scholarly journals Physiological Changes and Pathological Pain Associated with Sedentary Lifestyle-Induced Body Systems Fat Accumulation and Their Modulation by Physical Exercise

2021 ◽  
Vol 18 (24) ◽  
pp. 13333
Author(s):  
Enrique Verdú ◽  
Judit Homs ◽  
Pere Boadas-Vaello
Keyword(s):  
Adipose Tissue ◽  
Physical Exercise ◽  
Fat Body ◽  
Sedentary Lifestyle ◽  
Fat Accumulation ◽  
Functional Changes ◽  
Training Interventions ◽  
Systems Research ◽  
Body Tissues ◽  
Pathological Pain

A sedentary lifestyle is associated with overweight/obesity, which involves excessive fat body accumulation, triggering structural and functional changes in tissues, organs, and body systems. Research shows that this fat accumulation is responsible for several comorbidities, including cardiovascular, gastrointestinal, and metabolic dysfunctions, as well as pathological pain behaviors. These health concerns are related to the crosstalk between adipose tissue and body systems, leading to pathophysiological changes to the latter. To deal with these health issues, it has been suggested that physical exercise may reverse part of these obesity-related pathologies by modulating the cross talk between the adipose tissue and body systems. In this context, this review was carried out to provide knowledge about (i) the structural and functional changes in tissues, organs, and body systems from accumulation of fat in obesity, emphasizing the crosstalk between fat and body tissues; (ii) the crosstalk between fat and body tissues triggering pain; and (iii) the effects of physical exercise on body tissues and organs in obese and non-obese subjects, and their impact on pathological pain. This information may help one to better understand this crosstalk and the factors involved, and it could be useful in designing more specific training interventions (according to the nature of the comorbidity).

scholarly journals Interleukin-6 mediated exercise-induced alleviation of adiposity and hepatic steatosis in mice

2021 ◽  
Vol 9 (1) ◽  
pp. e001431
Author(s):  
Long Li ◽  
Caoxin Huang ◽  
Hongyan Yin ◽  
Xiaofang Zhang ◽  
Dongmei Wang ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Exercise Training ◽  
Hepatic Steatosis ◽  
Interleukin 6 ◽  
Body Weight Gain ◽  
Treadmill Running ◽  
Alcoholic Fatty Liver ◽  
Fat Accumulation ◽  
Ppar Γ

IntroductionExercise training has been shown to be the most effective strategy to combat obesity and non-alcoholic fatty liver disease. However, exercise promotes loss of adipose tissue mass and improves obesity-related hepatic steatosis through mechanisms that remain obscure.Research design and methodsTo study the role of interleukin-6 (IL-6) in high-fat diet (HFD)-induced adiposity and hepatic steatosis during treadmill running, IL-6 knockout (IL-6 KO) mice and wild-type (WT) mice were randomly divided into lean, obese (fed a HFD) and trained obese groups (fed a HFD and exercise trained).ResultsAfter 20 weeks of HFD feeding and 8 weeks of treadmill running, we found that exercise obviously reduced HFD-induced body weight gain, inhibited visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) expansion and almost completely reversed obesity-related intrahepatic fat accumulation in WT mice. However, IL-6 knockout (IL-6 KO) mice are refractory to the benefits of treadmill training on body weight, VAT and SAT mass elevation, and hepatic steatosis. Moreover, a panel of lipolytic-related and thermogenic-related genes, including ATGL, HSL and PGC-1α, was upregulated in the VAT and SAT of WT mice that received exercise training compared with untrained mice, which was not observed in IL-6 KO mice. In addition, exercise training resulted in a significant inhibition of hepatic peroxisome proliferator-activated receptor gamma (PPAR-γ) expression in WT mice, and these effects were not noted in IL-6 KO mice.ConclusionThese results revealed that IL-6 is involved in the prevention of obesity and hepatic fat accumulation during exercise training. The mechanisms underlying these antiobesity effects may be associated with enhanced lipolysis and thermogenesis in white adipose tissue. The improvement in hepatic steatosis by exercise training may benefit from the marked inhibition of PPAR-γ expression by IL-6.

scholarly journals Vascular Adhesion Protein 1 Mediates Gut Microbial Flagellin-Induced Inflammation, Leukocyte Infiltration, and Hepatic Steatosis

