Neuronal regulation of substrate cycle between glucose 6-phosphate and glucose in brown adipose tissues of cold-exposed mice

1990 ◽  
Vol 226 (3) ◽  
pp. 314-319 ◽  
Author(s):  
Hiroshi Suzuki ◽  
Jun Watanabe ◽  
Tsuyoshi Itani ◽  
Ryokei Ogawa ◽  
Shinsuke Kanamura
Keyword(s):  
Adipose Tissues ◽  
Brown Adipose ◽  
Neuronal Regulation

scholarly journals Reduced Expression of Urokinase Plasminogen Activator in Brown Adipose Tissue of Obese Mouse Models

2021 ◽  
Vol 22 (7) ◽  
pp. 3407
Author(s):  
Chung-Ze Wu ◽  
Li-Chien Chang ◽  
Chao-Wen Cheng ◽  
Te-Chao Fang ◽  
Yuh-Feng Lin ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Glomerular Filtration Rate ◽  
Brown Adipose Tissue ◽  
Glomerular Filtration ◽  
Plasminogen Activator ◽  
Mouse Models ◽  
Filtration Rate ◽  
Obese Mouse ◽  
Adipose Tissues ◽  
Brown Adipose

In recent decades, the obesity epidemic has resulted in morbidity and mortality rates increasing globally. In this study, using obese mouse models, we investigated the relationship among urokinase plasminogen activator (uPA), metabolic disorders, glomerular filtration rate, and adipose tissues. Two groups, each comprised of C57BL/6J and BALB/c male mice, were fed a chow diet (CD) and a high fat diet (HFD), respectively. Within the two HFD groups, half of each group were euthanized at 8 weeks (W8) or 16 weeks (W16). Blood, urine and adipose tissues were collected and harvested for evaluation of the effects of obesity. In both mouse models, triglyceride with insulin resistance and body weight increased with duration when fed a HFD in comparison to those in the groups on a CD. In both C57BL/6J and BALB/c HFD mice, levels of serum uPA initially increased significantly in the W8 group, and then the increment decreased in the W16 group. The glomerular filtration rate declined in both HFD groups. The expression of uPA significantly decreased in brown adipose tissue (BAT), but not in white adipose tissue, when compared with that in the CD group. The results suggest a decline in the expression of uPA in BAT in obese m models as the serum uPA increases. There is possibly an association with BAT fibrosis and dysfunction, which may need further study.

scholarly journals Feedback looping between ChREBP and PPAR^|^alpha; in the regulation of lipid metabolism in brown adipose tissues

2013 ◽  
Vol 60 (10) ◽  
pp. 1145-1153 ◽  
Author(s):  
Katsumi Iizuka ◽  
Wudelehu Wu ◽  
Yukio Horikawa ◽  
Masayuki Saito ◽  
Jun Takeda
Keyword(s):  
Lipid Metabolism ◽  
Ppar Alpha ◽  
Adipose Tissues ◽  
Brown Adipose

Transport of fatty acids and monoacylglycerols in white and brown adipose tissues

1991 ◽  
Vol 27 (3-4) ◽  
pp. 487-491 ◽  
Author(s):  
Robert O. Scow ◽  
E.Joan Blanchette-Mackie
Keyword(s):  
Fatty Acids ◽  
Adipose Tissues ◽  
Brown Adipose

scholarly journals Metabolic inflexibility of white and brown adipose tissues in abnormal fatty acid partitioning of type 2 diabetes

2012 ◽  
Vol 2 (S2) ◽  
pp. S37-S42 ◽  
Author(s):  
T Grenier-Larouche ◽  
S M Labbé ◽  
C Noll ◽  
D Richard ◽  
A C Carpentier
Keyword(s):  
Type 2 Diabetes ◽  
Fatty Acid ◽  
Adipose Tissues ◽  
Brown Adipose ◽  
Metabolic Inflexibility

scholarly journals ASKA technology-based pull-down method reveals a suppressive effect of ASK1 on the inflammatory NOD-RIPK2 pathway in brown adipocytes

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Saki Takayanagi ◽  
Kengo Watanabe ◽  
Takeshi Maruyama ◽  
Motoyuki Ogawa ◽  
Kazuhiro Morishita ◽  
...  
Keyword(s):  
Uncoupling Protein ◽  
Biological Significance ◽  
Suppressive Effect ◽  
Brown Adipocyte ◽  
Brown Adipocytes ◽  
Adipose Tissues ◽  
Signaling Complex ◽  
Brown Adipose ◽  
Immune Pathway

