scholarly journals Aquaglyceroporins Are Differentially Expressed in Beige and White Adipocytes

2020 ◽  
Vol 21 (2) ◽  
pp. 610
Author(s):  
Inês Vieira da Silva ◽  
Francisco Díaz-Sáez ◽  
António Zorzano ◽  
Anna Gumà ◽  
Marta Camps ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Adipocyte Differentiation ◽  
Expression Patterns ◽  
Physiological Role ◽  
Glycerol Metabolism ◽  
Metabolic Complications ◽  
Altered Expression ◽  
Beige Adipocyte ◽  
White Adipocyte ◽  
White Adipocytes

Browning of white adipocytes has been proposed as a powerful strategy to overcome metabolic complications, since brown adipocytes are more catabolic, expending energy as a heat form. However, the biological pathways involved in the browning process are still unclear. Aquaglyceroporins are a sub-class of aquaporin water channels that also permeate glycerol and are involved in body energy homeostasis. In the adipose tissue, aquaporin-7 (AQP7) is the most representative isoform, being crucial for white adipocyte fully differentiation and glycerol metabolism. The altered expression of AQP7 is involved in the onset of obesity and metabolic disorders. Herein, we investigated if aquaglyceroporins are implicated in beige adipocyte differentiation, similar to white cells. Thus, we optimized a protocol of murine 3T3-L1 preadipocytes browning that displayed increased beige and decreased white adipose tissue features at both gene and protein levels and evaluated aquaporin expression patterns along the differentiation process together with cellular lipid content. Our results revealed that AQP7 and aquaporin-9 (AQP9) expression was downregulated throughout beige adipocyte differentiation compared to white differentiation, which may be related to the beige physiological role of heat production from oxidative metabolism, contrasting with the anabolic/catabolic lipid metabolism requiring glycerol gateways occurring in white adipose cells.

scholarly journals CD90 Is Dispensable for White and Beige/Brown Adipocyte Differentiation

2020 ◽  
Vol 21 (21) ◽  
pp. 7907
Author(s):  
Meike Dahlhaus ◽  
Julian Roos ◽  
Daniel Engel ◽  
Daniel Tews ◽  
Daniel Halbgebauer ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Stromal Cells ◽  
Adipocyte Differentiation ◽  
Human Adipose Tissue ◽  
Brown Adipocyte ◽  
White Adipocyte ◽  
White Adipocytes ◽  
Brown Adipose ◽  
Adipose Tissue Stromal Cells ◽  
Flow Cytometric Sorting

Brown adipose tissue (BAT) is a thermogenic organ in rodents and humans. In mice, the transplantation of BAT has been successfully used to combat obesity and its comorbidities. While such beneficial properties of BAT are now evident, the developmental and cellular origins of brown, beige, and white adipocytes have remained only poorly understood, especially in humans. We recently discovered that CD90 is highly expressed in stromal cells isolated from human white adipose tissue (WAT) compared to BAT. Here, we studied whether CD90 interferes with brown or white adipogenesis or white adipocyte beiging. We applied flow cytometric sorting of human adipose tissue stromal cells (ASCs), a CRISPR/Cas9 knockout strategy in the human Simpson-Golabi-Behmel syndrome (SGBS) adipocyte model system, as well as a siRNA approach in human approaches supports the hypothesis that CD90 affects brown or white adipogenesis or white adipocyte beiging in humans. Taken together, our findings call the conclusions drawn from previous studies, which claimed a central role of CD90 in adipocyte differentiation, into question.

RANKL induces beige adipocyte differentiation in preadipocytes

2020 ◽  
Vol 318 (6) ◽  
pp. E866-E877
Author(s):  
Flávia Sayuri Matsuo ◽  
Paulo Henrique Cavalcanti de Araújo ◽  
Ryerson Fonseca Mota ◽  
Ana Júlia Rossoni Carvalho ◽  
Mariana Santos de Queiroz ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Adipocyte Differentiation ◽  
Stromal Vascular Fraction ◽  
Nuclear Factor Κb ◽  
Whole Body ◽  
Brown Adipocyte ◽  
Marker Genes ◽  
Beige Adipocyte ◽  
White Adipocyte

