Brown adipose tissue and alzheimer’s disease

Tayanloo-Beik, Akram; Nikkhah, Amirabbas; Alaei, Setareh; Goodarzi, Parisa; Rezaei‐Tavirani, Mostafa; Mafi, Ahmad R.; Larijani, Bagher; Shouroki, Fatemeh Fazeli; Arjmand, Babak

doi:10.1007/s11011-022-01097-z

Cited by 4 publications

(2 citation statements)

References 131 publications

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“…Recent studies have shown that BAT activation is an effective approach in cancer therapy (80) and benefits patients with Alzheimer's disease (AD) (81)(82)(83). Cold-stimulated BAT mitigates glucose uptake in the tumor tissues and is used for BAT-mediated thermogenesis at cold temperatures (80).…”

Section: Discussionmentioning

confidence: 99%

GPR84-mediated signal transduction affects metabolic function by promoting brown adipocyte activity

Sun,

An,

Paschoal

et al. 2023

Journal of Clinical Investigation

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The G protein–coupled receptor 84 (GPR84), a medium-chain fatty acid receptor, has garnered attention because of its potential involvement in a range of metabolic conditions. However, the precise mechanisms underlying this effect remain elusive. Our study has shed light on the pivotal role of GPR84, revealing its robust expression and functional significance within brown adipose tissue (BAT). Mice lacking GPR84 exhibited increased lipid accumulation in BAT, rendering them more susceptible to cold exposure and displaying reduced BAT activity compared with their WT counterparts. Our in vitro experiments with primary brown adipocytes from GPR84-KO mice revealed diminished expression of thermogenic genes and reduced O 2 consumption. Furthermore, the application of the GPR84 agonist 6- n -octylaminouracil (6-OAU) counteracted these effects, effectively reinstating the brown adipocyte activity. These compelling in vivo and in vitro findings converge to highlight mitochondrial dysfunction as the primary cause of BAT anomalies in GPR84-KO mice. The activation of GPR84 induced an increase in intracellular Ca 2+ levels, which intricately influenced mitochondrial respiration. By modulating mitochondrial Ca 2+ levels and respiration, GPR84 acts as a potent molecule involved in BAT activity. These findings suggest that GPR84 is a potential therapeutic target for invigorating BAT and ameliorating metabolic disorders.

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Section: Discussionmentioning

confidence: 99%

GPR84-mediated signal transduction affects metabolic function by promoting brown adipocyte activity

Sun,

An,

Paschoal

et al. 2023

Journal of Clinical Investigation

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show abstract

“…While white adipocytes primarily serve as energy reservoirs, brown and beige adipocytes specialize in energy expenditure through thermogenesis. This thermogenic capacity holds significant promise for influencing overall energy homeostasis, especially in the context of metabolic disorders (Tayanloo-Beik et al, 2023; Seki et al, 2022; Wibmer et al, 2021; Becher et al, 2021; Razzoli et al, 2016, Nedergaard et al, 2007). Non-shivering thermogenesis, a crucial component of the body’s heat-producing mechanisms, can be initiated by cold exposure and various environmental cues, yet the intricate mechanisms remain incompletely understood (Hoang et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

Deciphering Species-Specific and Conserved Regulation of HumanUCP1Gene Expression: Insights from Predicted Homeodomain Family Transcription Factor Binding Sites

B. Tóth,

Hegedűs,

Virág

et al. 2024

Preprint

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While the potential of adipocyte thermogenesis in influencing metabolic diseases is well-recognized, its precise regulatory mechanisms remain elusive. To address this, we explore the complex network of transcription factors (TFs) governing the human UCP1 gene, a central player in thermogenesis, to shed light on regulatory processes driving human fat cell phenotypes. By employing computational analyses, we screen UCP1 ortholog and paralog promoters across humans, mice and rats to uncover conserved and species-specific regulatory elements. Leveraging transcriptomic data, chipSeq results and AdioNET phenotyping we delineate TFs potentially bind to the human UCP1 promoter. Significant sequence variation is revealed in the enhancer regions of UCP1s, characterised by the absence of large segments in the rodent genome, potentially influenced by the presence/absence of repetitive elements. Furthermore, our analyses identify species-specific regulatory hotspots mostly recognized by homeodomain family TFs providing the potential for the formation of enhanceosomes with nearby TFs. Exploring phylogenetically conserved regulatory elements reveals TFs exhibiting binding sites across species and UCP paralogs assigning again homeodomain family TFs among others, and bHLH TFs, respectively. These results potentially advance our understanding of thermogenic fat cell development and offer new targets for intervention in metabolic disorders.

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Intranasal insulin treatment ameliorates spatial memory, muscular strength, and frailty deficits in 5xFAD mice

Gendron,

Fertan,

Roddick

et al. 2024

Physiology & Behavior

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Brown adipose tissue and alzheimer’s disease

Cited by 4 publications

References 131 publications

GPR84-mediated signal transduction affects metabolic function by promoting brown adipocyte activity

GPR84-mediated signal transduction affects metabolic function by promoting brown adipocyte activity

Deciphering Species-Specific and Conserved Regulation of HumanUCP1Gene Expression: Insights from Predicted Homeodomain Family Transcription Factor Binding Sites

Intranasal insulin treatment ameliorates spatial memory, muscular strength, and frailty deficits in 5xFAD mice

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