AbstractRecent studies have shown that adipose tissue is an immunological organ. While inflammation in energy-storing white adipose tissues has been the focus of intense research, the regulatory mechanisms of inflammation in heat-producing brown adipose tissues remain largely unknown. We previously identified apoptosis signal-regulating kinase 1 (ASK1) as a critical regulator of brown adipocyte maturation; the PKA-ASK1-p38 axis facilitates uncoupling protein 1 (UCP1) induction cell-autonomously. Here, we show that ASK1 suppresses an innate immune pathway and contributes to maintenance of brown adipocytes. We report a novel chemical pull-down method for endogenous kinases using analog sensitive kinase allele (ASKA) technology and identify an ASK1 interactor in brown adipocytes, receptor-interacting serine/threonine-protein kinase 2 (RIPK2). ASK1 disrupts the RIPK2 signaling complex and inhibits the NOD-RIPK2 pathway to downregulate the production of inflammatory cytokines. As a potential biological significance, an in vitro model for intercellular regulation suggests that ASK1 facilitates the expression of UCP1 through the suppression of inflammatory cytokine production. In parallel to our previous report on the PKA-ASK1-p38 axis, our work raises the possibility of an auxiliary role of ASK1 in brown adipocyte maintenance through neutralizing the thermogenesis-suppressive effect of the NOD-RIPK2 pathway.

Integrated application of metabolomics and RNA‐seq reveals thermogenic regulation in goat brown adipose tissues

2021 ◽  
Vol 35 (9) ◽  
Author(s):  
Yan Wang ◽  
Xingyue Chen ◽  
Wenli Fan ◽  
Xujia Zhang ◽  
Siyuan Zhan ◽  
...  
Keyword(s):  
Rna Seq ◽  
Adipose Tissues ◽  
Brown Adipose

scholarly journals Treatment with atrial natriuretic peptide induces adipose tissue browning and exerts thermogenic actions in vivo

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Haruka Kimura ◽  
Tomohisa Nagoshi ◽  
Yuhei Oi ◽  
Akira Yoshii ◽  
Yoshiro Tanaka ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Hepatic Steatosis ◽  
Cold Exposure ◽  
Lipid Droplets ◽  
Adipose Tissues ◽  
Brown Adipose ◽  
Ucp1 Expression ◽  
Tissue Browning

AbstractIncreasing evidence suggests natriuretic peptides (NPs) coordinate inter-organ metabolic crosstalk with adipose tissues and play a critical role in energy metabolism. We recently reported A-type NP (ANP) raises intracellular temperature in cultured adipocytes in a low-temperature-sensitive manner. We herein investigated whether exogenous ANP-treatment exerts a significant impact on adipose tissues in vivo. Mice fed a high-fat-diet (HFD) or normal-fat-diet (NFD) for 13 weeks were treated with or without ANP infusion subcutaneously for another 3 weeks. ANP-treatment significantly ameliorated HFD-induced insulin resistance. HFD increased brown adipose tissue (BAT) cell size with the accumulation of lipid droplets (whitening), which was suppressed by ANP-treatment (re-browning). Furthermore, HFD induced enlarged lipid droplets in inguinal white adipose tissue (iWAT), crown-like structures in epididymal WAT, and hepatic steatosis, all of which were substantially attenuated by ANP-treatment. Likewise, ANP-treatment markedly increased UCP1 expression, a specific marker of BAT, in iWAT (browning). ANP also further increased UCP1 expression in BAT with NFD. Accordingly, cold tolerance test demonstrated ANP-treated mice were tolerant to cold exposure. In summary, exogenous ANP administration ameliorates HFD-induced insulin resistance by attenuating hepatic steatosis and by inducing adipose tissue browning (activation of the adipose tissue thermogenic program), leading to in vivo thermogenesis during cold exposure.

Fatty acid synthesis in adipose tissues of physically trained rats in vivo

1983 ◽  
Vol 245 (1) ◽  
pp. E8-E13
Author(s):  
K. Tokuyama ◽  
H. Okuda
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Fatty Acid Synthesis ◽  
Physical Training ◽  
Dark Period ◽  
Acid Synthesis ◽  
Free Access ◽  
Adipose Tissues ◽  
Brown Adipose

The effect of physical training on fatty acid synthesis in vivo was studied. After the rats had free access to a running wheel for 50 days, the rate of fatty acid synthesis estimated using 3H2O in adipose tissues of trained rats was about three times higher than that of sedentary rats in both the light and dark period. The rate of fatty acid synthesis in the liver but not in the brown adipose tissue was also slightly enhanced by physical training. The number of adipocytes was not affected, but the size of adipocytes was reduced by physical training. In trained rats, the rate of fatty acid synthesis in adipocytes whose diameter was similar to that of sedentary rats was about 10 times higher than that of sedentary rats. Within adipose tissue, the rate of fatty acid synthesis correlated positively to the diameter of adipocytes both in the sedentary and trained rats. These findings mean that the adaptive increase in fatty acid synthesis seen in adipocytes of trained rats is not secondary to the reduction in size of adipocytes.

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