scholarly journals Adaptative decrease in expression of the mRNA for uncoupling protein and subunit II of cytochrome c oxidase in rat brown adipose tissue during pregnancy and lactation

1989 ◽  
Vol 263 (3) ◽  
pp. 965-968 ◽  
Author(s):  
I Martin ◽  
M Giralt ◽  
O Viñas ◽  
R Iglesias ◽  
T Mampel ◽  
...  

Uncoupling-protein (UCP) mRNA expression is decreased to 15% of virgin control levels between days 10 and 15 of pregnancy, and remains at these low values during late pregnancy and lactation. Abrupt weaning of mid-lactating rats causes a slight but significant increase in UCP mRNA. Expression of mRNA for subunit II of cytochrome c oxidase (COII) decreased to half that of virgin control in late pregnancy and during lactation. Whereas COII mRNA expression is in step with the known modifications of brown-fat mitochondria content during the breeding cycle of the rat, UCP mRNA expression appears to be diminished much earlier than the mitochondrial proton-conductance-pathway activity. On the other hand, the reactivity of brown fat to increase expression of UCP and COII mRNAs in response to acute cold or noradrenaline treatment is not impaired during lactation.

1988 ◽  
Vol 255 (2) ◽  
pp. 457-461 ◽  
Author(s):  
O Viñas ◽  
M Giralt ◽  
M J Obregón ◽  
R Iglesias ◽  
F Villarroya ◽  
...  

Brown adipose tissue iodothyronine 5′-deiodinase activity is significantly lower in 17-day pregnant rats compared with virgin controls and remains low during late pregnancy and lactation. It fully recovers with abrupt weaning, but only partially with spontaneous weaning. Even though this profile of changes is remarkably in step with the known pattern of modifications in brown fat thermogenesis during the breeding cycle, the lowered iodothyronine 5′-deiodinase activity appearing between days 15 and 17 of pregnancy occurs earlier than the reduction in brown adipose tissue thermogenesis. Brown fat 3,3′,5-tri-iodothyronine content is also reduced in late pregnant, early and mid-lactating rats, most probably as a consequence of the lowered 5′-deiodination of thyroxine in situ. Acute insulin treatment increases brown fat iodothyronine 5′-deiodinase activity in virgin animals as well as in late-pregnant and lactating rats, despite the lowered basal enzyme activity levels in the latter groups. Thus an impaired response to insulin in brown fat does not appear to be a factor leading to the lowered iodothyronine 5′-deiodinase activity during late pregnancy and lactation.


1995 ◽  
Vol 308 (3) ◽  
pp. 749-752 ◽  
Author(s):  
I Martin ◽  
M Giralt ◽  
O Viñas ◽  
R Iglesias ◽  
T Mampel ◽  
...  

The relative abundance of the mitochondrial-encoded mRNAs for cytochrome c oxidase subunit II and NADH dehydrogenase subunit I was lower in brown adipose tissue (BAT) from lactating rats than in virgin controls. This decrease was in parallel with a significant decrease in mitochondrial 16 S rRNA levels and in the relative content of mitochondrial DNA in the tissue. BAT from lactating rats showed lowered mRNA expression of the nuclear-encoded genes for the mitochondrial uncoupling protein, subunit IV of cytochrome c oxidase and the adenine nucleotide translocase isoforms ANT1 and ANT2, whereas mRNA levels for the ATP synthase beta-subunit were unchanged. However, the relative content of this last protein was lower in BAT mitochondria from lactating rats than in virgin controls. It is concluded that lactation-induced mitochondrial hypotrophy in BAT is associated with a co-ordinate decrease in the expression of the mitochondrial genome and nuclear genes for mitochondrial proteins. This decrease is caused by regulatory events acting at different levels, including pre- and post-transcriptional regulation. BAT appears to be a useful model with which to investigate the molecular mechanisms involved in the co-ordination of the expression of the mitochondrial and nuclear genomes during mitochondrial biogenesis.


2010 ◽  
Vol 105 (3) ◽  
pp. 329-338 ◽  
Author(s):  
Alannah D. Maurer ◽  
Raylene A. Reimer

