GDP binding to rat brown fat mitochondria: effects of thyroxine at different ambient temperatures

1981 ◽  
Vol 241 (3) ◽  
pp. C134-C139 ◽  
Author(s):  
U. Sundin
Keyword(s):  
Linear Increase ◽  
Reciprocal Relationship ◽  
Brown Fat ◽  
Hormone Activity ◽  
Ambient Temperatures ◽  
Heating Capacity ◽  
Brown Adipose ◽  
Induced Changes ◽  
Brown Fat Mitochondria

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.

Influence of subdiaphragmatic vagotomy and brown fat sympathectomy on thermogenesis in rats

1985 ◽  
Vol 249 (3) ◽  
pp. E239-E243 ◽  
Author(s):  
P. L. Andrews ◽  
N. J. Rothwell ◽  
M. J. Stock
Keyword(s):  
Insulin Treatment ◽  
Brown Fat ◽  
Guanosine Diphosphate ◽  
Subdiaphragmatic Vagotomy ◽  
Brown Adipose ◽  
Adrenergic Antagonist ◽  
Brown Adipose Tissue Activity ◽  
Acute Injection ◽  
Brown Fat Mitochondria ◽  
Thermogenic Response

Infusion of rats with insulin (8 U/day via implanted minipump) for 7 days caused a 22% rise in resting oxygen consumption, which was inhibited by acute injection of the beta-adrenergic antagonist propranolol. Insulin treatment produced significant increases in brown fat mass, protein content, and total thermogenic activity (assessed from binding of guanosine diphosphate to isolated brown fat mitochondria), but these responses were inhibited by prior surgical sympathectomy of the tissue. Animals subjected to subdiaphragmatic vagotomy gained more weight than pair-fed, sham-operated controls and showed reductions in total energy expenditure, the acute thermogenic response to a meal and brown adipose tissue activity. Daily injections of insulin (1 U/day) prevented all of these effects of vagotomy. These data demonstrate that the changes in brown fat activity induced by exogenous insulin are mediated by the sympathetic nervous system and that the depressed thermogenesis and brown fat activity associated with vagotomy appear to be due to a relative insulin deficiency and can be reversed by treatment with the hormone.

scholarly journals Evidence that microtubules do not mediate opsin vesicle transport in photoreceptors.

1989 ◽  
Vol 109 (6) ◽  
pp. 3053-3062 ◽  
Author(s):  
D K Vaughan ◽  
S K Fisher ◽  
S A Bernstein ◽  
I L Hale ◽  
K A Linberg ◽  
...  
Keyword(s):  
Outer Segment ◽  
Lucifer Yellow ◽  
Lateral Displacement ◽  
Linear Increase ◽  
Rod Photoreceptor ◽  
Drug Induced ◽  
Membrane Assembly ◽  
Induced Changes ◽  
Vectorial Transport

The organization of the rod photoreceptor cytoskeleton suggests that microtubules (MTs) and F actin are important in outer segment (OS) membrane renewal. We studied the role of the cytoskeleton in this process by first quantifying OS membrane assembly in rods from explanted Xenopus eyecups with a video assay for disc morphogenesis and then determining if the rate of assembly was reduced after drug disassembly of either MTs or F actin. Membrane assembly was quantified by continuously labeling newly forming rod OS membranes with Lucifer Yellow VS (LY) and following the tagged membranes' distal displacement along the OS. LY band displacement displayed a linear increase over 16 h in culture. These cells possessed a longitudinally oriented network of ellipsoid MTs between the sites of OS protein synthesis and OS membrane assembly. Incubation of eyecups in nocodazole, colchicine, vinblastine, or podophyllotoxin disassembled the ellipsoid MTs. Despite their absence, photoreceptors maintained a normal rate of OS assembly. In contrast, photoreceptors displayed a reduced distal displacement of LY-labeled membranes in eyecups treated with cytochalasin D, showing that our technique can detect drug-induced changes in basal rod outer segment assembly. The reduction noted in the cytochalasin-treated cells was due to the abnormal lateral displacement of newly added OS disc membranes that occurs with this drug (Williams, D. S., K. A. Linberg, D. K. Vaughan, R. N. Fariss, and S. K. Fisher. 1988. J. Comp. Neurol. 272:161-176). Together, our results indicate that the vectorial transport of OS membrane constituents through the ellipsoid and their assembly into OS disc membranes are not dependent on elliposid MT integrity.

scholarly journals Cold Exposure Distinctively Modulates Parathyroid and Thyroid Hormones in Cold-Acclimatized and Non-Acclimatized Humans

Endocrinology ◽  
2020 ◽  
Vol 161 (7) ◽  
Author(s):  
Zuzana Kovaničová ◽  
Tímea Kurdiová ◽  
Miroslav Baláž ◽  
Patrik Štefanička ◽  
Lukáš Varga ◽  
...  
Keyword(s):  
Thyroid Hormones ◽  
Cold Exposure ◽  
Neck Surgery ◽  
Whole Body ◽  
Free T4 ◽  
Free T3 ◽  
Brown Adipose ◽  
Induced Changes ◽  
Ice Water

