRS and Infrared Thermography

2017 ◽  
Vol 2017 ◽  
pp. 1-6 ◽  
Author(s):  
Valentina Hartwig ◽  
Letizia Guiducci ◽  
Martina Marinelli ◽  
Laura Pistoia ◽  
Tommaso Minutoli Tegrimi ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Pilot Study ◽  
Brown Adipose Tissue ◽  
Infrared Thermography ◽  
Pharmacological Intervention ◽  
Oral Glucose ◽  
Cold Stimulation ◽  
Standard Clinical Practice ◽  
Obesity And Diabetes ◽  
Brown Adipose

Purpose. A clear link between obesity and brown adipose tissue (BAT) dysfunction has been recently demonstrated. The purpose of this pilot study is to determine if near-infrared spectroscopy (NIRS) 2D imaging together with infrared thermography (IRT) is capable of identifying thermal and vascular response in the supraclavicular (SCV) areas after the ingestion of an oral glucose load as a thermogenic stimulation. Method. We studied two groups of women (obese versus lean) for discerning their different responses. NIRS and IRT images were acquired on the neck in the left SCV region during a 3 h oral glucose tolerance test (OGTT) and immediately after a cold stimulation. Results. We detected a significant thermal response of BAT in SCV fossa in both groups. Both during OGTT and after cold stimulation, skin temperature was persistently higher in lean versus obese. This response was not coupled with changes in oxygen saturation of subcutaneous tissue in that area. Discussion and Conclusion. The results show that NIRS/IRT may be a novel, noninvasive, radiation-free, easy to use, and low-cost method for monitoring, during the standard clinical practice, the diet and pharmacological intervention which aims to stimulate BAT as a potential therapeutic target against obesity and diabetes.

Enhanced gene expression of endothelial nitric oxide synthase in brown adipose tissue during cold exposure

2002 ◽  
Vol 282 (2) ◽  
pp. R623-R626 ◽  
Author(s):  
Kazue Kikuchi-Utsumi ◽  
Bihu Gao ◽  
Hiroshi Ohinata ◽  
Masaaki Hashimoto ◽  
Noriyuki Yamamoto ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
Inos Mrna ◽  
No Production ◽  
Mrna Levels ◽  
Cold Stimulation ◽  
Brown Adipose ◽  
Enos Mrna

It has been shown that norepinephrine (NE) can mediate vasodilatation by stimulating the production of nitric oxide (NO) in brown adipose tissue (BAT), resulting in an increase in BAT blood flow. We speculated that constitutive NO synthase (NOS) is involved in this NO production. However, it is not known whether constitutive NOS is expressed in BAT. To answer this question, we assessed the expression of two types of constitutive NOS, endothelial (eNOS) and neuronal NOS (nNOS), in BAT of rats. eNOS was abundantly expressed in both BAT and isolated brown adipocytes, whereas nNOS was not. Cold exposure, which is known to stimulate NE release from sympathetic nerve terminals in BAT, led to a significant increase in eNOS mRNA in this tissue. In contrast, very low levels of inducible NOS (iNOS) mRNA were expressed, and cold stimulation failed to increase iNOS mRNA levels in BAT. These results suggest that eNOS is the primary isoform that is responsible for NO production in BAT and that its expression may be under sympathetic control.

scholarly journals ACE2 Pathway Regulates Thermogenesis and Energy Metabolism

2021 ◽  
Author(s):  
Xi Cao ◽  
Tingting Shi ◽  
Chuanhai Zhang ◽  
Wanzhu Jin ◽  
Lini Song ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Energy Expenditure ◽  
Brown Adipose Tissue ◽  
Knockout Mice ◽  
Metabolic Disorders ◽  
Energy Homeostasis ◽  
Cold Stimulation ◽  
Obesity And Diabetes ◽  
Brown Adipose ◽  
Pka Pathway

