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Chronic cold exposure enhances glucose oxidation in brown adipose tissue

ABSTRACT: The cultured brown adipocytes can oxidize glucose in vitro, but it is still not fully clear whether brown adipose tissue (BAT) could completely oxidize glucose in vivo. Although positron emission tomography (PET) with 18F-fluorodeoxyglucose (18F-FDG) showed a high level of glucose uptake in the activated BAT, the non-metabolizable 18F-FDG cannot fully demonstrate intracellular glucose metabolism. Through in vivo [U-13C]glucose tracing, here we show that chronic cold exposure dramatically activates glucose oxidation in BAT and the browning/beiging subcutaneous white adipose tissue (sWAT). Specifically, chronic cold exposure enhances glucose flux into the mitochondrial TCA cycle. Metabolic flux analysis models that ?3-adrenergic receptor (?3-AR) agonist significantly enhances the flux of mitochondrial pyruvate uptake through mitochondrial pyruvate carrier (MPC) in the differentiated primary brown adipocytes. Furthermore, in vivo MPC inhibition blocks cold-induced glucose oxidation, and impairs body temperature maintenance in mice. Together, mitochondrial pyruvate uptake and oxidation serves an important energy source in the chronic cold exposure activated BAT and beige adipose tissue, which supports a role for glucose oxidation in brown fat thermogenesis.

SUBMITTER: Dr. Lei Jiang

PROVIDER: S-SCDT-EMBOR-2020-50085V1 | biostudies-other |

REPOSITORIES: biostudies-other

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Chronic cold exposure enhances glucose oxidation in brown adipose tissue.

Project description:The cultured brown adipocytes can oxidize glucose in vitro, but it is still not fully clear whether brown adipose tissue (BAT) could completely oxidize glucose in vivo. Although positron emission tomography (PET) with 18 F-fluorodeoxyglucose (18 F-FDG) showed a high level of glucose uptake in the activated BAT, the non-metabolizable 18 F-FDG cannot fully demonstrate intracellular glucose metabolism. Through in vivo [U-13 C]glucose tracing, here we show that chronic cold exposure dramatically activates glucose oxidation in BAT and the browning/beiging subcutaneous white adipose tissue (sWAT). Specifically, chronic cold exposure enhances glucose flux into the mitochondrial TCA cycle. Metabolic flux analysis models that β3-adrenergic receptor (β3-AR) agonist significantly enhances the flux of mitochondrial pyruvate uptake through mitochondrial pyruvate carrier (MPC) in the differentiated primary brown adipocytes. Furthermore, in vivo MPC inhibition blocks cold-induced glucose oxidation and impairs body temperature maintenance in mice. Together, mitochondrial pyruvate uptake and oxidation serve an important energy source in the chronic cold exposure activated BAT and beige adipose tissue, which supports a role for glucose oxidation in brown fat thermogenesis.

| S-EPMC7645266 | biostudies-literature

Chronic cold exposure induces autophagy to promote fatty acid oxidation, mitochondrial turnover, and thermogenesis in brown adipose tissue.

Project description:Autophagy plays an important role in lipid breakdown, mitochondrial turnover, and mitochondrial function during brown adipose tissue (BAT) activation by thyroid hormone, but its role in BAT during adaptive thermogenesis remains controversial. Here, we examined BAT from mice exposed to 72 h of cold challenge as well as primary brown adipocytes treated with norepinephrine and found increased autophagy as well as increased β-oxidation, mitophagy, mitochondrial turnover, and mitochondrial activity. To further understand the role of autophagy of BAT in vivo, we generated BAT-specific Atg5 knockout (Atg5cKO) mice and exposed them to cold for 72 h. Interestingly, BAT-specific Atg5cKO mice were unable to maintain body temperature after chronic cold exposure and displayed deranged mitochondrial morphology and reactive oxygen species damage in their BAT. Our findings demonstrate the critical role of autophagy in adaptive thermogenesis, fatty acid metabolism, and mitochondrial function in BAT during chronic cold exposure.