The receptor activator of nuclear factor-κB (NF-κB) (RANK), its ligand (RANKL), and the decoy receptor osteoprotegerin (OPG) are a triad of proteins that regulate bone metabolism, and serum OPG is considered a biomarker for cardiovascular diseases and Type 2 diabetes; however, the implications of OPG in adipose tissue metabolism remains elusive. In this study, we investigate RANK-RANKL-OPG signaling in white adipose tissue browning. Histological analysis of osteoprotegerin knockout (OPG−/−) mice showed subcutaneous white adipose tissue (sWAT) browning, resistance for high-fat diet-induced weight gain, and preserved glucose metabolism compared with wild-type (WT) mice. Stromal vascular fraction (SVF) cells from sWAT of OPG−/− mice showed multilocular morphology and higher expression of brown adipocyte marker genes compared with those from the WT group. Infusion of RANKL induced browning and elevated respiratory rates in sWAT, along with increased whole body oxygen consumption in mice measured by indirect calorimetry. Subcutaneous WAT-derived SVF and 3T3-L1 cells, but not mature white adipocytes, differentiated into beige adipose tissue in the presence of RANKL. Moreover, SVF cells, even under white adipocyte differentiation, showed multilocular lipid droplet, lower lipid content, and increased expression of beige adipocyte markers with RANKL stimulation. In this study, we show for the first time the contribution of RANKL to increase energy expenditure by inducing beige adipocyte differentiation in preadipocytes.

scholarly journals Orphan GPR116 mediates the insulin sensitizing effects of the hepatokine FNDC4 in adipose tissue

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Anastasia Georgiadi ◽  
Valeria Lopez-Salazar ◽  
Rabih El- Merahbi ◽  
Rhoda Anane Karikari ◽  
Xiaochuan Ma ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Dependent Manner ◽  
Metabolic Dysfunction ◽  
Functional Interaction ◽  
White Adipocyte ◽  
White Adipocytes ◽  
Obesity And Diabetes ◽  
Adhesion Gpcr ◽  
Circulating Levels

AbstractThe proper functional interaction between different tissues represents a key component in systemic metabolic control. Indeed, disruption of endocrine inter-tissue communication is a hallmark of severe metabolic dysfunction in obesity and diabetes. Here, we show that the FNDC4-GPR116, liver-white adipose tissue endocrine axis controls glucose homeostasis. We found that the liver primarily controlled the circulating levels of soluble FNDC4 (sFNDC4) and lowering of the hepatokine FNDC4 led to prediabetes in mice. Further, we identified the orphan adhesion GPCR GPR116 as a receptor of sFNDC4 in the white adipose tissue. Upon direct and high affinity binding of sFNDC4 to GPR116, sFNDC4 promoted insulin signaling and insulin-mediated glucose uptake in white adipocytes. Indeed, supplementation with FcsFNDC4 in prediabetic mice improved glucose tolerance and inflammatory markers in a white-adipocyte selective and GPR116-dependent manner. Of note, the sFNDC4-GPR116, liver-adipose tissue axis was dampened in (pre) diabetic human patients. Thus our findings will now allow for harnessing this endocrine circuit for alternative therapeutic strategies in obesity-related pre-diabetes.

scholarly journals Lsd1 prevents age-programed loss of beige adipocytes

2017 ◽  
Vol 114 (20) ◽  
pp. 5265-5270 ◽  
Author(s):  
Delphine Duteil ◽  
Milica Tosic ◽  
Dominica Willmann ◽  
Anastasia Georgiadi ◽  
Toufike Kanouni ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Peroxisome Proliferator ◽  
Fat Cell ◽  
White Adipocyte ◽  
White Adipocytes ◽  
Age Related ◽  
Beige Adipocytes ◽  
Beige Fat ◽  
And Function