Sci ◽  
2021 ◽  
Vol 3 (1) ◽  
pp. 13
Author(s):  
Raine Toivonen ◽  
Sanja Vanhatalo ◽  
Maija Hollmén ◽  
Eveliina Munukka ◽  
Anniina Keskitalo ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Hepatic Steatosis ◽  
Visceral Adipose Tissue ◽  
Leukocyte Infiltration ◽  
Fat Accumulation ◽  
Adhesion Protein ◽  
Hepatic Fat ◽  
Vascular Adhesion ◽  
Visceral Adipose ◽  
Vascular Adhesion Protein 1

Toll-like receptor 5 ligand, flagellin, and vascular adhesion protein 1 (VAP-1) are involved in non-alcoholic fatty liver disease. This study aimed to determine whether VAP-1 mediates flagellin-induced hepatic fat accumulation. The effects of flagellin on adipocyte VAP-1 expression were first studied in vitro. Then, flagellin (100 ng/mouse) or saline was intraperitoneally injected into C57BL/6J (WT) and C57BL/6-Aoc3-/- (VAP-1 KO) mice on a high-fat diet twice a week every 2 weeks for 10 weeks. After that, the effects on inflammation, insulin signaling, and metabolism were studied in liver and adipose tissues. Hepatic fat was quantified histologically and biochemically. Because flagellin challenge increased VAP-1 expression in human adipocytes, we used VAP-1 KO mice to determine whether VAP-1 regulates the inflammatory and metabolic effects of flagellin in vivo. In mice, VAP-1 mediated flagellin-induced inflammation, leukocyte infiltration, and lipolysis in visceral adipose tissue. Consequently, an increased release of glycerol led to hepatic steatosis in WT, but not in KO mice. Flagellin-induced hepatic fibrosis was not mediated by VAP-1. VAP-1 KO mice harbored more inflammation-related microbes than WT mice, while flagellin did not affect the gut microbiota. Our results suggest that by acting on visceral adipose tissue, flagellin increased leukocyte infiltration that induced lipolysis. Further, the released glycerol participated in hepatic fat accumulation. In conclusion, the results describe that gut microbial flagellin through VAP-1 induced hepatic steatosis.

scholarly journals Consumption of Cherry out of Season Changes White Adipose Tissue Gene Expression and Morphology to a Phenotype Prone to Fat Accumulation

Nutrients ◽  
2018 ◽  
Vol 10 (8) ◽  
pp. 1102 ◽  
Author(s):  
Albert Gibert-Ramos ◽  
Anna Crescenti ◽  
M. Salvadó
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Serum Levels ◽  
Standard Diet ◽  
Fischer 344 Rats ◽  
Fat Accumulation ◽  
Fischer 344 ◽  
Obesogenic Diet ◽  
Adipose Tissue Gene Expression ◽  
Biometric Measurements

The aim of this study was to determine whether the consumption of cherry out of its normal harvest photoperiod affects adipose tissue, increasing the risk of obesity. Fischer 344 rats were held over a long day (LD) or a short day (SD), fed a standard diet (STD), and treated with a cherry lyophilizate (CH) or vehicle (VH) (n = 6). Biometric measurements, serum parameters, gene expression in white (RWAT) and brown (BAT) adipose tissues, and RWAT histology were analysed. A second experiment with similar conditions was performed (n = 10) but with a cafeteria diet (CAF). In the STD experiment, Bmal1 and Cry1 were downregulated in the CHSD group compared to the VHSD group. Pparα expression was downregulated while Ucp1 levels were higher in the BAT of the CHSD group compared to the VHSD group. In the CAF-fed rats, glucose and insulin serum levels increased, and the expression levels of lipogenesis and lipolysis genes in RWAT were downregulated, while the adipocyte area increased and the number of adipocytes diminished in the CHSD group compared to the VHSD group. In conclusion, we show that the consumption of cherry out of season influences the metabolism of adipose tissue and promotes fat accumulation when accompanied by an obesogenic diet.

scholarly journals Functional changes in adipose tissue in a randomised controlled trial of physical activity

2012 ◽  
Vol 11 (1) ◽  
pp. 80 ◽  
Author(s):  
Per Sjögren ◽  
Justo Sierra-Johnson ◽  
Lena V Kallings ◽  
Tommy Cederholm ◽  
Maria Kolak ◽  
...  
Keyword(s):  
Physical Activity ◽  
Adipose Tissue ◽  
Randomised Controlled Trial ◽  
Controlled Trial ◽  
Functional Changes ◽  
Randomised Controlled

scholarly journals Contribution of Neuroinflammation to the Pathogenesis of Cancer Cachexia

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Alessio Molfino ◽  
Gianfranco Gioia ◽  
Filippo Rossi Fanelli ◽  
Alessandro Laviano
Keyword(s):  
Adipose Tissue ◽  
Food Intake ◽  
Proinflammatory Cytokines ◽  
Adaptive Response ◽  
Energy Homeostasis ◽  
Cancer Cachexia ◽  
Behavioral Changes ◽  
Brain Areas ◽  
Functional Changes ◽  
The Brain