| S-EPMC8134067 | biostudies-literature

Maternal Cold Exposure Enhances Fetal Brown Adipose Tissue Development

Project description:Brown adipose tissue (BAT) is specialized for dissipating energy in the form of heat. BAT-mediated heat production is critical for effective adaption of newborns to the extrauterine environment. However, very little is known about whether and how fetal BAT development is modulated in-utero in response to changes in maternal thermal environment during pregnancy. The present study aims at determining whether maternal cold exposure influences fetal BAT development via placental remodeling. BL6 female mice were acclimated at 28C or 18C for 7 days prior to mating with male mice and maintained at their respective temperature until embryonic day 18.5. Placental and fetal BAT samples were collected for transcriptome analysis.

2021-06-18 | GSE151905 | GEO

SIRT1 enhances glucose tolerance by potentiating brown adipose tissue function.

Project description:OBJECTIVE: SIRT1 has been proposed to be a key signaling node linking changes in energy metabolism to transcriptional adaptations. Although SIRT1 overexpression is protective against diverse metabolic complications, especially in response to high-fat diets, studies aiming to understand the etiology of such benefits are scarce. Here, we aimed to identify the key tissues and mechanisms implicated in the beneficial effects of SIRT1 on glucose homeostasis. METHODS: We have used a mouse model of moderate SIRT1 overexpression, under the control of its natural promoter, to evaluate glucose homeostasis and thoroughly characterize how different tissues could influence insulin sensitivity. RESULTS: Mice with moderate overexpression of SIRT1 exhibit better glucose tolerance and insulin sensitivity even on a low fat diet. Euglycemic-hyperinsulinemic clamps and in-depth tissue analyses revealed that enhanced insulin sensitivity was achieved through a higher brown adipose tissue activity and was fully reversed by housing the mice at thermoneutrality. SIRT1 did not influence brown adipocyte differentiation, but dramatically enhanced the metabolic transcriptional responses to ?3-adrenergic stimuli in differentiated adipocytes. CONCLUSIONS: Our work demonstrates that SIRT1 improves glucose homeostasis by enhancing BAT function. This is not consequent to an alteration in the brown adipocyte differentiation process, but as a result of potentiating the response to ?3-adrenergic stimuli.

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Amino acid and glucose uptake by rat brown adipose tissue. Effect of cold-exposure and acclimation.

Project description:The net uptake/release of glucose, lactate and amino acids from the bloodstream by the interscapular brown adipose tissue of control, cold-exposed and cold-acclimated rats was estimated by measurement of arteriovenous differences in their concentrations. In the control animals amino acids contributed little to the overall energetic needs of the tissue; glucose uptake was more than compensated by lactate efflux. Cold-exposure resulted in an enhancement of amino acid utilization and of glucose uptake, with high lactate efflux. There was a net glycine and proline efflux that partly compensated the positive nitrogen balance of the tissue; amino acids accounted for about one-third of the energy supplied by glucose to the tissue. Cold-acclimation resulted in a very high increase in glucose uptake, with a parallel decrease in lactate efflux and amino acid consumption. Branched-chain amino acids, however, were more actively utilized. This was related with a much higher alanine efflux, in addition to that of glycine and proline. It is suggested that most of the glucose used during cold-exposure is returned to the bloodstream as lactate under conditions of active lipid utilization, amino acids contributing their skeletons largely in anaplerotic pathways. On the other hand, cold-acclimation resulted in an important enhancement of glucose utilization, with lowered amino acid oxidation. Amino acids are thus used as metabolic substrates by the brown adipose tissue of rats under conditions of relatively scarce substrate availability, but mainly as anaplerotic substrates, in parallel to glucose. Cold-acclimation results in a shift of the main substrates used in thermogenesis from lipid to glucose, with a much lower need for amino acids.

| S-EPMC1149224 | biostudies-other

Effects of cold exposure on metabolites in brown adipose tissue of rats.

