Catecholamines suppress fatty acid re-esterification and increase oxidation in white adipocytes via STAT3

Reilly, Shannon M.; Hung, Chao‐Wei; Ahmadian, Maryam; Zhao, Peng; Keinan, Omer; Gomez, Andrew V.; DeLuca, Julia H; Dadpey, Benyamin; Lu, Donald; Zaid, Jessica; Poirier, BreAnne; Peng, Xiaoling; Yu, Ruth T.; Downes, Michael; Liddle, Christopher; Evans, Ronald M.; Murphy, Anne N.; Saltiel, Alan R.

doi:10.1038/s42255-020-0217-6

Cited by 29 publications

(25 citation statements)

References 136 publications

(60 reference statements)

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“…This might facilitate a finely tuned management of triacylglycerol synthesis and breakdown, that varies rapidly between bouts of energy intake (post-prandial periods) or energy dissipation (exercise, fasting, cold exposure). Besides providing FA for other tissues via their lipolytic effect, catecholamines have recently been described to also increase FA oxidation rate in the adipocytes themselves, via the phosphorylation of signal transducer and activator of transcription 3 (STAT3), which, in turn regulates FA metabolism in a non-genomic manner[ 62 ]. Alongside these two fates of released FA, mobilization and oxidation, there is also a third way, consisting in FA reesterification, which is predominant in adipocytes, since it limits excessive FA release and subsequent lipotoxicity.…”

Section: Discussionmentioning

confidence: 99%

Vanadium-dependent activation of glucose transport in adipocytes by catecholamines is not mediatedviaadrenoceptor stimulation or monoamine oxidase activity

Fontaine¹,

Tavernier²,

Morin³

et al. 2020

WJD

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BACKGROUND Benzylamine and methylamine activate glucose uptake in adipocytes. For tyramine, this effect has even been extended to cardiomyocytes. AIM To investigate the effects of catecholamines and other amines on glucose uptake. METHODS A screening compared 25 biogenic amines on 2-deoxyglucose (2-DG) uptake activation in rat adipocytes. Pharmacological approaches and transgenic mouse models were then used to decipher the mode of action of several hits. RESULTS In rat adipocytes, insulin stimulation of 2-DG uptake was reproduced with catecholamines. 100 µmol/L or 1 mmol/L adrenaline, noradrenaline, dopamine and deoxyepinephrine, maximally activated hexose transport only when sodium orthovanadate was added at 100 µmol/L. Such activation was similar to that already reported for benzylamine, methylamine and tyramine, well-recognized substrates of semicarbazide-sensitive amine oxidase (SSAO) and monoamine oxidase (MAO). Several, but not all, tested agonists of β-adrenoreceptors (β-ARs) also activated glucose transport while α-AR agonists were inactive. Lack of blockade by α- and β-AR antagonists indicated that catecholamine-induced 2-DG uptake was not mediated by AR stimulation. Adipocytes from mice lacking β 1 -, β 2 - and β 3 -ARs (triple KO) also responded to millimolar doses of adrenaline or noradrenaline by activating hexose transport in the presence of 100 µmol/L vanadate. The MAO blocker pargyline, and SSAO inhibitors did not block the effects of adrenaline or noradrenaline plus vanadate, which were blunted by antioxidants. CONCLUSION Catecholamines exert unexpected insulin-like actions in adipocytes when combined with vanadium. For limiting insulin resistance by activating glucose consumption at least in fat stores, we propose that catecholamine derivatives combined with vanadium can generate novel complexes that may have low toxicity and promising anti-diabetic properties.

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Section: Discussionmentioning

confidence: 99%

Vanadium-dependent activation of glucose transport in adipocytes by catecholamines is not mediatedviaadrenoceptor stimulation or monoamine oxidase activity

Fontaine¹,

Tavernier²,

Morin³

et al. 2020

WJD

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“…The constant breakdown and release of FFAs from adipocytes has been observed in fasting in rats, mice, and humans, with 40% of FFAs being rapidly recycled back to triglycerides [ 54 ]. More recently, it has been shown that β 3 AR signaling blocks the re-esterification of FFAs to TGs, potentially allowing for an inter-organ GL/FFA cycle [ 55 ].…”

Section: Inter-organ Lipid Signaling From White Adipose Tissuementioning

confidence: 99%

Mitochondrial Lipid Signaling and Adaptive Thermogenesis

et al. 2021

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Thermogenesis is an energy demanding process by which endotherms produce heat to maintain their body temperature in response to cold exposure. Mitochondria in the brown and beige adipocytes play a key role in thermogenesis, as the site for uncoupling protein 1 (UCP1), which allows for the diffusion of protons through the mitochondrial inner membrane to produce heat. To support this energy demanding process, the mitochondria in brown and beige adipocytes increase oxidation of glucose, amino acids, and lipids. This review article explores the various mitochondria-produced and processed lipids that regulate thermogenesis including cardiolipins, free fatty acids, and acylcarnitines. These lipids play a number of roles in thermogenic adipose tissue including structural support of UCP1, transcriptional regulation, fuel source, and activation of cell signaling cascades.

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“…The hyperactivation of neurohormonal systems especially β-adrenergic receptors (βARs) signaling abnormalities plays a pivotal role in HF pathogenesis 59 . And activated βARs directly lead to the phosphorylation of signal transducer and activator of transcription 3 (Stat3) which integrates multiple signaling pathways in the development of cardiac hypertrophy and eventual heart failure in cardiomyocytes 60 . Zhang et al investigated the molecular mechanism underlying βAR-mediated Stat3 activation and then proved that Src, Yes and Fyn, the main SFKs in MEF cells were critical mediators for βAR-initiated Stat3 phosphorylation to maintain the physiological function of the heart 61 .…”

Section: Sfks and Cardiovascular Diseasesmentioning

confidence: 99%

Src-family Protein Tyrosine Kinases: A promising target for treating Cardiovascular Diseases

Zhai¹,

Yang²,

Zhang³

et al. 2021

Int. J. Med. Sci.

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The Src-family protein tyrosine kinases (SFKs), a subfamily of non-receptor tyrosine kinases, are ubiquitously expressed in various cell types. Numerous studies have suggested that SFKs are related to signal transduction in major cardiac physiological and pathological processes, it is the activity of SFKs that is connected with the maintenance of cardiovascular homeostasis. Upon stimulation of various injury factors or stress, the phosphorylation state of SFKs is changed, which has been found to modulate different cardiac pathological conditions, such as hypertension, coronary heart disease, ischemic heart disease, myocardial ischemia-reperfusion injury, arrhythmia and cardiomyopathy via regulating cell growth, differentiation, movement and function, electrophysiologic signals. This review summarizes the basic information about SFKs, updates its role in the different processes underlying the development of multiple cardiovascular diseases (CVDs), and highlights their potential role as disease biomarkers and therapeutic targets, which would help understand the pathophysiology of CVDs and promote the further potential clinical adhibition.

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Catecholamines suppress fatty acid re-esterification and increase oxidation in white adipocytes via STAT3

Cited by 29 publications

References 136 publications

Vanadium-dependent activation of glucose transport in adipocytes by catecholamines is not mediatedviaadrenoceptor stimulation or monoamine oxidase activity

Vanadium-dependent activation of glucose transport in adipocytes by catecholamines is not mediatedviaadrenoceptor stimulation or monoamine oxidase activity

Mitochondrial Lipid Signaling and Adaptive Thermogenesis

Src-family Protein Tyrosine Kinases: A promising target for treating Cardiovascular Diseases

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