Adipose tissue development: The role of precursor cells and adipogenic factors

1987 ◽  
Vol 65 (17) ◽  
pp. 803-811 ◽  
Author(s):  
H. Hauner ◽  
G. Löffler
Keyword(s):  
Adipose Tissue ◽  
Precursor Cells ◽  
Tissue Development ◽  
Adipose Tissue Development

scholarly journals Enhanced nutritionally induced adipose tissue development in mice with stromelysin-1 gene inactivation

2003 ◽  
Vol 89 (04) ◽  
pp. 696-704 ◽  
Author(s):  
Erik Maquoi ◽  
Diego Demeulemeester ◽  
Gabor Vörös ◽  
Désire Collen ◽  
H. Lijnen
Keyword(s):  
Adipose Tissue ◽  
Research Society ◽  
The Body ◽  
Tissue Development ◽  
Cholesterol Levels ◽  
Fat Deposits ◽  
Adipose Tissue Development ◽  
Adipocyte Hypertrophy ◽  
Deficient Mice

SummaryTo investigate a potential role of stromelysin-1 (MMP-3) in development of adipose tissue, 5 week old male MMP-3 deficient mice (MMP-3-/-) and wild-type (MMP-3+/+) controls were kept on a high fat diet (HFD) for 15 weeks. MMP-3-/- mice were hyperphagic and gained more weight than the MMP-3+/+ mice. At the time of sacrifice, the body weight of the MMP-3-/- mice was significantly higher than that of the MMP-3+/+ mice, as was the weight of the isolated subcutaneous (SC) and gonadal (GON) fat deposits. Significant adipocyte hypertrophy was observed in the GON but not in the SC adipose tissue of MMP-3-/- mice. Fasting plasma glucose and cholesterol levels were comparable in both genotypes, whereas triglyceride levels were significantly lower in MMP-3-/- mice. Staining with an endothelial cell specific lectin revealed a significantly higher blood vessel density and larger total stained area in the GON adipose tissues of MMP-3-/- mice. Thus, in a murine model of nutritionally induced obesity, MMP-3 impairs adipose tissue development, possibly by affecting food intake and/or adipose tissue-related angiogenesis.Theme paper: Part of this paper was originally presented at the joint meetings of the 16th International Congress of the International Society of Fibrinolysis and Proteolysis (ISFP) and the 17th International Fibrinogen Workshop of the International Fibrinogen Research Society (IFRS) held in Munich, Germany, September, 2002.

Influence of t-PA and u-PA on Adipose Tissue Development in a Murine Model of Diet-Induced Obesity

2002 ◽  
Vol 87 (02) ◽  
pp. 306-310 ◽  
Author(s):  
P.E. Morange ◽  
D. Bastelica ◽  
M.F. Bonzi ◽  
B. Van Hoef ◽  
D. Collen ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Plasminogen Activator ◽  
The Body ◽  
Tissue Type ◽  
Tissue Development ◽  
Diet Induced Obesity ◽  
Type Plasminogen Activator ◽  
Urokinase Type Plasminogen Activator ◽  
Adipose Tissue Development

SummaryTo investigate the potential role of tissue-type plasminogen activator (t-PA) or urokinase-type plasminogen activator (u-PA) in development of adipose tissue, we have used a nutritionally induced obesity model in t-PA (t-PA−/−) and u-PA (u-PA−/−) deficient mice. Five week old male wild-type (WT), t-PA−/− or u-PA−/− mice (n = 9 to 16) were fed a high fat diet (HFD, 42% fat). After 16 weeks of HFD, the body weight of t-PA−/− mice was significantly higher than that of WT mice (48 ± 1.1 g vs. 39 ± 2.2 g, p = 0.004). The total weight of the isolated subcutaneous (sc) fat deposit was higher in t-PA−/− than in WT mice (2.4 ± 0.22 g vs. 1.2 ± 0.29 g, p = 0.002), accompanied with higher adipocyte diameters (80 ± 1.7 µm vs. 61 ± 4.7 µm, p < 0.01). These differences were not observed in the intra-abdominal fat deposit. The number of stroma cells in both adipose tissue territories was increased in t-PA−/− as compared to WT mice (2.0 ± 0.13 vs. 1.5 ± 0.10 p = 0.02 and 3.0 ± 0.17 vs 1.6 ± 0.17, p = 0.0001, stroma cells/ adipocytes in sc and intra-abdominal tissue, respectively), partly as a result of an increased number of endothelial cells (192 ± 9 vs. 154 ± 18 p = 0.06 and 108 ± 13 vs. 69 ± 8 p = 0.04 CD31 stained/adipocyte area). In contrast the weight gain and adipose tissue development in u-PA−/− mice was not different from that in WT mice. These data suggest that t-PA but not u-PA plays a role in adipose tissue development.

