Adipose Tissue as an Endocrine Organ

Hui, Hannah Xiaoyan; Feng, Tianshi

doi:10.5772/intechopen.76220

Cited by 6 publications

(6 citation statements)

References 112 publications

(139 reference statements)

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“…Finally, FoxO1 plays a pivotal role in ameliorating fat metabolism, maintaining redox homeostasis and thus counteracting pathologies such as obesity and type II diabetes. In fact, when molecular cascades that ensure systemic metabolic homeostasis are impaired, the metabolic disease can develop and eventually give rise to other correlated diseases spanning from hepatic steatosis to cancer [40,51]. The studies developed so far pose a starting point for future investigations to collocate FoxO1 in a therapeutic research plan focusing on metabolic syndrome and the aforementioned diseases.…”

Section: Discussionmentioning

confidence: 99%

“…Adipose tissue has the main function to store energy inside adipocytes in the form of neutral lipids during excess nutrient conditions and to release them by lipolysis during fasting, to guarantee whole-body energetic homeostasis. Indeed, adipose tissue is a very dynamic organ that rapidly readapts under many physiological stimuli, by changing number, size, metabolic and endocrine functions of adipocytes [40]. Several adipose tissue-resident cells, including immune cells and mesenchymal stem cells of the stromal vascular fractions, are necessary to support the remodeling of adipose tissue assuring clearance of dead adipocytes, adipogenic differentiation, and proper vascularization [41,42].…”

Section: Foxo1 Signaling In Adipose Tissuementioning

confidence: 99%

“…Responding to insulin and glucagon respectively during feeding and fasted state, the adipose tissue activates precise molecular pathways able to modify the expression and subcellular localization of metabolic enzymes and transcription factors [52]. Feeding stimulates the lipogenic pathway and storage of triglycerides in adipocytes, while fasting induces the activation of the lipolytic pathway and promotes the breakdown of triglycerides and the release of free fatty acids from adipose tissue [40,53,54]. In this scenario, FoxO1 inactivation by insulin signaling is necessary for activating the lipogenic program in adipocytes, whereas, in the fasted condition, it transcribes genes involved in lipid catabolism [10].…”

Section: Foxo1 Signaling In Adipose Tissuementioning

confidence: 99%

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Adipose Tissue and FoxO1: Bridging Physiology and Mechanisms

Ioannilli

Ciccarone

Ciriolo

2020

Cells

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Forkhead box O class proteins (FoxOs) are expressed nearly in all tissues and are involved in different functions such as energy metabolism, redox homeostasis, differentiation, and cell cycle arrest. The plasticity of FoxOs is demonstrated by post-translational modifications that determine diverse levels of transcriptional regulations also controlled by their subcellular localization. Among the different members of the FoxO family, we will focus on FoxO1 in adipose tissue, where it is abundantly expressed and is involved in differentiation and transdifferentiation processes. The capability of FoxO1 to respond differently in dependence of adipose tissue subtype underlines the specific involvement of the transcription factor in energy metabolism and the “browning” process of adipocytes. FoxO1 can localize to nuclear, cytoplasm, and mitochondrial compartments of adipocytes responding to different availability of nutrients and source of reactive oxygen species (ROS). Specifically, fasted state produced-ROS enhance the nuclear activity of FoxO1, triggering the transcription of lipid catabolism and antioxidant response genes. The enhancement of lipid catabolism, in combination with ROS buffering, allows systemic energetic homeostasis and metabolic adaptation of white/beige adipocytes. On the contrary, a fed state induces FoxO1 to accumulate in the cytoplasm, but also in the mitochondria where it affects mitochondrial DNA gene expression. The importance of ROS-mediated signaling in FoxO1 subcellular localization and retrograde communication will be discussed, highlighting key aspects of FoxO1 multifaceted regulation in adipocytes.

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Section: Discussionmentioning

confidence: 99%

Section: Foxo1 Signaling In Adipose Tissuementioning

confidence: 99%

Section: Foxo1 Signaling In Adipose Tissuementioning

confidence: 99%

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Adipose Tissue and FoxO1: Bridging Physiology and Mechanisms

Ioannilli

Ciccarone

Ciriolo

2020

Cells

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“…The AT secretory status depends on the changes of cellular tissue composition, including alterations in the phenotypes, numbers, and site of adipose tissue depots ( Ouchi et al, 2011 ). There are two types of adipokines- pro-inflammatory such as leptin, monocyte chemoattractant protein 1 (MCP-1), tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6) and anti-inflammatory such as adiponectin and interleukin 10 (IL-10) ( Mancuso, 2016 ; Hui and Feng, 2018 ; Henriques et al, 2019 ).…”

Section: Introductionmentioning

confidence: 99%

White adipose tissue as a target for cadmium toxicity

Attia

Das²,

Varadharajan³

et al. 2022

Front. Pharmacol.

