Resistin is co-secreted with adiponectin in white mouse adipocytes

2021 ◽  
Vol 534 ◽  
pp. 707-713
Author(s):  
Saliha Musovic ◽  
Man Mohan Shrestha ◽  
Ali M. Komai ◽  
Charlotta S. Olofsson
Keyword(s):  
BMJ ◽  
1960 ◽  
Vol 2 (5212) ◽  
pp. 1596-1596
Author(s):  
H. Ogilvie
Keyword(s):  

2008 ◽  
Vol 150 (1-3) ◽  
pp. 33-37 ◽  
Author(s):  
Anne Mazzucotelli ◽  
Carole Ribet ◽  
Isabelle Castan-Laurell ◽  
Danièle Daviaud ◽  
Charlotte Guigné ◽  
...  

1969 ◽  
Vol 3 (1) ◽  
pp. 1-6
Author(s):  
J. O. L. King

Mice of two strains (a laboratory strain of white mouse and a fancy strain of coloured mouse) were fed on a proprietary cubed diet and were given to drink tap water, or water containing 26 mg per litre of one of the following antibiotics: chortetracycline hydrochloride, ampicillin, or tylosin tartrate. In the first experiment growing mice were given these diets for 8 weeks from 4 weeks of age. Ampicillin produced weight increases in both strains (significant in the white mice), chlortetracycline produced an increase in the coloured mice and a reduction in the white mice, while tylosin reduced weight increases in both strains. The results of fortnightly weighings of the control mice and those receiving ampicillin showed that in the coloured mice the effect was marked at an early age, while in the white mice it tended to spread over the growing period. In a second experiment with breeding mice, using does of both strains, ampicillin increased litter size in both strains (significantly in the case of the coloured mice), chlortetracycline increased litter size in the white mice only, and tylosin did so in the coloured mice only. All three antibiotics increased litter birth weights in coloured mice (ampicillin significantly), but reduced them in white mice. Weight increases from birth to weaning of selected groups of 8 mice showed that antibiotics had little effect in the white mice, and that ampicillin and tylosin improved the rate of gain in the coloured mice (ampicillin significantly).


1989 ◽  
Vol 169 (5) ◽  
pp. 1841-1846 ◽  
Author(s):  
E P Benditt ◽  
R L Meek

Three homologous genes that code for three related proteins comprise the serum amyloid A (SAA) family in the mouse. Endotoxin induces equally vigorous expression of mRNAs for the three SAA genes in liver. In extrahepatic tissues SAA1 and/or SAA2 mRNAs have been found only in kidney and intestine, however, SAA3 is expressed in all extrahepatic tissues thus far examined. This observation raised the question: is SAA3 mRNA expressed by a single cell system dispersed throughout all tissues, or by differentiated cells of each tissue? This question was explored in various tissues by in situ hybridization with a single-stranded cRNA probe specific for SAA3 mRNA. We found expression in the liver of SAA3 mRNA by other cells as well as by hepatocytes. A common feature among extrahepatic tissues was SAA3 mRNA expression in adipocytes. SAA3 mRNA was also found in two nonadipose cells, Leydig cells of the testis, and some of the cells located in parafollicular zones of the spleen.


2021 ◽  
Author(s):  
Fubiao Shi ◽  
Zoltan Simandi ◽  
Laszlo Nagy ◽  
Sheila Collins

AbstractIn addition to their established role to maintain blood pressure and fluid volume, the cardiac natriuretic peptides (NPs) can stimulate adipocyte lipolysis and control the brown fat gene program of nonshivering thermogenesis. The NP “clearance” receptor C (NPRC) functions to clear NPs from the circulation via peptide internalization and degradation and thus is an important regulator of NP signaling and adipocyte metabolism. It is well appreciated that the Nprc gene is highly expressed in adipose tissue and is dynamically regulated with nutrition and environmental changes. However, the molecular basis for how Nprc gene expression is regulated is still poorly understood. Here we identified Peroxisome Proliferator-Activated Receptor gamma (PPARγ) as a transcriptional regulator of Nprc expression in mouse adipocytes. During 3T3-L1 adipocyte differentiation, levels of Nprc expression increase in parallel with PPARγ induction. Rosiglitazone, a classic PPARγ agonist, increases, while siRNA knockdown of PPARγ reduces, Nprc expression in 3T3-L1 adipocytes. We demonstrate that PPARγ controls Nprc gene expression in adipocytes through its long-range distal enhancers. Furthermore, the induction of Nprc expression in adipose tissue during high-fat diet feeding is associated with increased PPARγ enhancer activity. Our findings define PPARγ as a mediator of adipocyte Nprc gene expression and establish a new connection between PPARγ and the control of adipocyte NP signaling in obesity.


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