Aging is accompanied by major changes in adipose tissue distribution and function. In particular, with time, thermogenic-competent beige adipocytes progressively gain a white adipocyte morphology. However, the mechanisms controlling the age-related transition of beige adipocytes to white adipocytes remain unclear. Lysine-specific demethylase 1 (Lsd1) is an epigenetic eraser enzyme positively regulating differentiation and function of adipocytes. Here we show that Lsd1 levels decrease in aging inguinal white adipose tissue concomitantly with beige fat cell decline. Accordingly, adipocyte-specific increase of Lsd1 expression is sufficient to rescue the age-related transition of beige adipocytes to white adipocytes in vivo, whereas loss of Lsd1 precipitates it. Lsd1 maintains beige adipocytes by controlling the expression of peroxisome proliferator-activated receptor α (Ppara), and treatment with a Ppara agonist is sufficient to rescue the loss of beige adipocytes caused by Lsd1 ablation. In summary, our data provide insights into the mechanism controlling the age-related beige-to-white adipocyte transition and identify Lsd1 as a regulator of beige fat cell maintenance.

Expression characteristics of ANGPTL-3 and ANGPTL-4 in duck liver and adipose tissues during early post-hatching development

2016 ◽  
Vol 50 (4) ◽  
Author(s):  
Jie Kou ◽  
Yangmei Zhao ◽  
Hehe Liu ◽  
Wanxia Wang ◽  
Jiwei Hu ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Tissue Distribution ◽  
Real Time Pcr ◽  
Adipocyte Differentiation ◽  
Expression Patterns ◽  
Quantitative Real Time Pcr ◽  
Adipose Tissues ◽  
Abdominal Adipose Tissue ◽  
Peking Duck

Angiopoietin-like protein 3 and -4 (ANGPTL-3 and -4) are generally related to lipid metabolism as well as angiogenesis in animals, however very less was known about their mRNA expression characterizations in tissue development. In this study, the mRNA expressions of ANGPTL-3 and ANGPTL-4 (ANGPTL-3 and -4) and tissue distribution in Peking duck (Anas platyrhynchos) of 1 to 8 weeks of age were analyzed using quantitative real-time PCR methods. It was observed that ANGPTL-3 and -4 mRNAs were broadly expressed in duck liver and adipose tissues and were most abundant in intra-abdominal adipose tissue (AD). ANGPTL-3 and -4 had different expression patterns in tissues. These data suggested that both duck ANGPTL-3 and -4 could be related to the development of tissues, and ANGPTL-4 may contribute to the development of adipose tissue through promoting adipocyte differentiation.

scholarly journals Extra-adrenal regeneration of glucocorticoids by 11β-hydroxysteroid dehydrogenase type 1: physiological regulator and pharmacological target for energy partitioning

2007 ◽  
Vol 66 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Brian R. Walker
Keyword(s):  
Adipose Tissue ◽  
Human Subjects ◽  
Physiological Role ◽  
Hydroxysteroid Dehydrogenase ◽  
Receptor Activation ◽  
Energy Partitioning ◽  
Metabolic Complications ◽  
Cortisol Levels ◽  
Specific Regulation

The major glucocorticoid in man, cortisol, plays important roles in regulating fuel metabolism, energy partitioning and body fat distribution. In addition to the control of cortisol levels in blood by the hypothalamic–pituitary–adrenal axis, intracellular cortisol levels within target tissues can be controlled by local enzymes. 11β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) catalyses the regeneration of active cortisol from inert cortisone, thereby amplifying cortisol levels and glucocorticoid receptor activation in adipose tissue, liver and other tissues. 11β-HSD1 is under complex tissue-specific regulation and there is evidence that it adjusts local cortisol concentrations independently of the plasma cortisol concentrations, e.g. in response to changes in diet. In obesity 11β-HSD1 mRNA and activity in adipose tissue are increased. The mechanism of this up-regulation remains uncertain; polymorphisms in the HSD11B1 gene have been associated with metabolic complications of obesity, including hypertension and type 2 diabetes, but not with obesity per se. Extensive data have been obtained in mice with transgenic over-expression of 11β-HSD1 in liver and adipocytes, targeted deletion of 11β-HSD1, and using novel selective 11β-HSD1 inhibitors; these data support the use of 11β-HSD1 inhibitors to lower intracellular glucocorticoid levels and treat both obesity and its metabolic complications. Moreover, in human subjects the non-selective ‘prototype’ inhibitor carbenoxolone enhances insulin sensitivity. Results of clinical studies with novel potent selective 11β-HSD1 inhibitors are therefore eagerly awaited. The present article focuses on the physiological role of glucocorticoids in regulating energy partitioning, and the evidence that this process is modulated by 11β-HSD1 in human subjects.

