The measurement of human adipose tissue mass

Author(s):  
William I. Morse ◽  
J. Stuart Soeldner
1977 ◽  
Vol 11 (4) ◽  
pp. 435-435
Author(s):  
Fredda V Ginsberg-Fellner ◽  
Andrew Davis ◽  
Gary J Bergman ◽  
Jacqueline S Schenkein-Stern ◽  
Jerome L Knittle

1981 ◽  
Vol 53 (1) ◽  
pp. 192-199 ◽  
Author(s):  
J. PETER FORNEY ◽  
LEON MILEWICH ◽  
GRACE T. CHEN ◽  
JUDY L. GARLOCK ◽  
BARRY E. SCHWARZ ◽  
...  

Cell Reports ◽  
2020 ◽  
Vol 33 (1) ◽  
pp. 108228 ◽  
Author(s):  
John M. Dean ◽  
Anyuan He ◽  
Min Tan ◽  
Jun Wang ◽  
Dongliang Lu ◽  
...  

2009 ◽  
Vol 68 (4) ◽  
pp. 378-384 ◽  
Author(s):  
Henrike Sell ◽  
Jürgen Eckel

A strong causal link between increased adipose tissue mass and insulin resistance in tissues such as liver and skeletal muscle exists in obesity-related disorders such as type 2 diabetes. Increased adipose tissue mass in obese patients and patients with diabetes is associated with altered secretion of adipokines, which also includes chemotactic proteins. Adipose tissue releases a wide range of chemotactic proteins including many chemokines and chemerin, which are interesting targets for adipose tissue biology and for biomedical research in obesity and obesity-related diseases. This class of adipokines may be directly linked to a chronic state of low-grade inflammation and macrophage infiltration in adipose tissue, a concept intensively studied in adipose tissue biology in recent years. The inflammatory state of adipose tissue in obese patients may be the most important factor linking increased adipose tissue mass to insulin resistance. Furthermore, chemoattractant adipokines may play an important role in this situation, as many of these proteins possess biological activity beyond the recruitment of immune cells including effects on adipogenesis and glucose homeostasis in insulin-sensitive tissues. The present review provides a summary of experimental evidence of the role of adipose tissue-derived chemotactic cytokines and their function in insulin resistancein vivoandin vitro.


2014 ◽  
Vol 393 (1-2) ◽  
pp. 120-128 ◽  
Author(s):  
M. Holubová ◽  
V. Nagelová ◽  
Z. Lacinová ◽  
M. Haluzík ◽  
D. Sýkora ◽  
...  

2009 ◽  
Vol 296 (1) ◽  
pp. E121-E131 ◽  
Author(s):  
C. H. Widberg ◽  
F. S. Newell ◽  
A. W. Bachmann ◽  
S. N. Ramnoruth ◽  
M. C. Spelta ◽  
...  

Cell number is an important determinant of adipose tissue mass, and the coordinated proliferation and differentiation of preadipocytes into mature lipid-laden adipocytes underpins the increased adipose tissue mass associated with obesity. Despite this, the molecular cues governing such adipose tissue expansion are poorly understood. We previously reported that fibroblast growth factor-1 (FGF-1) promotes both proliferation and differentiation of human preadipocytes and that the major adipogenic effect of FGF-1 occurs during proliferation, priming the cells for adipose conversion. In the current study, we examined whether this effect was linked to the mitogenic action of FGF-1 by investigating the mitogenic and adipogenic potential of other growth factors, platelet-derived growth factor (PDGF; AA and BB) and vascular endothelial growth factor. Although PDGF-AA and PDGF-BB showed comparable mitogenic potential to FGF-1, only FGF-1 treatment resulted in priming and subsequent differentiation. Pharmacological inhibition of FGF receptor (FGFR) tyrosine kinase activity, using the FGFR-specific inhibitors PD-173074 and SU-5402, revealed an obligate requirement for FGFR activity in these processes. A combination of biochemical and genetic approaches revealed an important role for FGFR1. Knock down of FGFR1 expression by small-interfering RNA reduced FGF-1-stimulated signaling events, proliferation, and priming. Together these data highlight the unique nature of the role of FGF-1 during the earliest stages of adipogenesis and establish a role for FGFR1 in human adipogenesis, identifying FGFR1 as a potential therapeutic target to reduce obesity.


2018 ◽  
Vol 49 (1) ◽  
pp. 9-15 ◽  
Author(s):  
Takashi Abe ◽  
Jeremy P. Loenneke ◽  
Robert S. Thiebaud

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