scholarly journals Age related changes in the antilipolytic effects of nicotinic acid in rat adipose tissue

1983 ◽  
Vol 80 (4) ◽  
pp. 663-670 ◽  
Author(s):  
L. Caparrotta ◽  
G. Fassina ◽  
R.M. Gaion ◽  
F. Tessari
Life Sciences ◽  
1983 ◽  
Vol 32 (23) ◽  
pp. 2701-2708 ◽  
Author(s):  
Elisabetta Scotini ◽  
Laura Caparrotta ◽  
Francesco Tessari ◽  
Giuliana Fassina

1993 ◽  
Vol 123 (1) ◽  
pp. 52-58 ◽  
Author(s):  
James W. Bailey ◽  
Rebekah L. Barker ◽  
Roy E. Beauchene

2016 ◽  
Vol 29 (4) ◽  
pp. 175-183 ◽  
Author(s):  
Sylvie Devaux ◽  
Markus Adrian ◽  
Pascal Laurant ◽  
Alain Berthelot ◽  
Annie Quignard-Boulangé

2011 ◽  
pp. P2-351-P2-351
Author(s):  
Lucila Sackmann Sala ◽  
Clare B Vesel ◽  
Ellen R Lubbers ◽  
Rachel D Munn ◽  
Katie M Troike ◽  
...  

1982 ◽  
Vol 242 (2) ◽  
pp. E93-E96 ◽  
Author(s):  
W. H. Miller ◽  
I. M. Faust

Rats raised in the cold showed an unusual pattern of adipose tissue morphology. Male Sprague-Dawley rats were maintained in a 5 degrees C environment for up to 24 wk and the cellularity of their major adipose depots was determined. Normal age-related increases in adipocyte number were absent in two major fat depots (retroperitoneal and inguinal), whereas there was a supranormal increase in a third (epididymal). This pattern of hyperplasia contrasts sharply with that seen in rats fed highly palatable high-fat or high-carbohydrate diets in which retroperitoneal depots show the most hyperplasia and epididymal pads the least. Such variations of response across depots suggest that the features of adipose tissue responsible for adipocyte proliferation in the various depots may not be homogeneous both in their nature and in their distribution.


2020 ◽  
Author(s):  
Emily L. Goldberg ◽  
Irina Shchukina ◽  
Yun-Hee Youm ◽  
Christina D. Camell ◽  
Tamara Dlugos ◽  
...  

AbstractAging impairs the integrated immunometabolic responses which have evolved to maintain core body temperature in homeotherms to survive cold-stress, infections, and dietary restriction. Adipose tissue inflammation regulates the thermogenic stress response but how adipose tissue-resident cells instigate thermogenic failure in aged are unknown. Here, we define alterations in the adipose-resident immune system and identify that type 2 innate lymphoid cells (ILC2) are lost in aging. Restoration of ILC2 numbers in aged mice to levels seen in adults through IL-33 supplementation failed to rescue old mice from metabolic impairment and cold-induced lethality. Transcriptomic analyses revealed intrinsic defects in aged ILC2, and adoptive transfer of adult ILC2 are sufficient to protect old mice against cold. Thus, the functional defects in adipose ILC2 during aging drive thermogenic failure.One Sentence SummaryAge-related changes in adipose tissue drive reprogramming of ILC2 that leads to impaired cold tolerance


2021 ◽  
Vol 12 ◽  
Author(s):  
Xing-Hui Song ◽  
Ning He ◽  
Yue-Ting Xing ◽  
Xiao-Qin Jin ◽  
Yan-Wei Li ◽  
...  

Adipose tissue-derived stromal cells are promising candidates investigating the stem cell-related treatment. However, their proportion and utility in the human body decline with time, rendering stem cells incompetent to complete repair processes in vivo. The involvement of circRNAs in the aging process is poorly understood. Rat subcutaneous adipose tissue from 10-week-old and 27-month-old rats were used for hematoxylin and eosin (H and E) staining, TUNEL staining, and circRNA sequencing. Rat adipose tissue-derived stromal cells were cultured and overexpressed with circ-ATXN2. Proliferation was examined using xCELLigence real-time cell analysis, EdU staining, and cell cycle assay. Apoptosis was induced by CoCl2 and examined using flow cytometry. RT-PCR assay and Oil Red O staining were used to measure adipogenesis at 48 h and 14 days, respectively. H and E staining showed that the diameter of adipocytes increased; however, the number of cells decreased in old rats. TUNEL staining showed that the proportion of apoptotic cells was increased in old rats. A total of 4,860 and 4,952 circRNAs was detected in young and old rats, respectively. Among them, 67 circRNAs exhibited divergent expression between the two groups (fold change ≥2, p ≤ 0.05), of which 33 were upregulated (49.3%) and 34 were downregulated (50.7%). The proliferation of circ-ATXN2-overexpressing cells decreased significantly in vitro, which was further validated by xCELLigence real-time cell analysis, EdU staining, and cell cycle assay. Overexpression of circ-ATXN2 significantly increased the total apoptotic rate from 5.78 ± 0.46% to 11.97 ± 1.61%, early apoptotic rate from 1.76 ± 0.22% to 5.50 ± 0.66%, and late apoptosis rate from 4.02 ± 0.25% to 6.47 ± 1.06% in adipose tissue-derived stromal cells. Furthermore, in circ-ATXN2-overexpressing cells, RT-PCR assay revealed that the expression levels of adipose differentiation-related genes PPARγ and CEBP/α were increased and the Oil Red O staining assay showed more lipid droplets. Our study revealed the expression profile of circRNAs in the adipose tissue of old rats. We found a novel age-related circular RNA—circ-ATXN2—that inhibits proliferation and promotes cell death and adipogenesis in rat adipose tissue-derived stromal cells.


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