Inflammation characterizes the course of acute and chronic diseases and is largely responsible for the metabolic and behavioral changes occurring during the clinical journey of patients. Robust data indicate that, during cancer, functional modifications within brain areas regulating energy homeostasis contribute to the onset of anorexia, reduced food intake, and increased catabolism of muscle mass and adipose tissue. In particular, functional changes are associated with increased hypothalamic concentration of proinflammatory cytokines, which suggests that neuroinflammation may represent the adaptive response of the brain to peripheral challenges, including tumor growth. Within this conceptual framework, the vagus nerve appears to be involved in conveying alert signals to the hypothalamus, whereas hypothalamic serotonin appears to contribute to triggering catabolic signals.

scholarly journals PPA1 Regulates Systemic Insulin Sensitivity by Maintaining Adipocyte Mitochondria Function as a Novel PPARγ Target Gene

2021 ◽  
Author(s):  
Ye Yin ◽  
Yangyang Wu ◽  
Xu Zhang ◽  
Yeting Zhu ◽  
Yue Sun ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Mitochondrial Function ◽  
Metabolic Disorders ◽  
Target Gene ◽  
Fat Body ◽  
Whole Body ◽  
Inorganic Pyrophosphatase ◽  
Severe Insulin Resistance ◽  
Adipose Tissue Development ◽  
First Time

<a>Downregulation of mitochondrial function in adipose tissue is considered as one important driver for the development of obesity-associated metabolic disorders. Inorganic Pyrophosphatase 1 (PPA1) is an enzyme catalyzes the hydrolysis of PPi to Pi, and is required for anabolism to take place in cells. Although alternation of PPA1 has been related to some diseases, the importance of PPA1 in metabolic syndromes has never been discussed before. In this study, we found that global PPA1 knockout mice (PPA1<sup>+/-</sup>) showed impaired glucose tolerance and severe insulin resistance under HFD feeding. In addition, impaired adipose tissue development and ectopic lipid accumulation were also observed. Conversely, overexpression of PPA1 in adipose tissue by AAV injection can partly reverse the metabolic disorders in PPA1<sup>+/-</sup> mice, suggesting that impaired adipose tissue function is responsible for the metabolic disorders observed in PPA1<sup>+/- </sup>mice. Mechanistic studies revealed that PPA1 acted as a PPARγ target gene to maintain mitochondrial function in adipocytes. Furthermore, specific knockdown of PPA1 in fat body of <i>Drosophila</i> led to impaired mitochondria morphology, decreased lipid storage, and made <i>Drosophila</i> more sensitive to starvation. In conclusion, for the first time, our findings demonstrated the importance of PPA1 in maintaining adipose tissue function and whole body metabolic homeostasis.</a>

scholarly journals Anti-Obesity Effect of Galacto-Oligosaccharides in Obese Rats

2021 ◽  
Author(s):  
Shang Kong ◽  
Xingjun Huang ◽  
Hua Cao ◽  
Yan Bai ◽  
Qishi Che ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fat Body ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Protective Role ◽  
Lipoprotein Cholesterol ◽  
Fat Cells ◽  
Expression Levels ◽  
Brown Adipose ◽  
Obese Rats

Abstract Background: Galacto-oligosaccharides (GOS) is a commonly used as a prebiotic with a variety of metabolic benefits. Whether GOS plays a protective role in obesity is still unknown. Here we demonstrated that GOS possesses an anti-obesity activity by promoting adipose tissue browning and thermogenesis. Results: Our results showed that GOS effectively slow weight gain of diet-induced obese (DIO) rats without affecting energy intake. GOS significantly suppressed the hypertrophy and hyperplasia of white adipose tissue (WAT), as well as markedly lessened the ratio of fat pad to fat body. Consistently, GOS significantly improved serum total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C) levels, which indicated an appropriate weight loss activity of GOS. Interestingly, GOS also significantly increased the expression levels of browning proteins (UCP1, PPARγ, PGC1α and PRMD16) both in the WAT and brown adipose tissue (BAT). We further found that GOS markedly increased the expression levels of LXRα, PPARα, LDLR and CYP7A1 proteins in the liver of obese rats. Conclusions: Taken together, we concluded that GOS inhibits obesity by accelerating the browning of white fat cells and the thermogenesis of brown fat cells, moreover GOS improves host lipid homeostasis by promoting cholesterol catabolism.

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