Mitochondrial Lipid Signaling and Adaptive Thermogenesis

Bank, Helaina Von; Hurtado-Thiele, Mae; Oshimura, Nanami; Simcox, Judith

doi:10.3390/metabo11020124

Cited by 29 publications

(16 citation statements)

References 97 publications

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“…Exerting an autocrine-paracrine regulation, FGF9 binds to FGFR3 receptor in adipocytes to regulate Ucp1 expression [ 399 ]. In addition to proteins, cold exposure induces the secretion of lipid species from BAT including 12,13-diHOME and 12-HEPE, which enhance BAT fatty acids [ 6 ] and glucose uptake [ 400 ] respectively. Altogether, cold exposure triggers an intricate metabolic network between the central nervous system (CNS) and AT which redirects the utilization of circulating glucose and FFAs to support heat production ultimately improving WAT and BAT function and whole-body metabolism.…”

Section: Activation Of Thermogenesis As Therapy For Obesity-associated Metabolic Diseasesmentioning

confidence: 99%

Thermogenic Fat: Development, Physiological Function, and Therapeutic Potential

Brandão

Poojari

Rabiee

2021

IJMS

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The concerning worldwide increase of obesity and chronic metabolic diseases, such as T2D, dyslipidemia, and cardiovascular disease, motivates further investigations into preventive and alternative therapeutic approaches. Over the past decade, there has been growing evidence that the formation and activation of thermogenic adipocytes (brown and beige) may serve as therapy to treat obesity and its associated diseases owing to its capacity to increase energy expenditure and to modulate circulating lipids and glucose levels. Thus, understanding the molecular mechanism of brown and beige adipocytes formation and activation will facilitate the development of strategies to combat metabolic disorders. Here, we provide a comprehensive overview of pathways and players involved in the development of brown and beige fat, as well as the role of thermogenic adipocytes in energy homeostasis and metabolism. Furthermore, we discuss the alterations in brown and beige adipose tissue function during obesity and explore the therapeutic potential of thermogenic activation to treat metabolic syndrome.

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Section: Activation Of Thermogenesis As Therapy For Obesity-associated Metabolic Diseasesmentioning

confidence: 99%

Thermogenic Fat: Development, Physiological Function, and Therapeutic Potential

Brandão

Poojari

Rabiee

2021

IJMS

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“…Melatonin is known for its role in maintaining systemic energy homeostasis [ 499 ]. In the mitochondria of brown and beige adipose tissue, CL biosynthesis is robustly induced upon cold exposure [ 500 , 501 ] because CL can bind tightly to uncoupling protein 1 (UCP1), stabilizing its conformation and enhancing functionality [ 502 ]. The ability of melatonin to protect CL from peroxidation may account for the increased thermogenic response in Zücker diabetic fatty (ZDF) rats via the restoration of UCP1 mRNA expression, increased mitochondrial mass and brown adipose tissue (BAT) weight, as well as enhanced mitochondrial OXPHOS activities in complex I and IV [ 503 ].…”

Section: Melatonin Is a Potent Ancient Antioxidant That Protects Atp Levels To Regulate The Formation And Dissolution Of Mlosmentioning

confidence: 99%

Melatonin: Regulation of Biomolecular Condensates in Neurodegenerative Disorders

Loh¹,

Reíter

2021

Antioxidants

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Biomolecular condensates are membraneless organelles (MLOs) that form dynamic, chemically distinct subcellular compartments organizing macromolecules such as proteins, RNA, and DNA in unicellular prokaryotic bacteria and complex eukaryotic cells. Separated from surrounding environments, MLOs in the nucleoplasm, cytoplasm, and mitochondria assemble by liquid–liquid phase separation (LLPS) into transient, non-static, liquid-like droplets that regulate essential molecular functions. LLPS is primarily controlled by post-translational modifications (PTMs) that fine-tune the balance between attractive and repulsive charge states and/or binding motifs of proteins. Aberrant phase separation due to dysregulated membrane lipid rafts and/or PTMs, as well as the absence of adequate hydrotropic small molecules such as ATP, or the presence of specific RNA proteins can cause pathological protein aggregation in neurodegenerative disorders. Melatonin may exert a dominant influence over phase separation in biomolecular condensates by optimizing membrane and MLO interdependent reactions through stabilizing lipid raft domains, reducing line tension, and maintaining negative membrane curvature and fluidity. As a potent antioxidant, melatonin protects cardiolipin and other membrane lipids from peroxidation cascades, supporting protein trafficking, signaling, ion channel activities, and ATPase functionality during condensate coacervation or dissolution. Melatonin may even control condensate LLPS through PTM and balance mRNA- and RNA-binding protein composition by regulating N6-methyladenosine (m6A) modifications. There is currently a lack of pharmaceuticals targeting neurodegenerative disorders via the regulation of phase separation. The potential of melatonin in the modulation of biomolecular condensate in the attenuation of aberrant condensate aggregation in neurodegenerative disorders is discussed in this review.

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“…Exerting an autocrineparacrine regulation, FGF9 binds to FGFR3 receptor in adipocytes to regulate Ucp1 expression [399]. In addition to proteins, cold exposure induces the secretion of lipid species from BAT including 12,13-diHOME and 12-HEPE, which enhance BAT fatty acids [6] and glucose uptake [400] respectively. Altogether, cold exposure triggers an intricate metabolic network between the central nervous system (CNS) and AT which redirects the utilization of circulating glucose and FFAs to support heat production ultimately improving WAT and BAT function and whole-body metabolism.…”

Section: Cold-induced Thermogenesismentioning

confidence: 99%

Thermogenic Fat: Development, Physiological Function, and Therapeutic Potential

Brandão¹,

Poojari²,

Rabiee³

2021

Preprint

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The concerning worldwide increase of obesity and chronic metabolic diseases such as T2D, dyslipidemia, and cardiovascular disease motivates further investigations into preventive and alternative therapeutic approaches. Over the past decade, there is growing evidence that the formation and activation of thermogenic adipocytes (brown and beige) may serve as therapy to treat obesity and its associated diseases owing to its capacity to increase energy expenditure and to modulate circulating lipids and glucose levels. Thus, understanding the molecular mechanism of brown and beige adipocytes formation and activation will facilitate the development of strategies to combat metabolic disorders. Here, we provide a comprehensive overview of pathways and players involved in the development of brown and beige fat as well as the role of thermogenic adipocytes in energy homeostasis and metabolism. Also, we discuss the alterations in brown and beige adipose tissue function during obesity and, explore the therapeutic potential of thermogenic activation to treat metabolic syndrome.

show abstract

Mitochondrial Lipid Signaling and Adaptive Thermogenesis

Cited by 29 publications

References 97 publications

Thermogenic Fat: Development, Physiological Function, and Therapeutic Potential

Thermogenic Fat: Development, Physiological Function, and Therapeutic Potential

Melatonin: Regulation of Biomolecular Condensates in Neurodegenerative Disorders

Thermogenic Fat: Development, Physiological Function, and Therapeutic Potential

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