scholarly journals Effect of acute cold exposure on uncoupling protein gene expression in brown adipose tissue of monosodium-L-glutamate-induced obese mice.

1993 ◽  
Vol 61 ◽  
pp. 137
Author(s):  
Fujiko Tsukahara ◽  
Yoko Uchida ◽  
Teruko Nomoto ◽  
Takamura Muraki
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
Protein Gene ◽  
Uncoupling Protein ◽  
Obese Mice ◽  
Acute Cold Exposure ◽  
Brown Adipose ◽  
Uncoupling Protein Gene

scholarly journals Blunted Expression of PPARa in Mice with FABP-4 and -5 Deficiency under Acute Cold Exposure

2017 ◽  
Vol 3 (6) ◽  
pp. 443
Author(s):  
Mas Rizky A.A Syamsunarno ◽  
Mirasari Putri ◽  
Tatsuya Iso ◽  
Rini Widyastuti ◽  
Ramdan Panigoro ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
Uncoupling Protein ◽  
Nuclear Hormone Receptor ◽  
Fatty Acid Binding ◽  
Acute Cold Exposure ◽  
Brown Adipose

Brown Adipose Tissue (BAT) is a nonshivering thermogenesis organ during cold exposure. Peroxisomal proliferator activated receptor alpha (PPARa) is the member of the nuclear hormone receptor superfamily and primarily expressed in BAT and liver. PPARa is coordinated with uncoupling protein 1 (UCP1) to regulate fatty acid metabolism in BAT. Fatty acid binding protein (FABP)-4 and-5 play role in adaptive response under fasting and cold exposure. The purpose of this study was to investigate the expression of PPARa in mice with FABP4/5 deficiency (DKO). Wildtype (WT) and DKO mice were exposed to cold for 2 hours under fed or 20 hours-fasted conditions. BAT was collected and further mRNA level of PPARa was examined using quantitative real-time PCR. As the result, PPARa gene expression in WT mice were increased 50% and 100% in fed and fasted condition respectively after cold exposure. There was no alteration in PPARa expression in  BAT of DKO mice. As conclusion, The functional FABP-4 and -5 are necessary to modulate PPARa gene expression in Brown Adipose Tissue under acute cold exposure  Keywords: Acute cold exposure; FABP4; FABP5; Fasting  PPARa

scholarly journals PACAP is essential for the adaptive thermogenic response of brown adipose tissue to cold exposure

2014 ◽  
Vol 222 (3) ◽  
pp. 327-339 ◽  
Author(s):  
Abdoulaye Diané ◽  
Nikolina Nikolic ◽  
Alexander P Rudecki ◽  
Shannon M King ◽  
Drew J Bowie ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Metabolic Rate ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
Molecular Mechanisms ◽  
Uncoupling Protein ◽  
Morphological Properties ◽  
Brown Adipose ◽  
Thermogenic Response

Pituitary adenylate cyclase-activating polypeptide (PACAP) is a widely distributed neuropeptide that acts as a neurotransmitter, neuromodulator, neurotropic factor, neuroprotectant, secretagogue,and neurohormone. Owing to its pleiotropic biological actions, knockout ofPacap(Adcyap1) has been shown to induce several abnormalities in mice such as impaired thermoregulation. However, the underlying physiological and molecular mechanisms remain unclear. A previous report has shown that cold-exposedPacapnull mice cannot supply appropriate levels of norepinephrine (NE) to brown adipocytes. Therefore, we hypothesized that exogenous NE would rescue the impaired thermogenic response ofPacapnull mice during cold exposure. We compared the adaptive thermogenic capacity ofPacap−/−toPacap+/+mice in response to NE when housed at room temperature (24 °C) and after a 3.5-week cold exposure (4 °C). Biochemical parameters, expression of thermogenic genes, and morphological properties of brown adipose tissue (BAT) and white adipose tissue (WAT) were also characterized. Results showed that there was a significant effect of temperature, but no effect of genotype, on the resting metabolic rate in conscious, unrestrained mice. However, the normal cold-induced increase in the basal metabolic rate and NE-induced increase in thermogenesis were severely blunted in cold-exposedPacap−/−mice. These changes were associated with altered substrate utilization, reduced β3-adrenergic receptor (β3-Ar(Adrb3)) and hormone-sensitive lipase (Hsl(Lipe)) gene expression, and increased fibroblast growth factor 2 (Fgf2) gene expression in BAT. Interestingly,Pacap−/−mice had depleted WAT depots, associated with upregulated uncoupling protein 1 expression in inguinal WATs. These results suggest that the impairment of adaptive thermogenesis inPacapnull mice cannot be rescued by exogenous NE perhaps in part due to decreased β3-Ar-mediated BAT activation.