scholarly journals Mitochondria in White, Brown, and Beige Adipocytes

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Miroslava Cedikova ◽  
Michaela Kripnerová ◽  
Jana Dvorakova ◽  
Pavel Pitule ◽  
Martina Grundmanova ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Energy Metabolism ◽  
Oxygen Radicals ◽  
Adipocyte Differentiation ◽  
Nonshivering Thermogenesis ◽  
Adipose Tissues ◽  
White Adipocytes ◽  
Beige Adipocytes ◽  
Colour Appearance

Mitochondria play a key role in energy metabolism in many tissues, including cardiac and skeletal muscle, brain, liver, and adipose tissue. Three types of adipose depots can be identified in mammals, commonly classified according to their colour appearance: the white (WAT), the brown (BAT), and the beige/brite/brown-like (bAT) adipose tissues. WAT is mainly involved in the storage and mobilization of energy and BAT is predominantly responsible for nonshivering thermogenesis. Recent data suggest that adipocyte mitochondria might play an important role in the development of obesity through defects in mitochondrial lipogenesis and lipolysis, regulation of adipocyte differentiation, apoptosis, production of oxygen radicals, efficiency of oxidative phosphorylation, and regulation of conversion of white adipocytes into brown-like adipocytes. This review summarizes the main characteristics of each adipose tissue subtype and describes morphological and functional modifications focusing on mitochondria and their activity in healthy and unhealthy adipocytes.

scholarly journals Analysis of DYRK1B, PPARG, and CEBPB Expression Patterns in Adipose-Derived Stem Cells from Patients carrying DYRK1B R102C and Healthy Individuals During Adipogenesis

2021 ◽  
Author(s):  
Azam Armanmehr ◽  
Hossein Jafari Khamirani ◽  
Sina Zoghi ◽  
Mehdi Dianatpour
Keyword(s):  
Metabolic Syndrome ◽  
Stem Cells ◽  
Adipose Tissue ◽  
Transcription Factors ◽  
Adipocyte Differentiation ◽  
Expression Patterns ◽  
Signs And Symptoms ◽  
Adipose Derived Stem Cells ◽  
Healthy Individuals ◽  
Normal Individuals

Background: Metabolic syndrome (MetS) is a group of signs and symptoms that are associated with a higher risk of Type 2 Diabetes Mellitus (T2DM) and Cardiovascular Diseases (CVDs). The major risk factor for developing MetS is abdominal obesity that is caused by an increase in adipocyte size or number. Adipocyte number multiplication is caused by the differentiation of mesenchymal stem cells into adipose tissue. Numerous studies have evaluated the expression of key transcription factors including PPARG and CEBPB during adipocyte differentiation in murine cells such as 3T3-L1 cell line. In order to comprehend the expression changes during the process of fat accumulation in adipose tissue derived stem cells (ASCs), we compared the expression of DYRK1B, PPARG, and CEBPB in undifferentiated and differentiated ASCs into mature adipocytes between the patient (harboring DYRK1b R102C) and control (healthy individuals) groups. Methods: Gene expression was evaluated on eighth days pre-induction and days 1, 5, and 15 post-induction. The pluripotent capacity of ASCs and the potential for differentiation into adipocytes were confirmed by flow cytometry analysis of surface markers (CD34, CD44, CD105, and CD90), and Oil red O staining, respectively. Expressions of DYRK1B, PPARG, and CEBPB were assessed by RT-PCR in patients' and normal individuals' samples. Results: The expression of DYRK1B kinase and transcription factors (CEBPB and PPARG) are significantly higher in adipose derived stem cells harboring DYRK1b R102C compared to non-carriers on days 5 and 15 during adipocyte differentiation. These proteins may be suitable targets for therapeutic strategies in obesity and obesity related disorders like metabolic syndrome. Furthermore, AZ191 exhibited a potent and selective inhibitory activity toward DYRK1B and CEBPB. Conclusion: CEBPB, PPARA, and DYRK1B contribute to adipogenesis and the development of metabolic syndrome; thus, they can be harnessed in developing therapeutic agents against metabolic syndrome.