Abstract Cold-induced activation of thermogenesis modulates energy metabolism, but the role of humoral mediators is not completely understood. We aimed to investigate the role of parathyroid and thyroid hormones in acute and adaptive response to cold in humans. Examinations were performed before/after 15 minutes of ice-water swimming (n = 15) or 120 to 150 minutes of cold-induced nonshivering thermogenesis (NST) applied to cold-acclimatized (n = 6) or non-acclimatized (n = 11) individuals. Deep-neck brown adipose tissue (BAT) was collected from non-acclimatized patients undergoing elective neck surgery (n = 36). Seasonal variations in metabolic/hormonal parameters of ice-water swimmers were evaluated. We found that in ice-water swimmers, PTH and TSH increased and free T3, T4 decreased after a 15-minute winter swim, whereas NST-inducing cold exposure failed to regulate PTH and free T4 and lowered TSH and free T3. Ice-water swimming-induced increase in PTH correlated negatively with systemic calcium and positively with phosphorus. In non-acclimatized men, NST-inducing cold decreased PTH and TSH. Positive correlation between systemic levels of PTH and whole-body metabolic preference for lipids as well as BAT volume was found across the 2 populations. Moreover, NST-cooling protocol-induced changes in metabolic preference for lipids correlated positively with changes in PTH. Finally, variability in circulating PTH correlated positively with UCP1/UCP1, PPARGC1A, and DIO2 in BAT from neck surgery patients. Our data suggest that regulation of PTH and thyroid hormones during cold exposure in humans varies by cold acclimatization level and/or cold stimulus intensity. Possible role of PTH in NST is indicated by its positive relationships with whole-body metabolic preference for lipids, BAT volume, and UCP1 content.

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 ◽  
...  
Keyword(s):  
Cytochrome C ◽  
Mrna Expression ◽  
Cytochrome C Oxidase ◽  
Uncoupling Protein ◽  
Late Pregnancy ◽  
Brown Fat ◽  
Breeding Cycle ◽  
Brown Adipose ◽  
Pregnancy And Lactation ◽  
Brown Fat Mitochondria

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.

Brown fat mediates increased energy expenditure of cold-exposed overfed neonatal rats

1986 ◽  
Vol 251 (3) ◽  
pp. R518-R524
Author(s):  
B. J. Moore ◽  
J. S. Stern ◽  
B. A. Horwitz
Keyword(s):  
Energy Expenditure ◽  
Cold Exposure ◽  
Rapid Onset ◽  
Brown Fat ◽  
O2 Consumption ◽  
Neonatal Rats ◽  
Ambient Temperatures ◽  
Rat Pups ◽  
Acute Cold Exposure ◽  
Brown Adipose

Genetically lean rat pups, overfed by being raised in small litters of three from day 1 postpartum, rapidly become obese compared with pups raised in standard sized litters of eight. Because of the rapid onset of their obesity, we expected that overfed pups would exhibit defective brown fat thermogenesis as is seen in neonatal genetically obese rodents. O2 consumption (VO2) was measured in 2-, 4-, 6-, and 8-day-old homozygous lean (Fa/Fa) Zucker pups from each treatment. We determined minimum rate of VO2 at thermoneutrality and maximum VO2 in response to progressively colder ambient temperatures. Overfed pups were fatter than standard-fed pups (P less than 0.001). But contrary to our prediction, overfed pups had a significantly increased maximum VO2 in response to acute cold exposure. To test the hypothesis that brown fat mediated the increased VO2 in the overfed pups, scapular brown fat lipectomies were performed on a new group of overfed pups at 2 days of age and compared with sham-operated littermate controls. On day 8, no differences in minimum VO2 were seen at thermoneutrality when brown fat is turned off. But maximum VO2 in response to cold, when brown fat is turned on maximally, was significantly reduced in the lipectomized overfed pups compared with sham-operated overfed littermates. These data suggest that manipulations of diet, accomplished by raising pups in small litters, can increase brown fat thermogenic function. The results of the lipectomy experiment imply that brown adipose tissue is a primary mediator of the increased energy expenditure in response to acute cold exposure in the overfed pups.

scholarly journals UCP1 inhibition in Cidea-overexpressing mice is physiologically counteracted by brown adipose tissue hyperrecruitment

2017 ◽  
Vol 312 (1) ◽  
pp. E72-E87 ◽  
Author(s):  
Alexander W. Fischer ◽  
Irina G. Shabalina ◽  
Charlotte L. Mattsson ◽  
Gustavo Abreu-Vieira ◽  
Barbara Cannon ◽  
...  
Keyword(s):  
Inhibitory Effect ◽  
Brown Fat ◽  
Transcriptional Level ◽  
Compensatory Mechanism ◽  
Adipose Tissues ◽  
Protein Levels ◽  
Brown Adipose ◽  
Specific Regulation ◽  
Thermogenic Capacity

