Cold-induced alterations of phospholipid fatty acyl composition in brown adipose tissue mitochondria are independent of uncoupling protein-1

Ocloo, Augustine; Shabalina, Irina G.; Nedergaard, Jan; Brand, Martin D.

doi:10.1152/ajpregu.00128.2007

Cited by 27 publications

(23 citation statements)

References 63 publications

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“…7C). The elevation in the content of both 18:2 and 20:4-6 in brown fat in response to cold exposure has been repeatedly shown in mitochondria of brown fat (33)(34)(35), and we show here that the level of only one of these (20:4-6) was mitigated by group housing.…”

Section: Methodssupporting

confidence: 81%

Group housing and nest building only slightly ameliorate the cold stress of typical housing in female C57BL/6J mice

Maher

Barbash

Lynch

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

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Maher RL, Barbash SM, Lynch DV, Swoap SJ. Group housing and nest building only slightly ameliorate the cold stress of typical housing in female C57BL/6J mice. Am J Physiol Regul Integr Comp Physiol 308: R1070 -R1079, 2015. First published April 15, 2015 doi:10.1152/ajpregu.00407.2014.-Huddling and nest building are two methods of behavioral thermoregulation used by mice under cold stress. In the laboratory, mice are typically housed at an ambient temperature (T a) of 20°C, well below the lower end of their thermoneutral zone. We tested the hypothesis that the thermoregulatory benefits of huddling and nest building at a T a of 20°C would ameliorate this cold stress compared with being singly housed at 20°C as assessed by heart rate (HR), blood pressure (BP), triiodothyronine (T3), brown adipose (BAT) expression of Elovl3 mRNA, and BAT lipid content. A series of experiments using C57BL/6J female mice exposed to 20°C in the presence or absence of nesting material and/or cage mates was used to test this hypothesis. Mice showed large differences in HR, BP, shivering, and core body temperature (T b) when comparing singly housed mice at 20°C and 30°C, but only a modest reduction in HR with the inclusion of cage mates or bedding. However, group housing and/or nesting at 20°C decreased T3 levels compared with singly housed mice at 20°C. Singly housed mice at 20°C had a 22-fold higher level of BAT Elovl3 mRNA expression and a significantly lower triacylglycerol (TAG) content of BAT compared with singly housed mice at 30°C. Group housing at 20°C led to blunted changes in both Elovl3 mRNA and TAG levels. These findings suggest that huddling and nest building have a limited effect to ameliorate the cold stress associated with housing at 20°C. ambient temperature; blood pressure; brown fat; nesting THE MOUSE (MUS MUSCULUS) IS an important model system for mammalian studies. Its genetic tractability with a short reproductive time, coupled with advances in the miniaturization of physiological tools, create an increased ease for the merging of physiological studies and "omic" studies. The ambient temperature (T a ) of animal housing facilities is within a standard range that, while comfortable for human caretakers, falls well below the mouse thermoneutral zone (TNZ), the range of T a s in which endotherms do not elevate their metabolic rate to maintain core body temperature (T b ) (19, 23). The T a at which metabolic rate begins to rise to offset heat loss (i.e., the lower critical temperature) is ϳ29 -30°C for mice (18). Housed at temperatures below this zone, mice are under cold stress (8).To elevate metabolic rate and minimize heat loss when exposed to cooler temperatures, endotherms engage one of many behavioral changes and/or several physiological adaptations, which vary across species and which are not mutually exclu-

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Section: Methodssupporting

confidence: 81%

Group housing and nest building only slightly ameliorate the cold stress of typical housing in female C57BL/6J mice

Maher

Barbash

Lynch

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Other studies have shown that, for example, surface area (Crichton et al 2009) and phospholipid content (Ocloo et al 2007) do not differ significantly between the wildtype and Ucp1KO models. This suggests that, while factors other than UCP1 content may influence basal proton conductance to some extent, they are unlikely to account for the large changes observed.…”

Section: Discussionmentioning

confidence: 78%

Uncoupling protein-1 (UCP1) contributes to the basal proton conductance of brown adipose tissue mitochondria