Identification of key regulators of energy homeostasis holds important therapeutic promise for metabolic disorders, such as obesity and diabetes. ACE2 cleaves angiotensin II (Ang II) to generate Ang-(1-7) which acts mainly through the Mas receptor. Here, we identify ACE2 pathway as a critical regulator in the maintenance of thermogenesis and energy expenditure. We found that ACE2 is highly expressed in brown adipose tissue (BAT) and that cold stimulation increases ACE2 and Ang-(1-7) levels in BAT and serum. ACE2 knockout mice (ACE2-/y), Mas knockout mice (Mas-/-), and the mice transplanted with brown adipose tissue from Mas-/- mice displayed impaired thermogenesis. In contrast, impaired thermogenesis of db/db obese diabetic mice and high-fat diet-induced obese mice were ameliorated by overexpression of ACE2 or continuous infusion of Ang-(1-7). Activation of ACE2 pathway was associated with improvement of metabolic parameters, including blood glucose, lipids and energy expenditure in multiple animal models. Consistently, ACE2 pathway remarkably enhanced the browning of white adipose tissue. Mechanistically, we showed that ACE2 pathway activated Akt/FoxO1 and PKA pathway, leading to induction of UCP1 and activation of mitochondrial function. Our data propose that adaptive thermogenesis requires regulation of ACE2 pathway and highlight novel therapeutic targets for the treatment of metabolic disorders.

Abstract 435: Brown Adipose Tissue Activation in the Postprandial State Reflects on Plasma Lipoproteins and Immune Cell Response in Humans

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Alexandra Mellerowicz ◽  
Madelene Ericsson ◽  
Mattias Hedlund ◽  
Stefan K Nilsson
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cell Response ◽  
Immune Cell ◽  
Plasma Lipoproteins ◽  
Emg Activity ◽  
Cold Stimulation ◽  
Postprandial State ◽  
Brown Adipose ◽  
Immune Cell Response

Background: Brown adipose tissue (BAT) has a unique to ability to use excess energy for heat production. It is therefore an attractive target organ for counteracting obesity and related metabolic diseases where overfeeding is an underlying cause. BAT has in murine models been shown to clear postprandial lipids quickly. The postprandial response is associated to systemic inflammatory alterations and an increased lipid pressure possibly driving atherosclerosis development. We hypothesized that BAT activation would affect postprandial lipid clearance and that this would reflect in an altered immune cell response. Methods: Young male volunteers were subject to an oral fat tolerance test at two separate occasions during both cold stimulation and in thermoneutral control conditions. Body temperature and EMG activity was monitored and energy expenditure (EE) was measured. Blood samples were taken at baseline and every 30 min for 2 h. Plasma lipids and the immune cell response. Results: Cold stimulation during OFTT resulted in a 19,4 % higher EE compared to warm conditions (P=0,007). Surprisingly, no changes in plasma TG were observed. A 2-fold elevation in free fatty acids (FFA) was seen in cold which also correlated positively with EE (P=0,008). Total plasma cholesterol increased compared to warm conditions by 0,56 mmol/L (P=0,050). LDL-c and HDL-c were increased in cold (0,20 mmol/L difference P=0,048 and 0,16 mmol/L P=0,002) whereas remnant-c was unaltered between the two thermal conditions. White blood cell count (WBC) after OFTT was significantly increased in cold (P = 0,018) by 0,29 х 109/L. Discussion: BAT activation in the postprandial state results in increased HDL-c, possibly indicating increased vascular lipolysis and associated pre-β HDL particle formation. Increased VLDL production due to elevated FFA levels in the cold state and might explain why plasma TG is unaltered and also why LDL-c remains at a higher concentration in the cold. Conclusions: BAT might be an attractive target for obesity treatment but potentially displays pro-atherogenic properties that must be addressed in longitudinal studies.

Liraglutide decreases energy expenditure and does not affect the fat fraction of supraclavicular brown adipose tissue in patients with type 2 diabetes

2020 ◽  
Vol 30 (4) ◽  
pp. 616-624 ◽  
Author(s):  
Huub J. van Eyk ◽  
Elisabeth H.M. Paiman ◽  
Maurice B. Bizino ◽  
Suzanne L. IJzermans ◽  
Fleur Kleiburg ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
Energy Expenditure ◽  
Brown Adipose Tissue ◽  
Brown Adipose ◽  
Fat Fraction

scholarly journals PET/MRI of glucose metabolic rate, lipid content and perfusion in human brown adipose tissue