Risk of developing the metabolic syndrome may be influenced by nutritional environment early in life. We examined the effects of high-fibre (HF) and high-protein (HP) diets consumed during pregnancy and lactation on satiety hormones and expression of genes involved in glucose and lipid metabolism in offspring. Wistar dams were fed a control (C), HF or HP diets during pregnancy and lactation. At parturition, litters were culled to ten pups. At 21 d, all pups were weaned onto C diet. At 7, 14, 21, 28 and 35 d after birth, blood was analysed for satiety hormones and tissues for mRNA expression in offspring. No differences were observed in litter size or birth weight. At 21 d, offspring of HF dams had greater adjusted intestinal mass and lower liver weight than those of C but not of HP dams. Plasma glucose at 28 d and amylin at 7, 14 and 28 d were lower in HF v. C and HP offspring. Glucagon-like peptide-1 was higher in HP offspring than in HF offspring at 7 d but was higher in HF v. C offspring at 21 d. Offspring of HF dams had higher glucose transporter (GLUT2 and Na+-dependent glucose/galactose transporter) mRNA expression at 21 d v. C and HP offspring. In brown adipose tissue, HF and HP up-regulated uncoupling protein-1 and PPAR-γ coactivator. HP was associated with increased resistin and IL-6 mRNA expression. The present study demonstrates that maternal diet composition differentially regulates circulating satiety hormones and genes involved in glucose transport and energy metabolism in offspring. These early changes could have long-term consequences for obesity risk.


Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1686
Author(s):  
Yukari Yamashita ◽  
Tamaki Takeuchi ◽  
Yuki Endo ◽  
Ayumi Goto ◽  
Setsuko Sakaki ◽  
...  

We investigated the effect of evodiamine-containing microalga Dunaliella tertiolecta (DT) on the prevention of diet-induced obesity in a thermoneutral C57BL/6J male (30 °C). It attenuates the activity of brown adipose tissue (BAT), which accelerates diet-induced obesity. Nine-week-old mice were fed a high-fat diet supplemented with 10 g (Low group) or 25 g (High group) DT powder per kg food for 12 weeks. Compared to control mice without DT supplementation, body weight gain was significantly reduced in the High group with no difference in food intake. Tissue analyses indicated maintenance of multilocular morphology in BAT and reduced fat deposition in liver in DT-supplemented mice. Molecular analysis showed a significant decrease in mammalian target of rapamycin−ribosomal S6 protein kinase signaling pathway in white adipose tissue and upregulation in mRNA expression of brown fat-associated genes including fibroblast growth factor-21 (Fgf21) and uncoupling protein 1 (Ucp1) in BAT in the High group compared to the control. In the experiments using C3H10T1/2 adipocytes, DT extract upregulated mRNA expression of brown fat-associated genes in dose-dependent and time-dependent manners, accompanied by a significant increase in secreted FGF21 levels. Our data show the ability of DT as a nutraceutical to prevent brown fat attenuation and diet-induced obesity in vivo.


1989 ◽  
Vol 257 (3) ◽  
pp. 665-671 ◽  
Author(s):  
L Casteilla ◽  
O Champigny ◽  
F Bouillaud ◽  
J Robelin ◽  
D Ricquier

Samples of adipose tissue were obtained from different sites in bovine and ovine foetuses and newborns. RNA was isolated and analysed using bovine cDNA and ovine genomic probe for uncoupling protein (UCP), cDNA for subunits III and IV of cytochrome c oxidase and cDNA for ADP/ATP carrier. UCP mRNA was characterized for the first time in foetal bovine and ovine adipose tissue. It appeared later than mRNA of cytochrome c oxidase subunit III, and increased dramatically at birth (10-fold). ADP/ATP carrier mRNA was expressed at a lower level but also increased 10-fold at birth. It was demonstrated that UCP mRNA reached its highest level at birth in all bovine adipose tissues studied, except subcutaneous tissue. It disappeared quickly afterwards, being no longer detectable two days after birth. Similar variations were observed in newborn lambs. ADP/ATP carrier mRNA showed the same pattern of expression as UCP mRNA; although it was still lightly expressed two days after birth, it disappeared soon afterwards. Only mRNAs for cytochrome c oxidase subunits III and IV remained at the same level during the first postnatal week. On the basis of these data and of observations reported in the literature a sequence of events for the development of brown adipose cells in vivo is proposed. Soon after birth the perirenal adipose tissue of ruminants, which still contains mitochondria of typical brown adipose tissue morphology and high levels of cytochrome c oxidase mRNA, lacks UCP mRNA. Can it still be considered as brown fat? Ruminant species appear to be attractive models to study both the differentiation of brown adipose tissue and its possible conversion to white fat in large animals.


