Brown Fat Thermoregulation in Developing Hamsters (&lt;i&gt;Mesocricetus auratus&lt;/i&gt;): a GDP-Binding Study

Sundin, Ulf; Herron, David K.; Cannon, Barbara

doi:10.1159/000241419

Cited by 30 publications

(4 citation statements)

References 22 publications

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“…The increase of BUG RNA level during the perinatal period could correspond to the successive recruitment of brown precursors before birth and during the days following it, when the BAT reaches its full development. 35,36 In adults, it is well established that cold exposure and obesity represent opposite situations leading to activation or inhibition of BAT, respectively, as determined by changes in UCP-1 content. 32,37,38 Interestingly, BUG transcript level in BAT was inversely regulated in these two opposite situations, with a 60% decrease at 5 days of cold exposure, and a 60% increase in obese compared to lean Zücker rats.…”

Section: Discussionmentioning

confidence: 99%

Cloning of BUG demonstrates the existence of a brown preadipocyte distinct from a white one

et al. 2001

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BACKGROUND: Several indirect arguments agree with the existence of a brown preadipocyte distinct from a white one. Nevertheless, to date, no molecular marker has been available to directly in vivo demonstrate this hypothesis. OBJECTIVE: The aim of this study was to find a gene expressed in brown preadipocyte but not in white and to use it as a molecular marker to analyse brown preadipocyte recruitment in different physiological and physiopathological situations. METHOD: Differential display was performed on stromal-vascular and adipocyte fractions of white and brown adipose tissues in rat. RESULTS: We identified a new gene, BUG, preferentially expressed in the stromal-vascular fraction of brown fat vs other adipose tissues fractions in adult rat. This RNA is also highly expressed in heart and, to a lesser extent, in other tissues such as kidney and brain. The BUG transcript is detected by in situ hybridization in putative preadipocytes within brown adipose tissue. Its level is transiently and specifically up-regulated during early stages of brown preadipocyte differentiation in a primary culture system, before the acquisition of late brown adipocyte phenotype. During development, BUG can be detected before the emergence of UCP-1 expression. In adult rats, BUG expression is inversely associated to brown adipose tissue (BAT) activation during cold exposure as well as in obese animals. CONCLUSIONS: The pattern of BUG expression agrees with an early divergence between brown and white adipocyte lineages. It also reveals the existence of a pool of committed brown preadipocytes within BAT that are recruited during cold exposure. BUG expression is increased in obese animals, suggesting that an early defect in brown preadipocyte differentiation could account for impaired BAT function in genetically obese rats.

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Section: Discussionmentioning

confidence: 99%

Cloning of BUG demonstrates the existence of a brown preadipocyte distinct from a white one

et al. 2001

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“…The GDP-binding assay has been widely used as a measure of the thermogenic capacity of BAT (Goodbody & Trayhurn, 1981 ;Sundin et al 1981) and was used in the present study, together with cytochrome c oxidase, as an index of total thermogenic activity. For the weanling rats, the enhanced 0, consumption of the R D group was accompanied by a reduction in BAT mitochondrial GDP binding.…”

Section: Discussionmentioning

confidence: 99%

Riboflavin deficiency, metabolic rate and brown adipose tissue function in sucking and weanling rats

Patterson

Bates

1989

Br J Nutr

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1. The effects of riboflavin deficiency on growth, whole-body oxygen consumption, cytochrome c oxidase (EC 1.9.3.1) activity and GDP-binding capacity of brown adipose tissue were measured in three groups of rats: sucking pups, weanling rats, and dams. Control groups were weight-matched, pair-fed or fed ad lib.2. Riboflavin deficiency reduced growth rate and increased the activation coefficient of erythrocyte glutathione reductase (NAD(P)H) (EC 1.6.4.2), as predicted. In sucking pups it also reduced whole-body O2 consumption per unit body-weight, especially after noradrenaline stimulation. In weanling rats, however, it increased O2 consumption both before and after noradrenaline stimulation.3. Cytochrome c oxidase (EC 1.9.9.1) activity of brown adipose tissue was not consistently affected by riboflavin deficiency. Binding of [3H]GDP to the mitochondria was increased in the deficient weanling rats.4. Weanling rats therefore, seemed better able to withstand the effects of severe depletion. Their reduced growth and increased non-shivering thermogenesis helped to counteract the unfavourable ratio of riboflavin: other tissuebuilding materials. The relevance for thermoregulation in riboflavin-deficient children is discussed.

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“…Characteristic for this group (which includes Syr-ian hamsters) is that the newborns are very poorly developed, in thermoregulatory, as well as in other, respects. Thermoregulation and brown adipose tissue recruitment occur simultaneously during the second week after birth, but not before (60,190,357,572,758,777); until then, the pups behave as poikilotherms, i.e., they are unable to maintain a higher temperature than that of the surroundings. Although there is very good correlation between the acquisition of nonshivering thermogenesis and the recruitment of brown adipose tissue, this is not a strict demonstration that the nonshivering thermogenesis observed is entirely brown fat derived, but this is very likely.…”

Section: Immature Newborns Recruit Brown Adipose Tissue With a Delaymentioning

confidence: 99%

Brown Adipose Tissue: Function and Physiological Significance

Cannon

Nedergaard

2004

Physiological Reviews

5,487

126

5,981

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The function of brown adipose tissue is to transfer energy from food into heat; physiologically, both the heat produced and the resulting decrease in metabolic efficiency can be of significance. Both the acute activity of the tissue, i.e., the heat production, and the recruitment process in the tissue (that results in a higher thermogenic capacity) are under the control of norepinephrine released from sympathetic nerves. In thermoregulatory thermogenesis, brown adipose tissue is essential for classical nonshivering thermogenesis (this phenomenon does not exist in the absence of functional brown adipose tissue), as well as for the cold acclimation-recruited norepinephrine-induced thermogenesis. Heat production from brown adipose tissue is activated whenever the organism is in need of extra heat, e.g., postnatally, during entry into a febrile state, and during arousal from hibernation, and the rate of thermogenesis is centrally controlled via a pathway initiated in the hypothalamus. Feeding as such also results in activation of brown adipose tissue; a series of diets, apparently all characterized by being low in protein, result in a leptin-dependent recruitment of the tissue; this metaboloregulatory thermogenesis is also under hypothalamic control. When the tissue is active, high amounts of lipids and glucose are combusted in the tissue. The development of brown adipose tissue with its characteristic protein, uncoupling protein-1 (UCP1), was probably determinative for the evolutionary success of mammals, as its thermogenesis enhances neonatal survival and allows for active life even in cold surroundings.

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Brown Fat Thermoregulation in Developing Hamsters (<i>Mesocricetus auratus</i>): a GDP-Binding Study

Cited by 30 publications

References 22 publications

Cloning of BUG demonstrates the existence of a brown preadipocyte distinct from a white one

Cloning of BUG demonstrates the existence of a brown preadipocyte distinct from a white one

Riboflavin deficiency, metabolic rate and brown adipose tissue function in sucking and weanling rats

Brown Adipose Tissue: Function and Physiological Significance

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