Erratum: Induction of lipogenesis in white fat during cold exposure in mice: link to lean phenotype

Flachs, Pavel; Adamcová, Kateřina; Zouhar, Petr; Marques, Cátia; Janovská, Petra; Viegas, Iván; Jones, John G.; Bardová, Kristina; Svobodová, Michaela; Hansikova, Jana; Kuda, Ondřej; Rossmeisl, Martin; Liisberg, Ulrike; Borkowska, Andzelika; Kristiansen, Karsten; Madsen, Lise; Kopecký, Jan

doi:10.1038/ijo.2017.61

Cited by 22 publications

(2 citation statements)

References 60 publications

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“…Interestingly, Flachs et al. ( 60 ) reported a connection between TAG/fatty acid cycling and lipogenesis in WAT in cold-exposed mice, suggesting that a reduction in fatty acid re-esterification may be partially offset by an increase in lipogenesis to support TAG synthesis. This provides additional support for our findings showing higher lipogenesis and lipolysis, concomitant with lower fatty acid re-esterification.…”

Section: Discussionmentioning

confidence: 99%

Delta-6 desaturase (Fads2) deficiency alters triacylglycerol/fatty acid cycling in murine white adipose tissue

Wang¹,

Hucik²,

Sarr³

et al. 2023

Journal of Lipid Research

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Section: Discussionmentioning

confidence: 99%

Delta-6 desaturase (Fads2) deficiency alters triacylglycerol/fatty acid cycling in murine white adipose tissue

Wang¹,

Hucik²,

Sarr³

et al. 2023

Journal of Lipid Research

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“…Though Ca 2+ futile cycling is dominant in skeletal muscle, several other substrate fluxes are critical for the maintenance of ATP production [151]. Lipid futile cycling through the lipolysis and re-esterification of free fatty acid (FFA) in white adipose is well documented, in both the presence and absence of UCP1 [152][153][154][155]. Data from cultured brown adipocytes suggests these mechanisms are also present in BAT, with little reliance on UCP1 [151].…”

Section: Ucp1-independent Thermogenic Mechanisms In Adipose Tissuementioning

confidence: 99%

Thermogenic adipocytes: lineage, function and therapeutic potential

Pollard

Carling

2020

Biochemical Journal

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Metabolic inflexibility, defined as the inability to respond or adapt to metabolic demand, is now recognised as a driving factor behind many pathologies associated with obesity and the metabolic syndrome. Adipose tissue plays a pivotal role in the ability of an organism to sense, adapt to and counteract environmental changes. It provides a buffer in times of nutrient excess, a fuel reserve during starvation and the ability to resist cold-stress through non-shivering thermogenesis. Recent advances in single-cell RNA sequencing combined with lineage tracing, transcriptomic and proteomic analyses have identified novel adipocyte progenitors that give rise to specialised adipocytes with diverse functions, some of which have the potential to be exploited therapeutically. This review will highlight the common and distinct functions of well-known adipocyte populations with respect to their lineage and plasticity, as well as introducing the most recent members of the adipocyte family and their roles in whole organism energy homeostasis. Finally, this article will outline some of the more preliminary findings from large data sets generated by single-cell transcriptomics of mouse and human adipose tissue and their implications for the field, both for discovery and for therapy.

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Prolonged FGF21 treatment increases energy expenditure and induces weight loss in obese mice independently of UCP1 and adrenergic signaling

Stanic,

Bardova,

Janovska

et al. 2024

Biochemical Pharmacology

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Erratum: Induction of lipogenesis in white fat during cold exposure in mice: link to lean phenotype

Cited by 22 publications

References 60 publications

Delta-6 desaturase (Fads2) deficiency alters triacylglycerol/fatty acid cycling in murine white adipose tissue

Delta-6 desaturase (Fads2) deficiency alters triacylglycerol/fatty acid cycling in murine white adipose tissue

Thermogenic adipocytes: lineage, function and therapeutic potential

Prolonged FGF21 treatment increases energy expenditure and induces weight loss in obese mice independently of UCP1 and adrenergic signaling

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