1987 ◽  
Vol 252 (5) ◽  
pp. R987-R993 ◽  
Author(s):  
I. Levin ◽  
P. Trayhurn

The effects of different food deprivation regimens on the thermogenic activity and capacity of brown adipose tissue in the golden hamster have been investigated. Thermogenesis in the tissue was assessed by measurements of tissue cytochrome-c oxidase activity, mitochondrial GDP binding, and the specific mitochondrial concentration of uncoupling protein. The thermogenic activity and capacity of brown adipose tissue were found to be markedly reduced in fasted or underweight hamsters. Measurements of cytochrome-c oxidase activity indicate that the reductions were caused exclusively by a loss in mitochondrial mass, uncoupling protein concentration and GDP binding to mitochondria remaining unchanged. The decrease in brown adipose tissue thermogenesis was associated with a reduction in the capacity for nonshivering thermogenesis in the whole animal. Hamsters recovered from weight losses without increasing their food intake, and the recovery was accompanied by a normalization in mitochondrial mass in brown adipose tissue. Mitochondrial mass was, however, restored only after 10 days of ad libitum refeeding. These results suggest that the reduction in energy expenditure in the fasted hamster could relate to a decrease in brown adipose tissue thermogenesis, in addition to the previously reported decreases in resting metabolic rate and locomotor activity. Reductions in thermogenesis may also represent a further mechanism by which energy stores recover in the golden hamster without postfast hyperphagia.


1985 ◽  
Vol 248 (3) ◽  
pp. C365-C371 ◽  
Author(s):  
J. Nedergaard ◽  
B. Cannon

Brown fat mitochondria were isolated from cold-exposed and control rats, and their content of the brown-fat-specific 32-kDa “uncoupling” protein thermogenin determined both by the traditional [3H]GDP-binding method and by the recently developed enzyme-linked immunosorbent assay (ELISA). In mitochondria isolated from both cold-acclimated (3 wk at 4 degrees C) and cold-exposed rats (24 h), an increase in thermogenin content was observable, both when estimated by the [3H]GDP-binding method and by the ELISA assay, and there was no statistically significant difference in the magnitude of these increases in the two methods. In 1 h cold-exposed rats there was no increase in [3H]GDP binding or in the ELISA reaction. When the amount of thermogenin was plotted against [3H]GDP binding in the different states, a relationship of 75,000 g thermogenin per mole GDP bound was obtained. Based on the resolution of these two methods, and under the three conditions investigated, it was concluded that there was no reason to postulate the existence of a “masked” form of thermogenin or of an “unmasking” process and that thermogenin in the mitochondria, as in the isolated state, has apparently one GDP binding site per dimer.


1994 ◽  
Vol 72 (1-2) ◽  
pp. 1-7 ◽  
Author(s):  
M. Desautels ◽  
R. A. Dulos

When a membrane suspension prepared from isolated rat brown fat mitochondria was incubated at 37 °C for 4 h, a loss of uncoupling protein (UCP) immunoreactivity was observed on Western blots. Analysis of [3H]GDP-binding characteristics to UCP in isolated membranes also showed a significant reduction in Bmax without significant effect on Kd. The loss of UCP was not due to protease contamination from lysosomes or mast cell granules, since loss of UCP was still observed when mitochondria were treated with digitonin to lyse lysosomes prior to membrane preparation and when mitochondria were isolated from rats injected with compound 48/80 to degranulate mast cells. Furthermore, loss of UCP was observed at alkaline pH and was not affected by inhibitors of lysosomal enzymes. Loss of UCP immunoreactivity was markedly reduced when membranes were incubated at 4 °C or in the presence of phenylmethylsulfonyl fluoride, but was not influenced by the addition of GDP. Overall, these results indicate the presence of a serine protease within brown fat mitochondrial membranes that may be involved in the breakdown of UCP.Key words: thermoregulation, body weight, mitochondria, uncoupling protein, protein degradation, protease.


1981 ◽  
Vol 241 (3) ◽  
pp. C134-C139 ◽  
Author(s):  
U. Sundin

Reports on a reciprocal relationship between sympathetic-nerve and experimentally induced changes in thyroid-hormone activity called into question the proposed role of thyroxine in the changes seen in the brown fat after cold adaptation. Rats reared at +30, +22, and +5 degrees C received daily injections of thyroxine (1 mg/kg). After 3 wk of treatment, the thermogenic state of the tissue was assessed by measuring the capacity of the brown fat mitochondria to bind guanosine 5'-diphosphate (GDP). GDP-inhibited mitochondrial swelling, brown adipose tissue (BAT) wet weights, and mitochondrial yields were also measured. The control animals showed a linear increase in GDP binding between +30 and +5 degrees C. Thyroxine was found to lower the GDP binding markedly at +5 degrees C, less so at +22 degrees C, while no effect was evident at +30 degrees C. The values at +22 and +30 degrees C were identical. The other parameters studied all confirmed these results. The conclusion made is that the thyroxine-induced rise in basal metabolic rate lowers the critical temperature and reduces the demand for nonshivering thermogenesis. This is reflected in the reduced GDP binding and hence heating capacity of the brown fat mitochondria.


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