scholarly journals Role of Gas-6 in Adipogenesis and Nutritionally Induced Adipose Tissue Development in Mice

2005 ◽  
Vol 25 (5) ◽  
pp. 1002-1007 ◽  
Author(s):  
Erik Maquoi ◽  
Gabor Vörös ◽  
Peter Carmeliet ◽  
Désiré Collen ◽  
H. Roger Lijnen
Keyword(s):  
Adipose Tissue ◽  
Tissue Development ◽  
Adipose Tissue Development

scholarly journals H3.3K4M destabilizes enhancer epigenomic writers MLL3/4 and impairs adipose tissue development

2018 ◽  
Author(s):  
Younghoon Jang ◽  
Chaochen Wang ◽  
Aaron Broun ◽  
Young-Kwon Park ◽  
Lenan Zhuang ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Precursor Cells ◽  
Tissue Development ◽  
Set Domain ◽  
H3k4 Methylation ◽  
Double Knockout ◽  
Histone H3k4 ◽  
Adipose Tissue Development ◽  
And Function ◽  
H3k4 Methyltransferases

AbstractHistone H3K4 mono-methyltransferases MLL3 and MLL4 (MLL3/4) are required for enhancer activation during cell differentiation, though the mechanism is incompletely understood. To address MLL3/4 enzymatic activity in enhancer regulation, we have generated two mouse lines: one expressing H3.3K4M, a lysine-4-to-methionine (K4M) mutation of histone H3.3 that inhibits H3K4 methylation, and the other carrying conditional double knockout of MLL3/4 enzymatic SET domains. Expression of H3.3K4M in lineage-specific precursor cells depletes H3K4 methylation and prevents adipogenesis and adipose tissue development. Mechanistically, H3.3K4M prevents enhancer activation in adipogenesis by destabilizing MLL3/4 proteins but not other Set1-like H3K4 methyltransferases. Notably, deletion of the enzymatic SET domain of MLL3/4 in lineage-specific precursor cells mimics H3.3K4M expression and prevents adipose tissue development. Interestingly, destabilization of MLL3/4 by H3.3K4M in adipocytes does not affect adipose tissue maintenance and function. Together, our findings indicate that H3.3K4M destabilizes enhancer epigenomic writers MLL3/4 and impairs adipose tissue development.

scholarly journals Nutrigenomic regulation of adipose tissue development — role of retinoic acid: A review

Meat Science ◽  
2016 ◽  
Vol 120 ◽  
pp. 100-106 ◽  
Author(s):  
Bo Wang ◽  
Qiyuan Yang ◽  
Corrine L. Harris ◽  
Mark L. Nelson ◽  
Jan R. Busboom ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Retinoic Acid ◽  
Tissue Development ◽  
Adipose Tissue Development

scholarly journals Long non-coding RNAs in regulation of adipogenesis and adipose tissue function

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Tiziana Squillaro ◽  
Gianfranco Peluso ◽  
Umberto Galderisi ◽  
Giovanni Di Bernardo
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Drug Targets ◽  
Metabolic Diseases ◽  
Tissue Development ◽  
Cellular Functions ◽  
Adipose Tissue Development ◽  
And Function

Complex interaction between genetics, epigenetics, environment, and nutrition affect the physiological activities of adipose tissues and their dysfunctions, which lead to several metabolic diseases including obesity or type 2 diabetes. Here, adipogenesis appears to be a process characterized by an intricate network that involves many transcription factors and long noncoding RNAs (lncRNAs) that regulate gene expression. LncRNAs are being investigated to determine their contribution to adipose tissue development and function. LncRNAs possess multiple cellular functions, and they regulate chromatin remodeling, along with transcriptional and post-transcriptional events; in this way, they affect gene expression. New investigations have demonstrated the pivotal role of these molecules in modulating white and brown/beige adipogenic tissue development and activity. This review aims to provide an update on the role of lncRNAs in adipogenesis and adipose tissue function to promote identification of new drug targets for treating obesity and related metabolic diseases.

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