Differential Regulation of Uncoupling Protein-2 and Uncoupling Protein-3 Gene Expression in Brown Adipose Tissue during Development and Cold Exposure

1998 ◽  
Vol 243 (1) ◽  
pp. 224-228 ◽  
Author(s):  
M.Carmen Carmona ◽  
Angel Valmaseda ◽  
Sonia Brun ◽  
Octavi Viñas ◽  
Teresa Mampel ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
Uncoupling Protein ◽  
Differential Regulation ◽  
Uncoupling Protein 2 ◽  
Uncoupling Protein 3 ◽  
Brown Adipose

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.

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

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.

Absence of uncoupling protein 3 at thermoneutrality influences brown adipose tissue mitochondrial functionality in mice

2020 ◽  
Vol 34 (11) ◽  
pp. 15146-15163
Author(s):  
Elena Silvestri ◽  
Rosalba Senese ◽  
Rita De Matteis ◽  
Federica Cioffi ◽  
Maria Moreno ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Uncoupling Protein ◽  
Uncoupling Protein 3 ◽  
Brown Adipose

scholarly journals Postnatal selective suppression of lipoprotein lipase gene expression in brown adipose tissue (relative to the expression of the gene for the uncoupling protein) is not due to adrenergic insensitivity: a possible specific inhibitory effect of colostrum

1996 ◽  
Vol 314 (1) ◽  
pp. 261-267 ◽  
Author(s):  
María-Jesus OBREGÓN ◽  
Barbara CANNON ◽  
Jan NEDERGAARD
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Lipoprotein Lipase ◽  
Uncoupling Protein ◽  
Mrna Levels ◽  
Selective Suppression ◽  
Brown Adipose ◽  
Adrenergic Antagonist ◽  
Lpl Gene

The levels of mRNA coding for the uncoupling protein (UCP) and for lipoprotein lipase (LPL) were monitored in the brown adipose tissue of newborn rat pups. At 5 h after birth, the mRNA levels of UCP and LPL were high in pups exposed singly to 28 °C and low in pups kept singly at thermoneutrality (36 °C); in pups staying with the dam, the UCP mRNA levels were intermediate. However, the LPL mRNA levels were lower in pups staying with the dam than in pups at 36 °C, implying that factors additional to environmental temperature influenced LPL gene expression. Injection of noradrenaline into pups at thermoneutrality (36 °C) led to increases in UCP and LPL gene expression, but noradrenaline injections had no further effect in cold-exposed pups. The adrenergic effects were mediated via β-adrenergic receptors. The cold-induced increases in both UCP and LPL gene expression were abolished by the β-adrenergic antagonist propranolol. Thus differences in adrenergic responsiveness could not explain the differential expression of the UCP and LPL genes observed in pups staying with the dam. The presence of a physiological suppressor was examined by feeding single pups at 28 °C with different foods: nothing, water, Intralipid, cow's milk, rat milk and rat colostrum. None of these agents led to suppression of UCP gene expression, but colostrum led to a selective suppression of LPL gene expression. It was concluded that the genes for UCP and LPL were responsive to adrenergic stimuli immediately after birth, and it is suggested that a component of rat colostrum can selectively suppress LPL gene expression.

scholarly journals ChREBP-β regulates thermogenesis in brown adipose tissue

2020 ◽  
Vol 245 (3) ◽  
pp. 343-356 ◽  
Author(s):  
Chunchun Wei ◽  
Xianhua Ma ◽  
Kai Su ◽  
Shasha Qi ◽  
Yuangang Zhu ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
Uncoupling Protein ◽  
Critical Role ◽  
Active Form ◽  
Negative Regulator ◽  
Mrna Levels ◽  
Brown Adipose ◽  
Metabolic Remodeling

Brown adipose tissue (BAT) plays a critical role in energy expenditure by uncoupling protein 1 (UCP1)-mediated thermogenesis. Carbohydrate response element-binding protein (ChREBP) is one of the key transcription factors regulating de novo lipogenesis (DNL). As a constitutively active form, ChREBP-β is expressed at extremely low levels. Up to date, its functional relevance in BAT remains unclear. In this study, we show that ChREBP-β inhibits BAT thermogenesis. BAT ChREBP-β mRNA levels were elevated upon cold exposure, which prompted us to generate a mouse model overexpressing ChREBP-β specifically in BAT using the Cre/LoxP approach. ChREBP-β overexpression led to a whitening phenotype of BAT at room temperature, as evidenced by increased lipid droplet size and decreased mitochondrion content. Moreover, BAT thermogenesis was inhibited upon acute cold exposure, and its metabolic remodeling induced by long-term cold adaptation was significantly impaired by ChREBP-β overexpression. Mechanistically, ChREBP-β overexpression downregulated expression of genes involved in mitochondrial biogenesis, autophagy, and respiration. Furthermore, thermogenic gene expression (e.g. Dio2, UCP1) was markedly inhibited in BAT by the overexpressed ChREBP-β. Put together, our work points to ChREBP-β as a negative regulator of thermogenesis in brown adipocytes.

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