scholarly journals Molecular and Cellular Bases of Lipodystrophy Syndromes

2022 ◽  
Vol 12 ◽  
Author(s):  
Jamila Zammouri ◽  
Camille Vatier ◽  
Emilie Capel ◽  
Martine Auclair ◽  
Caroline Storey-London ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Liver Disease ◽  
Adipocyte Differentiation ◽  
Systemic Diseases ◽  
Partial Loss ◽  
Metabolic Complications ◽  
Nonalcoholic Fatty Liver ◽  
Adipose Tissue Dysfunction ◽  
Gonadotropic Axis ◽  
Molecular Bases

Lipodystrophy syndromes are rare diseases originating from a generalized or partial loss of adipose tissue. Adipose tissue dysfunction results from heterogeneous genetic or acquired causes, but leads to similar metabolic complications with insulin resistance, diabetes, hypertriglyceridemia, nonalcoholic fatty liver disease, dysfunctions of the gonadotropic axis and endocrine defects of adipose tissue with leptin and adiponectin deficiency. Diagnosis, based on clinical and metabolic investigations, and on genetic analyses, is of major importance to adapt medical care and genetic counseling. Molecular and cellular bases of these syndromes involve, among others, altered adipocyte differentiation, structure and/or regulation of the adipocyte lipid droplet, and/or premature cellular senescence. Lipodystrophy syndromes frequently present as systemic diseases with multi-tissue involvement. After an update on the main molecular bases and clinical forms of lipodystrophy, we will focus on topics that have recently emerged in the field. We will discuss the links between lipodystrophy and premature ageing and/or immuno-inflammatory aggressions of adipose tissue, as well as the relationships between lipomatosis and lipodystrophy. Finally, the indications of substitutive therapy with metreleptin, an analog of leptin, which is approved in Europe and USA, will be discussed.

scholarly journals Oxyresveratrol Increases Energy Expenditure through Foxo3a-Mediated Ucp1 Induction in High-Fat-Diet-Induced Obese Mice

2018 ◽  
Vol 20 (1) ◽  
pp. 26 ◽  
Author(s):  
Jin Choi ◽  
No-Joon Song ◽  
A Lee ◽  
Dong Lee ◽  
Min-Ju Seo ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Energy Expenditure ◽  
High Fat Diet ◽  
Adipocyte Differentiation ◽  
Metabolic Diseases ◽  
Biological Activities ◽  
Obese Mice ◽  
High Fat ◽  
White Adipocyte

The phytochemical oxyresveratrol has been shown to exert diverse biological activities including prevention of obesity. However, the exact reason underlying the anti-obese effects of oxyresveratrol is not fully understood. Here, we investigated the effects and mechanism of oxyresveratrol in adipocytes and high-fat diet (HFD)-fed obese mice. Oxyresveratrol suppressed lipid accumulation and expression of adipocyte markers during the adipocyte differentiation of 3T3-L1 and C3H10T1/2 cells. Administration of oxyresveratrol in HFD-fed obese mice prevented body-weight gains, lowered adipose tissue weights, improved lipid profiles, and increased glucose tolerance. The anti-obese effects were linked to increases in energy expenditure and higher rectal temperatures without affecting food intake, fecal lipid content, and physical activity. The increased energy expenditure by oxyresveratrol was concordant with the induction of thermogenic genes including Ucp1, and the reduction of white adipocyte selective genes in adipose tissue. Furthermore, Foxo3a was identified as an oxyresveratrol-induced gene and it mimicked the effects of oxyresveratrol for induction of thermogenic genes and suppression of white adipocyte selective genes, suggesting the role of Foxo3a in oxyresveratrol-mediated anti-obese effects. Taken together, these data show that oxyresveratrol increases energy expenditure through the induction of thermogenic genes in adipose tissue and further implicates oxyresveratrol as an ingredient and Foxo3a as a molecular target for the development of functional foods in obesity and metabolic diseases.

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