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Cadmium (Cd) is a widespread heavy metal known as a toxic environmental pollutant. Cd exposure is threatening due to its bioaccumulation trait in living systems that exceeds 35 years without a beneficial biological role. Acute exposure to high Cd doses was reported to impact adipose tissue (AT) function adversely. The main aim of this study is to investigate the effect of low-dose chronic Cd exposure on the genes involved in adipose tissue (AT) functions. Adult male Sprague-Dawley rats were exposed to a low Cd dose (15 mg/kg B.W./day) for 10 weeks. Then, three AT depots-subcutaneous AT (SUB-AT), abdominal AT (AB-AT), and retroperitoneal AT (REtrop-AT) were excised for Cd accumulation measures and gene expression analysis. Adiponectin and leptin gene expression levels were investigated as markers for adipocytes function and homeostasis. Our results showed that Cd accumulated in all the tested adipose depots, but SUB-AT was found to be the depot to most accumulate Cd. Also, it was exhibited that chronic exposure to low Cd doses altered the gene expression of adipocytokines. The levels of adiponectin and leptin mRNA expression were downregulated in all tested AT-depots after Cd exposure. The significant adverse effect on SUB-AT compared to other depots indicates different responses based on AT depots location toward Cd exposure. Collectively, these results suggest a toxic effect of Cd that influenced adipocyte function.

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“…O TA é um tecido dinâmico e metabolicamente ativo e é responsável pela síntese e secreção de várias moléculas bioativas, como adipocinas e citocinas pró e anti-inflamatórias (FRANCISQUETI;NASCIMENTO;CORREA, 2015;HUI;FENG, 2018;LUO;LIU, 2016;MARTINS et al, 2014 PINTO, 2014;SZABLEWSKI, 2018).…”

Section: Introductionunclassified

Associação de variantes em >i<MC3R, MC4R, IRS1>/i< e >i<IRS2>/i< com obesidade e marcadores metabólicos, inflamatórios e adipocinas

Fajardo¹

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Introdução: A obesidade é uma doença metabólica crônica com diversas complicações de alto risco cardiovascular. Variantes em genes das vias da leptina-melanocortina e insulina foram associados com a obesidade e suas complicações. No entanto, a relação de variantes nesses genes com alterações antropométricas e metabólicas foram pouco exploradas na população brasileira. Objetivo: Analisar a associação de variantes em MC3R, MC4R, IRS1 e IRS2 com obesidade e biomarcadores metabólicos e inflamatórios e adipocinas, em indivíduos brasileiros. Métodos: Neste estudo do tipo caso controle, foram selecionados 168 indivíduos obesos, 99 com sobrepeso e 89 controles (grupo controle) classificados de acordo com o índice de massa corporal (IMC). Dados clínicos, antropométricos e composição corporal foram obtidos e os perfis metabólico, inflamatório e de adipocinas foram analisados. As variantes MC3R rs3746619 (c.-95C>A) e rs3827103 (c.130G>A), MC4R rs17782313 (g.57851097 T>C), IRS1 rs2943634 (g.226203364 A˃C) e IRS2 rs1865434 (g.109756261 C>T) foram analisadas por PCR em tempo real. Resultados: Os valores de parâmetros antropométricos e taxa de gordura corporal foram maiores nos grupos obeso e sobrepeso que no grupo controle (p<0,001). O grupo obeso apresentou maior frequência de hipertensão (46,5%), diabete tipo 2 (24,7%), dislipidemia (65,3%) e uso de medicamentos (74,1%) e menor prática de atividade física (32,4%) que os demais grupos (p<0,05). O grupo obeso também apresentou concentrações maiores de leptina, resistina, fibrinogênio, PAI-1, IL-1β, IL-6, PCRus e TNFα e concentrações menores de receptor de leptina solúvel que os demais grupos (p<0,05). As frequências alélicas das variantes genéticas deste estudo foram similares às da população geral (p>0,05). O genótipo AA do MC3R rs3827103 (c.130G>A) foi associado com sobrepeso (p=0,044). O alelo A das variantes MC3R rs3746619 (c.-95C>A) e rs3827103 (c.130G>A) foi associado com maior valor de HbA1 e menor concentração de apolipoproteina AI, respectivamente (p<0,05). O alelo C do IRS2 rs1865434 (g.109756261 C>T) foi associado com menor concentração de leptina (em homens) e de resistina (p<0,05). O alelo A do IRS1 rs2943634 A˃C e o genótipo CC do MC4R rs17782313 T˃C foram associados com maiores concentrações de fibrinogênio e PCRus (p<0,05). Esses resultados foram confirmados pela análise de regressão linear univariada. A análise de regressão logística univariada revelou associação da variante IRS1 A>C com maior risco de PCRus aumentado (OR=2,187; IC95%=1,237-3,866; p=0,007). Conclusões: As variantes MC3R rs3746619 e rs3827103, MC4R rs17782313, IRS1 rs2943634 e IRS2 rs1865434 parecem influenciar os perfis metabólico, inflamatório e de adipocinas, podendo ser biomarcadores úteis para avaliar o risco de alterações metabólicas e inflamatórias relacionadas com obesidade.

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Adipose Tissue as an Endocrine Organ

Cited by 6 publications

References 112 publications

Adipose Tissue and FoxO1: Bridging Physiology and Mechanisms

Adipose Tissue and FoxO1: Bridging Physiology and Mechanisms

White adipose tissue as a target for cadmium toxicity

Associação de variantes em >i<MC3R, MC4R, IRS1>/i< e >i<IRS2>/i< com obesidade e marcadores metabólicos, inflamatórios e adipocinas

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