Impact of physical exercise on visceral adipose tissue fatty acid profile and inflammation in response to a high-fat diet regimen

Author(s):  
Sílvia Rocha-Rodrigues ◽  
Amaia Rodríguez ◽  
Inês O. Gonçalves ◽  
Ana Moreira ◽  
Elisabete Maciel ◽  
...  
2017 ◽  
Vol 44 (3) ◽  
pp. 386-394 ◽  
Author(s):  
Sílvia Rocha-Rodrigues ◽  
Amaia Rodríguez ◽  
Sara Becerril ◽  
Beatriz Ramírez ◽  
Inês O Gonçalves ◽  
...  

2021 ◽  
pp. 1-24
Author(s):  
L. Irasema Chávaro-Ortiz ◽  
Brenda D. Tapia-Vargas ◽  
Mariel Rico-Hidalgo ◽  
Ruth Gutiérrez-Aguilar ◽  
María E. Frigolet

Abstract Obesity is defined as increased adiposity, which leads to metabolic disease. The growth of adipose tissue depends on its capacity to expand, through hyperplasia or hypertrophy, in order to buffer energy surplus. Also, during the establishment of obesity, adipose tissue expansion reflects adipose lipid metabolism (lipogenesis and/or lipolysis). It is well known that dietary factors can modify lipid metabolism promoting or preventing the development of metabolic abnormalities that concur with obesity. Trans-palmitoleic acid (TP), a biomarker of dairy consumption, has been associated with reduced adiposity in clinical studies. Thus, we aimed to evaluate the effect of TP over adiposity and lipid metabolism-related genes in a rodent model of diet-induced obesity (DIO). To fulfil this aim, we fed C57BL/6 mice with a Control or a High Fat diet, added with or without TP (3g/kg diet), during 11 weeks. Body weight and food intake were monitored, fat pads were weighted, histology of visceral adipose tissue was analysed, and lipid metabolism-related gene expression was explored by qPCR. Results show that TP consumption prevented weight gain induced by high fat diet, reduced visceral adipose tissue weight, and adipocyte size, while increasing the expression of lipolytic molecules. In conclusion, we show for the first time that TP influences adipose tissue metabolism, specifically lipolysis, resulting in decreased adiposity and reduced adipocyte size in a DIO mice model.


2015 ◽  
Vol 76 (2) ◽  
pp. 510-518 ◽  
Author(s):  
Benjamin Leporq ◽  
Simon A. Lambert ◽  
Maxime Ronot ◽  
Imane Boucenna ◽  
Pierre Colinart ◽  
...  

ACS Nano ◽  
2020 ◽  
Vol 14 (4) ◽  
pp. 5099-5110 ◽  
Author(s):  
Mengying Wei ◽  
Xiaotong Gao ◽  
Lijun Liu ◽  
Zhelong Li ◽  
Zhuo Wan ◽  
...  

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Cuiqing Liu ◽  
Guohua Lin ◽  
Guoqing Zhang ◽  
Huanhuan Wang ◽  
Hongping Yin ◽  
...  

Inflammation in insulin sensitive tissues, the visceral adipose tissue (VAT), is a central abnormality in obesity/insulin resistance (IR), with recruitment of innate immune cells such as monocytes into adipose tissue driving the development of glucose and lipoprotein dysregulation. We evaluated the role of Toll like receptor 3 (TLR3) in high fat diet-induced obesity and IR. Wild-type C57BL/6 and TLR3 -/- male mice were fed a high fat diet for 15 weeks. High fat feeding resulted in increased TLR3 expression in VAT. TLR3 deficiency attenuated the high fat diet-increased body weight, fasting blood glucose, whole body IR and impaired glucose tolerance. Morphologically, high fat diet induced adiposity and enlarged adipocyte area in VAT, which were attenuated in TLR3 -/- mice. Functionally, high fat diet induced dysregulation of adipocytokines such as downregulation of adiponectin and resistin, upregulation of leptin in VAT, with the disturbance of adiponectin and leptin was corrected in TLR3-/- mice. In addition, high fat diet inhibited insulin pathway, accompanied with decreased phosphorylation of AMPK and lowered expression of lipolysis-related enzymes such as HSL and ATGL, both at the mRNA levels and protein levels, all of which was corrected by TLR3 deficiency. Finally, TLR3 deletion suppressed the high fat feeding-mediated macrophage polarization, evidenced by increased type M1 macrophage (F4/80+/CD11c+/CD206-) infiltration and upregulation of M1 genes such as IL-6 and TNFα. TLR3 modulates high fat diet-induced IR and obesity by suppressing M1 macrophage-mediated VAT inflammation, facilitating secretion of adipocyte-derived hormones, thus enhanced AMPK activity and adipose lipolysis. These findings provide new mechanistic links between dietary factors-mediated IR and associated abnormalities in lipid metabolism and adipose inflammation.


Obesity ◽  
2008 ◽  
Vol 16 (6) ◽  
pp. 1226-1231 ◽  
Author(s):  
Hye-Seung Jun ◽  
Kyujung Hwang ◽  
Yunjung Kim ◽  
Taesun Park

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