Unconventional microarray design reveals the response to obesity is largely tissue specific: analysis of common and divergent responses to diet-induced obesity in insulin-sensitive tissues

2012 ◽  
Vol 37 (2) ◽  
pp. 257-268 ◽  
Author(s):  
Robyn K. Lee ◽  
Dustin S. Hittel ◽  
Vongai Z. Nyamandi ◽  
Li Kang ◽  
Jung Soh ◽  
...  
2011 ◽  
Vol 108 (6) ◽  
pp. 1025-1033 ◽  
Author(s):  
Sumithra Urs ◽  
Terry Henderson ◽  
Phuong Le ◽  
Clifford J. Rosen ◽  
Lucy Liaw

We recently characterised Sprouty1 (Spry1), a growth factor signalling inhibitor as a regulator of marrow progenitor cells promoting osteoblast differentiation at the expense of adipocytes. Adipose tissue-specific Spry1 expression in mice resulted in increased bone mass and reduced body fat, while conditional knockout of Spry1 had the opposite effect with decreased bone mass and increased body fat. Because Spry1 suppresses normal fat development, we tested the hypothesis that Spry1 expression prevents high-fat diet-induced obesity, bone loss and associated lipid abnormalities, and demonstrate that Spry1 has a long-term protective effect on mice fed a high-energy diet. We studied diet-induced obesity in mice with fatty acid binding promoter-driven expression or conditional knockout of Spry1 in adipocytes. Phenotyping was performed by whole-body dual-energy X-ray absorptiometry, microCT, histology and blood analysis. In conditional Spry1-null mice, a high-fat diet increased body fat by 40 %, impaired glucose regulation and led to liver steatosis. However, overexpression of Spry1 led to 35 % (P < 0·05) lower body fat, reduced bone loss and normal metabolic function compared with single transgenics. This protective phenotype was associated with decreased circulating insulin (70 %) and leptin (54 %; P < 0·005) compared with controls on a high-fat diet. Additionally, Spry1 expression decreased adipose tissue inflammation by 45 %. We show that conditional Spry1 expression in adipose tissue protects against high-fat diet-induced obesity and associated bone loss.


1988 ◽  
Vol 66 (8) ◽  
pp. 1767-1771 ◽  
Author(s):  
Kenneth B. Storey

Changes in the activity of glycogen phosphorylase and the content of fructose-2,6-bisphosphate (F-2, 6-P2) were monitored in tissues of the whelk, Busycotypus canaliculatum, over a 21-h course of environmental anoxia. Tissue-specific responses to anoxia were seen with respect to phosphorylase content: in the radular retractor muscle and foot, the content of phosphorylase a expressed rose rapidly over the initial hours of anoxia (maximal increases were 4.3- and 2.5-fold, respectively) while in the gill, content dropped 2-fold during anoxia. Phosphorylase content was modulated by two mechanisms, changes in the percentage of enzyme in the active a form and changes in the total amount (a + b) of enzyme expressed. Anoxia stimulated a dramatic reduction in F-2,6-P2 content in five tissues. In the ventricle, content fell by 224-fold with a t1/2 of only 35 min. Levels in gill, radular retractor, hepatopancreas, and kidney fell to 2.5–3.5% of control values within the first 8 h of anoxia. F-2,6-P2 content in foot muscle was not altered during anoxia. Changes in glycogen phosphorylase activities and F-2,6-P2 contents help to produce tissue-specific responses of glycolysis to environmental anoxia that acknowledge competing metabolic demands including metabolic rate depression, changes in fuel use, anaerobic energy needs, and carbohydrate use for anabolic purposes.


2013 ◽  
Vol 50 ◽  
pp. 118-130 ◽  
Author(s):  
Joshua P. Vandenbrink ◽  
Ryan E. Hammonds ◽  
Roger N. Hilten ◽  
K.C. Das ◽  
J. Michael Henson ◽  
...  

2011 ◽  
pp. P2-462-P2-462
Author(s):  
Erika Harno ◽  
Alice Yu ◽  
Andrew V Turnbull ◽  
Brendan Leighton ◽  
Anne White

2018 ◽  
Vol 7 (7) ◽  
pp. 453-463 ◽  
Author(s):  
Yun Hao ◽  
Kayla Quinnies ◽  
Ronald Realubit ◽  
Charles Karan ◽  
Nicholas P. Tatonetti

2009 ◽  
Vol 37 (7) ◽  
pp. 3177-3182 ◽  
Author(s):  
Chun-Mei Zhang ◽  
Ying Gu ◽  
Da-ni Qing ◽  
Jin-gai Zhu ◽  
Chun Zhu ◽  
...  

2020 ◽  
Vol 68 (7) ◽  
pp. 2256-2262
Author(s):  
Miao Ji ◽  
Ke Xu ◽  
Dawei Zhang ◽  
Tingting Chen ◽  
Liangcai Shen ◽  
...  

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