Uncoupling protein in embryonic brown adipose tissue — existence of nonthermogenic and thermogenic mitochondria

Houštěk, J; Kopecký, Jan; Rychter, Z; Soukup, Tomáš

doi:10.1016/0005-2728(88)90103-x

Cited by 64 publications

(35 citation statements)

References 18 publications

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“…2C). These patterns of brown adipocyte expression are consistent with those observed by others (24,(29)(30)(31)(32) and with previously published results from our laboratory with B6 mice (33). No strain-dependent variations in either Ucp1 expression or mitochondrial amount in iBAT were detected between A/J and B6 mice from 18 days of gestation to 4 months of age.…”

Section: Induction Of Ucp1 Expression In Ibat During Developmentsupporting

confidence: 93%

Genetic variability affects the development of brown adipocytes in white fat but not in interscapular brown fat

Xue¹,

Rim

Hogan

et al. 2007

Journal of Lipid Research

248

228

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Cold exposure induces brown adipocytes in retroperitoneal fat (RP) of adult A/J mice but not in C57BL/6J (B6) mice. In contrast, induction of the mitochondrial uncoupling protein 1 gene (Ucp1) in interscapular brown adipose tissue (iBAT) shows no strain dependence. We now show that unlike iBAT, in which Ucp1 was expressed in the fetus and continued throughout life, in RP, Ucp1 was transiently expressed between 10 and 30 days of age and then disappeared. Similar to the lack of genetic variation in the expression of Ucp1 in iBAT during cold induction of adult mice, no genetic variation in Ucp1 expression in iBAT was detected during development. In contrast, UCP1-positive multilocular adipocytes, together with corresponding increases in Ucp1 expression, appeared in RP at 10 days of age in A/J and B6 mice, but with much higher expression in A/J mice. At 20 days of age, brown adipocytes represent the major adipocyte present in RP of A/J mice. The disappearance of brown adipocytes by 30 days of age suggested that tissue remodeling occurred in RP. Genetic variability in Ucp1 expression could not be explained by variation in the expression of selective transcription factors and signaling molecules of adipogenesis. In summary, the existence of genetic variability between A/J and B6 mice during the development of brown adipocyte expression in RP, but not in iBAT, suggests that developmental mechanisms for the brown adipocyte differentiation program are different in these adipose tissues.-Xue, B., J-S. Rim, J. C. Hogan, A. A. Coulter, R. A. Koza, and L. P. Kozak. Genetic variability affects the development of brown adipocytes in white fat but not in interscapular brown fat. J. Lipid Res. 2007. 48: 41-51.

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Section: Induction Of Ucp1 Expression In Ibat During Developmentsupporting

confidence: 93%

Genetic variability affects the development of brown adipocytes in white fat but not in interscapular brown fat

Xue¹,

Rim

Hogan

et al. 2007

Journal of Lipid Research

248

228

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“…Regulation of BNIP3 during adipocyte remodelling, especially in obesity or PPARγ-related conditions The role of BNIP3 has been mostly investigated in myocytes in relation to hypoxia-induced apoptotic cell death and autophagic cell survival [14]. Here, we revealed that a considerable amount of BNIP3 expression is regulated in adipocytes under conditions in which higher mitochondrial content is required, including adipocyte differentiation [10], starvation [25] and in BAT [26], and also by rosiglitazone treatment [2,7,10]. We also found that BNIP3 was downregulated in adipose tissue under obese diabetic conditions.…”

Section: Discussionmentioning

confidence: 90%

BNIP3 is essential for mitochondrial bioenergetics during adipocyte remodelling in mice

Choi

Kim

et al. 2015

Diabetologia

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Aims/hypothesis Adipose tissue is a highly versatile system in which mitochondria in adipocytes undergo significant changes during active tissue remodelling. BCL2/adenovirus E1B 19 kDa protein-interacting protein 3 (BNIP3) is a mitochondrial protein and a known mitochondrial quality regulator. In this study, we investigated the role of BNIP3 in adipocytes, specifically under conditions of peroxisome proliferator-activated receptor-γ (PPARγ)-induced adipose tissue remodelling. Methods The expression of BNIP3 was evaluated in 3T3-L1 adipocytes in vitro, C57BL/6 mice fed a high-fat diet and db/db mice in vivo. Mitochondrial bioenergetics was investigated in BNIP3-knockdown adipocytes after rosiglitazone treatment. A putative peroxisome proliferator hormone responsive element (PPRE) was characterised by promoter assay and electrophoretic mobility shift assay (EMSA). ResultsThe protein BNIP3 was more abundant in brown adipose tissue than white adipose tissue. Furthermore, BNIP3 expression was upregulated by 3T3-L1 pre-adipocyte differentiation, starvation and rosiglitazone treatment. Conversely, BNIP3 expression in adipocytes decreased under various conditions associated with insulin resistance. This downregulation of BNIP3 was restored by rosiglitazone treatment. Knockdown of BNIP3 in adipocytes inhibited rosiglitazoneinduced mitochondrial biogenesis and function, partially mediated by the 5′ AMP-activated protein kinase (AMPK)-peroxisome proliferator-activated receptor γ, co-activator 1 α (PGC1α) signalling pathway. Rosiglitazone treatment increased the transcription level of Bnip3 in the reporter assay and the presence of the PPRE site in the Bnip3 promoter was demonstrated by EMSA. Conclusions/interpretation The protein BNIP3 contributes to the improvement of mitochondrial bioenergetics that occurs

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“…This is not surprising in the light of evidence that active 5'D and binding of locally produced T3 to nuclear receptors [27] is required for induction of UCP synthesis. Interestingly, the perinatal development of BAT in several species shows coincidental, but not exactly parallel changes in 5' D activity and UCP content [5,7,24,28]. The extent of stimulation of 5' D activity in cultured BAT cells exposed for 8 h to different adrenergic and cAMP modulating agents is shown in Table II.…”

Section: Abbreviationsmentioning

confidence: 99%

Induction of type II iodothyronine 5'‐deiodmase and mitochondrial uncoupling protein in brown adipocytes differentiated in cell culture

et al. 1990

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Brown adipocytes differentiated in primary cell culture were found to contain a type II iodothyronine 5'‐deiodinase (5'D), Incubation of confluent cells with norepinephrine or dibutyryl‐cAMP caused up to 17‐fold increase in 5'D activity with a maximum after 8 h. Activation of 5'D required mRNA and protein synthesis and was accompanied by parallel, up to 5.8‐fold increase in the amount of mitochondrial uncoupling protein with a maximum after 24 h. Analysis ofadrenergic stimulation of 5'D suggested predominant involvement of the β‐receptors and increased intracellular cAMP levels, while the contribution of x1,‐receptors was small.

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Uncoupling protein in embryonic brown adipose tissue — existence of nonthermogenic and thermogenic mitochondria

Cited by 64 publications

References 18 publications

Genetic variability affects the development of brown adipocytes in white fat but not in interscapular brown fat

Genetic variability affects the development of brown adipocytes in white fat but not in interscapular brown fat

BNIP3 is essential for mitochondrial bioenergetics during adipocyte remodelling in mice

Induction of type II iodothyronine 5'‐deiodmase and mitochondrial uncoupling protein in brown adipocytes differentiated in cell culture

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