Project description:Brown adipose tissue (BAT) plays an important role in regulation of energy expenditure while adapting to a cold environment. BAT thermogenesis depends on uncoupling protein 1 (UCP1), which is expressed in the inner mitochondrial membranes of BAT. Gene expression profiles induced by cold exposure in BAT have been studied, but the metabolomic biological pathway that contributes to the activation of thermogenesis in BAT remains unclear. In this study, we comprehensively compared the relative levels of metabolites between the BAT of rats kept at room temperature (22?°C) and of those exposed to a cold temperature (4?°C) for 48?h using capillary electrophoresis (CE) time-of-flight mass spectrometry (TOFMS) and liquid chromatography (LC)-TOFMS. We identified 218 metabolites (137 cations and 81 anions) by CE-TOFMS and detected 81 metabolites (47 positive and 34 negative) by LC-TOFMS in BAT. We found that cold exposure highly influenced the BAT metabolome. We showed that the cold environment lead to lower levels of glycolysis and gluconeogenesis intermediates and higher levels of the tricarboxylic acid (TCA) cycle metabolites, fatty acids, and acyl-carnitine metabolites than control conditions in the BAT of rats. These results indicate that glycolysis and ?-oxidation of fatty acids in BAT are positive biological pathways that contribute to the activation of thermogenesis by cold exposure, thereby facilitating the generation of heat by UCP1. These data provide useful information for understanding the basal metabolic functions of BAT thermogenesis in rats in response to cold exposure.

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Maternal Cold Exposure Enhances Fetal Brown Adipose Tissue Development

Project description:Maternal Cold Exposure Enhances Fetal Brown Adipose Tissue Development

| PRJNA637622 | ENA

Cold exposure induces dynamic, heterogeneous alterations in human brown adipose tissue lipid content.

Project description:Brown adipose tissue undergoes a dynamic, heterogeneous response to cold exposure that can include the simultaneous synthesis, uptake, and oxidation of fatty acids. The purpose of this work was to quantify these changes in brown adipose tissue lipid content (fat-signal fraction (FSF)) using fat-water magnetic resonance imaging during individualized cooling to 3 °C above a participant's shiver threshold. Eight healthy men completed familiarization, perception-based cooling, and MRI-cooling visits. FSF maps of the supraclavicular region were acquired in thermoneutrality and during cooling (59.5 ± 6.5 min). Brown adipose tissue regions of interest were defined, and voxels were grouped into FSF decades (0-10%, 10-20%…90-100%) according to their initial value. Brown adipose tissue contained a heterogeneous morphology of lipid content. Voxels with initial FSF values of 60-100% (P < 0.05) exhibited a significant decrease in FSF while a simultaneous increase in FSF occurred in voxels with initial FSF values of 0-30% (P < 0.05). These data suggest that in healthy young men, cold exposure elicits a dynamic and heterogeneous response in brown adipose tissue, with areas initially rich with lipid undergoing net lipid loss and areas of low initial lipid undergoing a net lipid accumulation.

| S-EPMC6753098 | biostudies-literature

Transcriptome profiling of brown adipose tissue during cold exposure

Project description:We applied a deep-sequencing based method – digital gene expression profiling (DGEP), to investigate gene expression in interscapular brown adipose tissue (iBAT), inguinal white adipose tissue (iWAT) and epididymal white adipose tissue (eWAT) in acute cold exposure

2014-12-19 | GSE63031 | GEO

Paternal cold exposure enhances brown adipose tissue sensitivity in offspring and ameliorates diet induced obesity

Project description:Research in recent years has focused on environmental effects that control tissue functionality and systemic metabolism. We show here in a retrospective analysis that presence of brown adipocytes and date of birth are correlated and linked to BMI. In a mouse model system, we demonstrate that pre-conception cold exposure leads to improved systemic metabolism and protects from diet induced obesity, through the sperm via the paternal lineage. Using a brown fat ablation model, we show that this effect is mediated by brown adipose tissue. Furthermore, through RNAseq and DNA methylation analysis we identify Adrb3 as a putative signaling mechanism which could mediate the effects of pre-conception cold exposure and could account for the heterogeneity of brown adipose tissue responsiveness. Taken together, our results identify paternal cold exposure as a stimulus which induces a hyper-active state in brown adipose tissue leading to improved adaptation to overnutrition and hypothermia in the offspring.

2018-06-30 | GSE100231 | GEO

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