Cidea is a gene highly expressed in thermogenesis-competent (UCP1-containing) adipose cells, both brown and brite/beige. Here, we initially demonstrate a remarkable adipose-depot specific regulation of Cidea expression. In classical brown fat, Cidea mRNA is expressed continuously and invariably, irrespective of tissue recruitment. However, Cidea protein levels are regulated posttranscriptionally, being conspicuously induced in the thermogenically recruited state. In contrast, in brite fat, Cidea protein levels are regulated at the transcriptional level, and Cidea mRNA and protein levels are proportional to tissue “briteness.” Although routinely followed as a thermogenic molecular marker, Cidea function is not clarified. Here, we employed a gain-of-function approach to examine a possible role of Cidea in the regulation of thermogenesis. We utilized transgenic aP2-hCidea mice that overexpress human Cidea in all adipose tissues. We demonstrate that UCP1 activity is markedly suppressed in brown-fat mitochondria isolated from aP2-hCidea mice. However, mitochondrial UCP1 protein levels were identical in wild-type and transgenic mice. This implies a regulatory effect of Cidea on UCP1 activity, but as we demonstrate that Cidea itself is not localized to mitochondria, we propose an indirect inhibitory effect. The Cidea-induced inhibition of UCP1 activity (observed in isolated mitochondria) is physiologically relevant since the mice, through an appropriate homeostatic compensatory mechanism, increased the total amount of UCP1 in the tissue to exactly match the diminished thermogenic capacity of the UCP1 protein and retain unaltered nonshivering thermogenic capacity. Thus, we verified Cidea as being a marker of thermogenesis-competent adipose tissues, but we conclude that Cidea, unexpectedly, functions molecularly as an indirect inhibitor of thermogenesis.

scholarly journals Essential Role of IGFIR in the Onset of Male Brown Fat Thermogenic Function: Regulation of Glucose Homeostasis by Differential Organ-Specific Insulin Sensitivity

Endocrinology ◽  
2016 ◽  
Vol 157 (4) ◽  
pp. 1495-1511 ◽  
Author(s):  
Vanesa Viana-Huete ◽  
Carlos Guillén ◽  
Ana García-Aguilar ◽  
Gema García ◽  
Silvia Fernández ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Uncoupling Protein ◽  
High Plasma ◽  
Brown Fat ◽  
Severe Insulin Resistance ◽  
Brown Adipose ◽  
Total Fat

Abstract Brown fat is a thermogenic tissue that generates heat to maintain body temperature in cold environments and dissipate excess energy in response to overfeeding. We have addressed the role of the IGFIR in the brown fat development and function. Mice lacking IGFIR exhibited normal brown adipose tissue/body weight in knockout (KO) vs control mice. However, lack of IGFIR decreased uncoupling protein 1 expression in interscapular brown fat and beige cells in inguinal fat. More importantly, the lack of IGFIR resulted in an impaired cold acclimation. No differences in the total fat volume were found in the KO vs control mice. Epididymal fat showed larger adipocytes but with a lower number of adipocytes in KO vs control mice at age 12 months. In addition, KO mice showed a sustained moderate hyperinsulinemia and hypertriglyceridemia upon time and hepatic insulin insensitivity associated with lipid accumulation, with the outcome of a global insulin resistance. In addition, we found that the expression of uncoupling protein 3 in the skeletal muscle was decreased and its expression was increased in the heart in parallel with the expression of beta-2 adrenergic receptors. Upon nonobesogenic high-fat diet, we found a severe insulin resistance in the liver and in the skeletal muscle, but unchanged insulin sensitivity in the heart. In conclusion, our data suggest that IGFIR it is not an essential growth factor in the brown fat development in the presence of the IR and very high plasma levels of IGF-I, but it is indispensable for full brown fat functionality.

Evidence for the Mediatory Role of Brown Adipose Tissue During Nonshivering Thermogenesis in the Cold-Acclimated Mouse

1972 ◽  
Vol 50 (2) ◽  
pp. 168-170 ◽  
Author(s):  
J. S. Hayward ◽  
P. F. Davies
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
The Body ◽  
Brown Fat ◽  
Interscapular Brown Adipose Tissue ◽  
Adult Mice ◽  
Brown Adipose ◽  
Rate Of Oxygen Consumption

The increased rate of oxygen consumption by cold-acclimated, adult mice after subcutaneous injection of noradrenaline has been measured for intact individuals and for those with the arterial supply to their interscapular brown adipose tissue ligated. An immediate reduction of 40% of this calorigenic response was noted in mice thus operated. Dissection of the total brown fat of the body indicated that the interscapular deposits comprise 43% by weight of the total brown adipose tissue, which in turn forms only 1% of the body weight. Since a 40% reduction in calorigenic response to noradrenaline cannot be ascribed to the loss of an amount of brown fat constituting less than 0.5%) of the body weight, the results support the hypothesis that brown fat can mediate calorigenic responses of other tissues.

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