Acute Cold Exposure Stimulates Uncoupling Protein Synthesis in Brown Adipose Tissue in Lean, but not Fatty Zucker Rats

1996 ◽  
Vol 90 (s34) ◽  
pp. 16P-17P
Author(s):  
C Bing ◽  
L Pickavance ◽  
J S Keith ◽  
H M Frankish ◽  
Q Wang ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
Uncoupling Protein ◽  
Zucker Rats ◽  
Acute Cold Exposure ◽  
Brown Adipose

Characterization and regulation of cold-induced heat shock protein expression in mouse brown adipose tissue

1995 ◽  
Vol 269 (1) ◽  
pp. R38-R47 ◽  
Author(s):  
J. M. Matz ◽  
M. J. Blake ◽  
H. M. Tatelman ◽  
K. P. Lavoi ◽  
N. J. Holbrook
Keyword(s):  
Adipose Tissue ◽  
Heat Shock ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
Elevated Temperatures ◽  
Uncoupling Protein ◽  
Hsp70 Expression ◽  
Mitochondrial Uncoupling ◽  
Ambient Temperatures ◽  
Brown Adipose

The accumulation of heat shock proteins (HSPs) after the exposure of cells or organisms to elevated temperatures is well established. It is also known that a variety of other environmental and cellular metabolic stressors can induce HSP synthesis. However, few studies have investigated the effect of cold temperature on HSP expression. Here we report that exposure of Institute of Cancer Research (ICR) mice to cold ambient temperatures results in a tissue-selective induction of HSPs in brown adipose tissue (BAT) coincident with the induction of mitochondrial uncoupling protein synthesis. Cold-induced HSP expression is associated with enhanced binding of heat shock transcription factors to DNA, similar to that which occurs after exposure of cells or tissues to heat and other metabolic stresses. Adrenergic receptor antagonists were found to block cold-induced HSP70 expression in BAT, whereas adrenergic agonists induced BAT HSP expression in the absence of cold exposure. These findings suggest that norepinephrine, released in response to cold exposure, induces HSP expression in BAT. Norepinephrine appears to initiate transcription of HSP genes after binding to BAT adrenergic receptors through, as yet, undetermined signal transduction pathways. Thermogenesis results from an increase in activity and synthesis of several metabolic enzymes in BAT of animals exposed to cold challenge. The concomitant increase in HSPs may function to facilitate the translocation and activity of the enzymes involved in this process.

The development of insulin resistance in brown adipose tissue may impair the acute cold-induced activation of thermogenesis in genetically obese (ob/ob) mice

1984 ◽  
Vol 4 (11) ◽  
pp. 933-940 ◽  
Author(s):  
Stewart W. Mercer ◽  
Paul Trayhurn
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
Brown Fat ◽  
Acute Cold Exposure ◽  
Brown Adipose

Genetically obese (ob/ob) mice develop insulin resistance in brown adipose tissue during the fifth week of life. Prior to this, at 26 days of age, oh/oh mice show a substantial increase in GDP binding to brownadipose-tissue mitochondria during acute cold exposure. When insulin resistance in brown fat develops, by 35 days of age, the increase in GDP binding in response to cold is markedly reduced. Studies with 2-deoxyglucose suggest that insulin resistance in brown adipose tissue could impair thermogenic responsiveness during acute cold exposure by limiting the ability of the tissue to take up glucose.

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