Parker

Crichton

Vidal-Puig

et al. 2009

J Bioenerg Biomembr

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Proton leak pathways uncouple substrate oxidation from ATP synthesis in mitochondria. These pathways are classified as basal (not regulated) or inducible (activated and inhibited). Previously it was found that over half of the basal proton conductance of muscle mitochondria was catalyzed by the adenine nucleotide translocase (ANT), an abundant mitochondrial anion carrier protein. To determine whether ANT is the unique protein catalyst, or one of many proteins that catalyze basal proton conductance, we measured proton leak kinetics in mitochondria isolated from brown adipose tissue (BAT). BAT can express another mitochondrial anion carrier, UCP1, at concentrations similar to ANT. Basal proton conductance was measured under conditions where UCP1 and ANT were catalytically inactive and was found to be lower in mitochondria from UCP1 knockout mice compared to wild-type. Ablation of another abundant inner membrane protein, nicotinamide nucleotide transhydrogenase, had no effect on proton leak kinetics in mitochondria from liver, kidney or muscle, showing that basal proton conductance is not catalyzed by all membrane proteins. We identify UCP1 as a second protein propagating basal proton leak, lending support to the hypothesis that basal leak pathways are perpetrated by members of the mitochondrial anion carrier family but not by other mitochondrial inner membrane proteins.

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“…However, these alterations are not secondary to UCP1-mediated uncoupling or to any other UCP1-dependent activity. 60 The angiogenic processes in brown adipose tissue It is presently discussed whether the increased vascularization in adipose tissues is secondary to hypoxia occurring in the tissues. However, in both interscapular brown adipose tissue and in inguinal white adipose tissue, cold-acclimationinduced angiogenesis is independent of the hypoxia that can occur in tissues during stimulation 61 (but the hypoxia itself is dependent on the presence of UCP1 61 ).…”

Section: Fevers Of Different Kindsmentioning

confidence: 99%

Metabolic consequences of the presence or absence of the thermogenic capacity of brown adipose tissue in mice (and probably in humans)

2010

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Only with the development of the uncoupling protein 1 (UCP1)-ablated mouse has it become possible to strictly delineate the physiological significance of the thermogenic capacity of brown adipose tissue. Considering the presence of active brown adipose tissue in adult humans, these insights may have direct human implications. In addition to classical nonshivering thermogenesis, all adaptive adrenergic thermogeneses, including diet-induced thermogenesis, is fully dependent on brown adipocyte activity. Any weight-reducing effect of b 3 -adrenergic agonists is fully dependent on UCP1 activity, as is any weightreducing effect of leptin (in excess of its effect on reduction of food intake). Consequently, in the absence of the thermogenic activity of brown adipose tissue, obesity develops spontaneously. The ability of brown adipose tissue to contribute to glucose disposal is also mainly related to thermogenic activity. However, basal metabolic rate, cold-induced thermogenesis, acute cold tolerance, fevers, nonadaptive adrenergic thermogenesis and processes such as angiogenesis in brown adipose tissue itself are not dependent on UCP1 activity. Whereas it is likely that these conclusions are also qualitatively valid for adult humans, the quantitative significance of brown adipose tissue for human metabolismFand the metabolic consequences for a single individual possessing more or less brown adipose tissueFawaits clarification.

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Cold-induced alterations of phospholipid fatty acyl composition in brown adipose tissue mitochondria are independent of uncoupling protein-1

Abstract: Ocloo A, Shabalina IG, Nedergaard J, Brand MD. Cold-induced alterations of phospholipid fatty acyl composition in brown adipose tissue mitochondria are independent of uncoupling protein-1.

Cited by 27 publications

References 63 publications

Group housing and nest building only slightly ameliorate the cold stress of typical housing in female C57BL/6J mice

Group housing and nest building only slightly ameliorate the cold stress of typical housing in female C57BL/6J mice

Uncoupling protein-1 (UCP1) contributes to the basal proton conductance of brown adipose tissue mitochondria

Metabolic consequences of the presence or absence of the thermogenic capacity of brown adipose tissue in mice (and probably in humans)

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