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Elin Lundström ◽  
Jonathan Andersson ◽  
Mathias Engström ◽  
Mark Lubberink ◽  
Robin Strand ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Metabolic Rate ◽  
Brown Adipose Tissue ◽  
Lipid Content ◽  
Cold Exposure ◽  
Arterial Blood ◽  
Brown Adipose ◽  
Glucose Metabolic Rate ◽  
Fat Fraction ◽  
Arterial Blood Volume

AbstractThis study evaluated the MRI-derived fat fraction (FF), from a Cooling-reheating protocol, for estimating the cold-induced brown adipose tissue (BAT) metabolic rate of glucose (MRglu) and changes in lipid content, perfusion and arterial blood volume (VA) within cervical-supraclavicular fat (sBAT). Twelve volunteers underwent PET/MRI at baseline, during cold exposure and reheating. For each temperature condition, perfusion and VA were quantified with dynamic [15O]water-PET, and FF, with water-fat MRI. MRglu was assessed with dynamic [18F]fluorodeoxyglucose-PET during cold exposure. sBAT was defined using anatomical criteria, and its subregion sBATHI, by MRglu > 11 μmol/100 cm3/min. For all temperature conditions, sBAT-FF correlated negatively with sBAT-MRglu (ρ ≤ − 0.87). After 3 h of cold, sBAT-FF decreased (− 2.13 percentage points) but tended to normalize during reheating although sBATHI-FF remained low. sBAT-perfusion and sBAT-VA increased during cold exposure (perfusion: + 5.2 ml/100 cm3/min, VA: + 4.0 ml/100 cm3). sBAT-perfusion remained elevated and sBAT-VA normalized during reheating. Regardless of temperature condition during the Cooling-reheating protocol, sBAT-FF could predict the cold-induced sBAT-MRglu. The FF decreases observed after reheating were mainly due to lipid consumption, but could potentially be underestimated due to intracellular lipid replenishment. The influence of perfusion and VA, on the changes in FF observed during cold exposure, could not be ruled out.

scholarly journals ACE2 pathway regulates thermogenesis and energy metabolism

eLife ◽  
2022 ◽  
Vol 11 ◽  
Author(s):  
Xi Cao ◽  
Tingting Shi ◽  
Chuanhai Zhang ◽  
Wanzhu Jin ◽  
Lini Song ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Energy Expenditure ◽  
Brown Adipose Tissue ◽  
Knockout Mice ◽  
Metabolic Disorders ◽  
Energy Homeostasis ◽  
Cold Stimulation ◽  
Obesity And Diabetes ◽  
Brown Adipose ◽  
Pka Pathway

Identification of key regulators of energy homeostasis holds important therapeutic promise for metabolic disorders, such as obesity and diabetes. ACE2 cleaves angiotensin II (Ang II) to generate Ang-(1-7) which acts mainly through the Mas1 receptor. Here, we identify ACE2 pathway as a critical regulator in the maintenance of thermogenesis and energy expenditure. We found that ACE2 is highly expressed in brown adipose tissue (BAT) and that cold stimulation increases ACE2 and Ang-(1-7) levels in BAT and serum. Ace2 knockout mice (Ace2-/y) and Mas1 knockout mice (Mas1-/-) displayed impaired thermogenesis. Mice transplanted with brown adipose tissue from Mas1-/- display metabolic abnormalities consistent with those seen in the Ace2 and Mas1 knockout mice. In contrast, impaired thermogenesis of Leprdb/db obese diabetic mice and high-fat diet-induced obese mice were ameliorated by overexpression of Ace2 or continuous infusion of Ang-(1-7). Activation of ACE2 pathway was associated with improvement of metabolic parameters, including blood glucose, lipids and energy expenditure in multiple animal models. Consistently, ACE2 pathway remarkably enhanced the browning of white adipose tissue. Mechanistically, we showed that ACE2 pathway activated Akt/FoxO1 and PKA pathway, leading to induction of UCP1 and activation of mitochondrial function. Our data propose that adaptive thermogenesis requires regulation of ACE2 pathway and highlight novel potential therapeutic targets for the treatment of metabolic disorders.

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