Differential Regulation of Mouse Uncoupling Proteins among Brown Adipose Tissue, White Adipose Tissue, and Skeletal Muscle in Chronic β3Adrenergic Receptor Agonist Treatment

1998 ◽  
Vol 253 (1) ◽  
pp. 85-91 ◽  
Author(s):  
Hideki Yoshitomi ◽  
Kazuto Yamazaki ◽  
Shinya Abe ◽  
Isao Tanaka
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
White Adipose Tissue ◽  
Receptor Agonist ◽  
Differential Regulation ◽  
Uncoupling Proteins ◽  
Brown Adipose

Upregulation of uncoupling proteins by oral administration of capsiate, a nonpungent capsaicin analog

2003 ◽  
Vol 95 (6) ◽  
pp. 2408-2415 ◽  
Author(s):  
Yoriko Masuda ◽  
Satoshi Haramizu ◽  
Kasumi Oki ◽  
Koichiro Ohnuki ◽  
Tatsuo Watanabe ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Body Weight ◽  
Adipose Tissue ◽  
Single Dose ◽  
Thyroid Hormones ◽  
Brown Adipose Tissue ◽  
Uncoupling Proteins ◽  
Brown Adipose ◽  
Pepper Cultivar ◽  
Ucp2 Mrna

Capsiate is a nonpungent capsaicin analog, a recently identified principle of the nonpungent red pepper cultivar CH-19 Sweet. In the present study, we report that 2-wk treatment of capsiate increased metabolic rate and promoted fat oxidation at rest, suggesting that capsiate may prevent obesity. To explain these effects, at least in part, we examined uncoupling proteins (UCPs) and thyroid hormones. UCPs and thyroid hormones play important roles in energy expenditure, the maintenance of body weight, and thermoregulation. Two-week treatment of capsiate increased the levels of UCP1 protein and mRNA in brown adipose tissue and UCP2 mRNA in white adipose tissue. This dose of capsiate did not change serum triiodothyronine or thyroxine levels. A single dose of capsiate temporarily raised both UCP1 mRNA in brown adipose tissue and UCP3 mRNA in skeletal muscle. These results suggest that UCP1 and UCP2 may contribute to the promotion of energy metabolism by capsiate, but that thyroid hormones do not.

scholarly journals Effect of diabetes and fasting on GLUT-4 (muscle/fat) glucose-transporter expression in insulin-sensitive tissues. Heterogeneous response in heart, red and white muscle

1992 ◽  
Vol 282 (3) ◽  
pp. 765-772 ◽  
Author(s):  
M Camps ◽  
A Castelló ◽  
P Muñoz ◽  
M Monfar ◽  
X Testar ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
White Adipose Tissue ◽  
White Muscle ◽  
Glucose Transporter ◽  
Mrna Levels ◽  
Glut 4 ◽  
Brown Adipose ◽  
Red Muscle

1. GLUT-4 glucose-transporter protein and mRNA levels were assessed in heart, red muscle and white muscle, as well as in brown and white adipose tissue from 7-day streptozotocin-induced diabetic and 48 h-fasted rats. 2. In agreement with previous data, white adipose tissue showed a substantial decrease in GLUT-4 mRNA and protein levels in response to both diabetes and fasting. Similarly, GLUT-4 mRNA and protein markedly decreased in brown adipose tissue in both insulinopenic conditions. 3. Under control conditions, the level of expression of GLUT-4 protein content differed substantially in heart, red and white skeletal muscle. Thus GLUT-4 protein was maximal in heart, and red muscle had a greater GLUT-4 content compared with white muscle. In spite of the large differences in GLUT-4 protein content, GLUT-4 mRNA levels were equivalent in heart and red skeletal muscle. 4. In heart, GLUT-4 mRNA decreased to a greater extent than GLUT-4 protein in response to diabetes and fasting. In contrast, red muscle showed a greater decrease in GLUT-4 protein than in mRNA in response to diabetes or fasting, and in fact no decrease in GLUT-4 mRNA content was detectable in fasting. On the other hand, preparations of white skeletal muscle showed a substantial increase in GLUT-4 mRNA under both insulinopenic conditions, and that was concomitant to either a modest decrease in GLUT-4 protein in diabetes or to no change in fasting. 5. These results indicate that (a) the effects of diabetes and fasting are almost identical and lead to changes in GLUT-4 expression that are tissue-specific, (b) white adipose tissue, brown adipose tissue and heart respond similarly to insulin deficiency by decreasing GLUT-4 mRNA to a larger extent than GLUT-4 protein, and (c) red and white skeletal muscle respond to insulinopenic conditions in a heterogeneous manner which is characterized by enhanced GLUT-4 mRNA/protein ratios.

