Measuring Respiratory Activity of Adipocytes and Adipose Tissues in Real Time

Bugge, Anne; Dib, Lea; Collins, Sheila

doi:10.1016/b978-0-12-800280-3.00013-x

Cited by 31 publications

(25 citation statements)

References 22 publications

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“…Protein concentrations were measured using a bicinchoninic acid (BCA) protein assay kit (HyClone Pierce). The production of ATP and basal respiration rate were determined by observing how the OCR changes in response to drugs that modulate mitochondrial activity (59). …”

Section: Methodsmentioning

confidence: 99%

Irisin protects mitochondria function during pulmonary ischemia/reperfusion injury

et al. 2017

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Limb remote ischemic preconditioning (RIPC) is an effective means of protection against ischemia/reperfusion (IR)–induced injury to multiple organs. Many studies are focused on identifying endocrine mechanisms that underlie the cross-talk between muscle and RIPC-mediated organ protection. We report that RIPC releases irisin, a myokine derived from the extracellular portion of fibronectin domain–containing 5 protein (FNDC5) in skeletal muscle, to protect against injury to the lung. Human patients with neonatal respiratory distress syndrome show reduced concentrations of irisin in the serum and increased irisin concentrations in the bronchoalveolar lavage fluid, suggesting transfer of irisin from circulation to the lung under physiologic stress. In mice, application of brief periods of ischemia preconditioning stimulates release of irisin into circulation and transfer of irisin to the lung subjected to IR injury. Irisin, via lipid raft–mediated endocytosis, enters alveolar cells and targets mitochondria. Interaction between irisin and mitochondrial uncoupling protein 2 (UCP2) allows for prevention of IR-induced oxidative stress and preservation of mitochondrial function. Animal model studies show that intravenous administration of exogenous irisin protects against IR-induced injury to the lung via improvement of mitochondrial function, whereas in UCP2-deficient mice or in the presence of a UCP2 inhibitor, the protective effect of irisin is compromised. These results demonstrate that irisin is a myokine that facilitates RIPC-mediated lung protection. Targeting the action of irisin in mitochondria presents a potential therapeutic intervention for pulmonary IR injury.

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Section: Methodsmentioning

confidence: 99%

Irisin protects mitochondria function during pulmonary ischemia/reperfusion injury

et al. 2017

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“…XF cell Mito stress test kit (Seahorse Bioscience) was used to measure mitochondrial function with a final concentration of 1 μM oligomycin and 0.5 μM rotenone. Uncoupled respiration was calculated by subtraction of rotenone-induced OCR from oligomycin A-induced OCR [22]. …”

Section: Methodsmentioning

confidence: 99%

Sex differences in sympathetic innervation and browning of white adipose tissue of mice

et al. 2016

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BackgroundThe higher prevalence of obesity-related metabolic disease in males suggests that female sex hormones provide protective mechanisms against the pathogenesis of metabolic syndrome. Because browning of white adipose tissue (WAT) is protective against obesity-related metabolic disease, we examined sex differences in β3-adrenergic remodeling of WAT in mice.MethodsEffects of the β3-adrenergic receptor agonist CL316,243 (CL) on browning of white adipose tissue were investigated in male and female C57BL mice. The role of ovarian hormones in female-specific browning was studied in control female C57BL mice and mice with ovarian failure induced by 4-vinylcyclohexene diepoxide treatment for 15 days.ResultsWe found that treatment with CL-induced upregulation of brown adipocyte markers and mitochondrial respiratory chain proteins in gonadal WAT (gWAT) of female mice, but was without effect in males. In contrast, CL treatment was equally effective in males and females in inducing brown adipocyte phenotypes in inguinal WAT. The tissue- and sex-specific differences in brown adipocyte recruitment were correlated with differences in sympathetic innervation, as determined by tyrosine hydroxylase immunostaining and western blotting. Levels of the neurotrophins NGF and BDNF were significantly higher in gWAT of female mice. CL treatment significantly increased NGF levels in gWAT of female mice but did not affect BDNF expression. In contrast, estradiol treatment doubled BDNF expression in female adipocytes differentiated in vitro. Ovarian failure induced by 4-vinylcyclohexene diepoxide treatment dramatically reduced BDNF and TH expression in gWAT, eliminated induction of UCP1 by CL, and reduced tissue metabolic rate.ConclusionsCollectively, these data demonstrate that female mice are more responsive than males to the recruitment of brown adipocytes in gonadal WAT and this difference corresponds to greater levels of estrogen-dependent sympathetic innervation.Electronic supplementary materialThe online version of this article (doi:10.1186/s13293-016-0121-7) contains supplementary material, which is available to authorized users.