scholarly journals Apelin, an APJ Receptor Ligand, Regulates Body Adiposity and Favors the Messenger Ribonucleic Acid Expression of Uncoupling Proteins in Mice

Endocrinology ◽  
2007 ◽  
Vol 148 (6) ◽  
pp. 2690-2697 ◽  
Author(s):  
Keiko Higuchi ◽  
Takayuki Masaki ◽  
Koro Gotoh ◽  
Seiichi Chiba ◽  
Isao Katsuragi ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Energy Expenditure ◽  
White Adipose Tissue ◽  
Adiponectin Level ◽  
Serum Levels ◽  
Uncoupling Proteins ◽  
Obese Mice ◽  
Body Adiposity ◽  
Brown Adipose

Apelin, the endogenous ligand of the APJ receptor, has been identified in a variety of tissues, including stomach, heart, skeletal muscle, and white adipose tissue. We sought to clarify the effects of apelin on body adiposity and the expression of uncoupling proteins (UCPs) in C57BL/6 mice. Treatment with ip apelin at a dose of 0.1 μmol/kg·d for 14 d decreased the weight of white adipose tissue and serum levels of insulin and triglycerides, compared with controls, without influencing food intake. Apelin treatment also decreased body adiposity and serum levels of insulin and triglycerides in obese mice fed a high-fat diet. Apelin increased the serum adiponectin level and decreased that of leptin. Additionally, apelin treatment increased mRNA expression of UCP1, a marker of peripheral energy expenditure, in brown adipose tissue (BAT) and of UCP3, a regulator of fatty acid export, in skeletal muscle. In addition, immunoblot bands and relative densities of UCP1 content in BAT were also higher in the apelin group than controls. Furthermore, apelin treatment increased body temperature and O2 consumption and decreased the respiratory quotient. In conclusion, apelin appears to regulate adiposity and lipid metabolism in both lean and obese mice. In addition, apelin regulates insulin resistance by influencing the circulating adiponectin level, the expression of BAT UCP1, and energy expenditure in mice.

scholarly journals Impact of thermogenesis induced by chronic β3-adrenergic receptor agonist treatment on inflammatory and infectious response during bacteremia in mice

PLoS ONE ◽  
2021 ◽  
Vol 16 (8) ◽  
pp. e0256768
Author(s):  
Patrick Munro ◽  
Samah Rekima ◽  
Agnès Loubat ◽  
Christophe Duranton ◽  
Didier F. Pisani ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Adrenergic Receptor ◽  
Receptor Agonist ◽  
Acute Infection ◽  
Immunomodulatory Activity ◽  
Inflammatory Parameters ◽  
Brown Adipose ◽  
Thermogenic Adipocytes ◽  
Adrenergic Receptor Agonist

White adipocytes store energy differently than brown and brite adipocytes which dissipate energy under the form of heat. Studies have shown that adipocytes are able to respond to bacteria thanks to the presence of Toll-like receptors at their surface. Despite this, little is known about the involvement of each class of adipocytes in the infectious response. We treated mice for one week with a β3-adrenergic receptor agonist to induce activation of brown adipose tissue and brite adipocytes within white adipose tissue. Mice were then injected intraperitoneally with E. coli to generate acute infection. The metabolic, infectious and inflammatory parameters of the mice were analysed during 48 hours after infection. Our results shown that in response to bacteria, thermogenic activity promoted a discrete and local anti-inflammatory environment in white adipose tissue characterized by the increase of the IL-1RA secretion. More generally, activation of brown and brite adipocytes did not modify the host response to infection including no additive effect with fever and an equivalent bacteria clearance and inflammatory response. In conclusion, these results suggest an IL-1RA-mediated immunomodulatory activity of thermogenic adipocytes in response to acute bacterial infection and open a way to characterize their effect along more chronic infection as septicaemia.

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