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“…Primary mouse adipocytes were prepared from inguinal adipose tissue as follows ( 50 ). Briefl y, inguinal fat pads were dissected from four-to six-week-old mice.…”

Section: Cell and Tissue Respiration Measurementsmentioning

confidence: 99%

LXRα fuels fatty acid-stimulated oxygen consumption in white adipocytes

Dib

Bugge

Collins

2014

Journal of Lipid Research

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Key hormonal regulatory mechanisms that control the balance between lipogenesis and lipolysis in adipose tissue are disrupted. Obese individuals are less sensitive to the antilipolytic actions of insulin and display an increase in basal lipolytic activity in their white adipose tissue (WAT), which results in high circulating levels of FFAs ( 6 ). These chronically elevated FFAs have been implicated in the pathogenesis of insulin resistance and type 2 diabetes ( 7 ). Thus utilization and/or sequestration of FFAs in WAT before they enter the circulation represent an important protective mechanism.The break-down of TG into FFA and glycerol in both WAT and brown adipose tissue (BAT) are largely under the control of the sympathetic nervous system (SNS) via catecholamines ( 8-10 ), and also by cardiac natriuretic peptides ( 11 ). In BAT the liberated FFAs provide not only the substrate for mitochondrial oxidative phosphorylation but they also directly activate the brown adipocyte-specifi c mitochondrial protonophoric uncoupling protein 1 (UCP1). UCP1 disengages energy stored in the proton gradient from ATP synthesis, resulting in a form of energy wastage known as thermogenesis ( 10,12 ). The existence of BAT has recently been affi rmed in adult humans ( 13,14 ). In WAT, on the other hand, it has been traditionally accepted that most of the FFAs liberated by lipolysis are released into the circulation to provide substrate for the energy requirements of other tissues in the body, including muscle, heart, and BAT ( 15, 16 ). Recent evidence, however, indicates a higher mitochondrial content in WAT than previously believed ( 17, 18 ), suggesting a greater role for white adipocyte mitochondria in the regulation of whole-body physiology ( 19 ). In addition to being released into the circulation and, to a much lesser extent, being reesterifi ed in situ ( 20 ), a portion of the liberated FFA undergoes mitochondrial oxidation within WAT itself ( 18,21,22 ). Obesity, which is characterized by an excessive increase in adipose tissue mass, is an escalating threat of epidemic proportions ( 1 ) and is highly correlated with a plethora of metabolic disorders ( 2, 3 ). Adipose tissue is a very plastic organ that can expand or contract to accommodate the needs of the organism. In cases of excess energy intake, adipose tissue engages in lipogenesis to store this energy as triglyceride (TG), while in times of inadequate dietary sources, it breaks down its reserves through lipolysis to provide substrate for oxidation and ATP synthesis within other tissues ( 4 ). Both lipogenesis and lipolysis are tightly controlled in adipocytes ( 5 ). However, in the obese condition, the normal homeostatic balance between lipogenesis and lipolysis is altered due to the excess caloric load ( 5 ). Abbreviations: AT-WT, aP2-Cre negative fl oxed (mice); ATaKO, adipose tissue LXR ␣ knockout (mice); BAT, brown adipose tissue; HFD, high-fat diet; HSL, hormone-sensitive lipase; LXR, liver X receptor; OCR, oxygen consumption rate; SNS, sympathetic nervous system...

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Measuring Respiratory Activity of Adipocytes and Adipose Tissues in Real Time

Cited by 31 publications

References 22 publications

Irisin protects mitochondria function during pulmonary ischemia/reperfusion injury

Irisin protects mitochondria function during pulmonary ischemia/reperfusion injury

Sex differences in sympathetic innervation and browning of white adipose tissue of mice

LXRα fuels fatty acid-stimulated oxygen consumption in white adipocytes

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