Voluntary exercise prevents colonic inflammation in high-fat diet-induced obese mice by up-regulating PPAR-γ activity

Liu, Weixin; Wang, Ting; Zhou, Feng; Wang, Ying; Jun-wei, Xing; Zhang, Shen; Gu, Shouzhi; Sang, Li-Xuan; Dai, Cong; Wang, Hailan

doi:10.1016/j.bbrc.2015.02.047

Cited by 38 publications

(35 citation statements)

References 30 publications

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“…In the present study, voluntary exercise reversed the fall in the plasma adiponectin levels and the expression of that adipokine in mWAT but simultaneously, the expression of the proinflammatory adipokine leptin was downregulated in the mice fed a HFD. Liu et al [7,65] have reported an increased expression of inflammatory mediators in the colons of sedentary mice fed a HFD, an effect mediated by a decrease in the expression and activity of protective PPAR-γ.…”

Section: Discussionmentioning

confidence: 99%

“…In CD, the hypertrophied mesenteric white adipose tissue (mWAT) could be a major contributor to the increase in the circulating proinflammatory cytokines and play a role in the pathogenesis and disease activity [2,3,4,5]. Diet-induced obesity (DIO) obtained by feeding rodents on high-fat diets is the most common model reported in the literature because DIO mimics the human characteristics of obesity and leads to increased mesenteric fat deposition, colonic inflammation and deterioration in experimental colitis [6,7,8,9]. …”

Section: Introductionmentioning

confidence: 99%

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Beneficial Effect of Voluntary Exercise on Experimental Colitis in Mice Fed a High-Fat Diet: The Role of Irisin, Adiponectin and Proinflammatory Biomarkers

et al. 2017

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Inflammatory bowel diseases (IBDs) are a heterogeneous group of disorders exhibited by two major phenotypic forms: Crohn‘s disease and ulcerative colitis. Although the aetiology of IBD is unknown, several factors coming from the adipose tissue and skeletal muscles, such as cytokines, adipokines and myokines, were suggested in the pathogenesis of ulcerative colitis; however, it has not been extensively studied whether voluntary exercise can ameliorate that disorder. We explored the effect of moderate exercise (i.e., voluntary wheel running) on the disease activity index (DAI), colonic blood flow (CBF), plasma irisin and adiponectin levels and real-time PCR expression of proinflammatory markers in mesenteric fat in mice with 2,4,6-trinitrobenzenesulfonic acid (TNBS) colitis fed a high-fat diet (HFD) compared to those on a standard chow diet (SD). Macroscopic and microscopic colitis in sedentary SD mice was accompanied by a significant fall in CBF, some increase in colonic tissue weight and a significant increase in the plasma levels of tumour necrosis factor-alpha (TNF-α), IL-6, monocyte chemotactic protein 1 (MCP-1) and IL-13 (p < 0.05). In sedentary HFD mice, colonic lesions were aggravated, colonic tissue weight increased and the plasma TNF-α, IL-6, MCP-1, IL-1β and leptin levels significantly increased. Simultaneously, a significant decrease in the plasma irisin and adiponectin levels was observed in comparison with SD mice (p < 0.05). Exercise significantly decreased macroscopic and microscopic colitis, substantially increased CBF and attenuated the plasma TNF-α, IL-6, MCP-1, IL-1β and leptin levels while raising the plasma irisin and the plasma and WAT concentrations of adiponectin in HFD mice (p < 0.05). We conclude that: (1) experimental colitis is exacerbated in HFD mice, possibly due to a fall in colonic microcirculation and an increase in the plasma and mesenteric fat content of proinflammatory biomarkers; and (2) voluntary physical activity can attenuate the severity of colonic damage in mice fed a HFD through the release of protective irisin and restoration of plasma adiponectin.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Beneficial Effect of Voluntary Exercise on Experimental Colitis in Mice Fed a High-Fat Diet: The Role of Irisin, Adiponectin and Proinflammatory Biomarkers

et al. 2017

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“…The white adipose tissue is the major energy reservoir in mammals and plays a key role in the maintenance of energy homeostasis [24]. PPAR is a key transcription factor in adipocyte differentiation, lipid storage, and glucose homeostasis [25] and it regulates the expression of adipocyte markers such as SREBP-1c,. FAS and aP2.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of hypocholesterolemic effect of oleuropein in cholesterol-fed rats

Hadrich

Mahmoudi

Bouallagui

et al. 2016

Chemico-Biological Interactions

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Oleuropein, which is the major compound of olive leaves, has been reported to exert several pharmacological properties, including anti-cancer, antidiabetic and anti-atherosclerotic activities. The objective of this study was to evaluate the effect of oleuropein on adiponectin level in high cholesterol diet (HCD) induced obesity in rat and the molecular mechanism underlying its activation. Our results showed that orally administered oleuropein (50 mg/kg) by gavage for 8 weeks decreased the body weight, adipose tissue mass and triglyceride and attenuated steatosis in liver. Moreover, the effect of oleuropein on adiponectin, an important hormone with fatty-acid oxidation properties, was evaluated and our data illustrated that oleuropein supplementation increased serum adiponectin concentration. The effects of oleuropein on protein expression related to lipogenic genes were investigated and our results showed that its administration significantly inhibited peroxisome proliferator-activated receptor γ (PPARγ), sterol regulatory element-binding protein-1c (SREBP-1c) and fatty-acid synthase (FAS). In addition, oleuropein stimulated the HCD-induced inhibition of AMP-activated protein kinase (AMPK) in epididymal adipose tissues. These results suggest that oleuropein exerts anti-obesity effects in HCD rats by activating AMPK and suppressing PPAR γ (Peroxisome proliferator-activated receptor γ) expression in adipose tissues. These data provide that oleuropein has important implications for preventing obesity.

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“…Numerous studies confirm that a high-fat diet (HFD) or high-fat and high-sugar diets (HF/HSD) can exacerbate experimentally induced colitis. In murine colitis models, the diet modifications are attributed to the alterations in the plasma levels of proinflammatory biomarkers and the expression of proinflammatory factors in VAT [102,108,128,[179][180][181][182][183][184][185][186][187]. It was demonstrated that the application of an HFD or HF/HSD diets and/or the development of obesity in mice increase(s) the intestinal permeability and bacterial translocation from the intestinal lumen to mesenteric fat, as well as profound changes in the microbiota [102,108,127,181,[184][185][186][187][188][189][190][191][192][193][194][195].…”

Section: Experimental Studies On Role Of Adipose Tissue In Ibdmentioning

confidence: 99%

Role of Obesity, Mesenteric Adipose Tissue, and Adipokines in Inflammatory Bowel Diseases

et al. 2019

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Inflammatory bowel diseases (IBDs) are a group of disorders which include ulcerative colitis and Crohn’s disease. Obesity is becoming increasingly more common among patients with inflammatory bowel disease and plays a role in the development and course of the disease. This is especially true in the case of Crohn’s disease. The recent results indicate a special role of visceral adipose tissue and particularly mesenteric adipose tissue, also known as “creeping fat”, in pathomechanism, leading to intestinal inflammation. The involvement of altered adipocyte function and the deregulated production of adipokines, such as leptin and adiponectin, has been suggested in pathogenesis of IBD. In this review, we discuss the epidemiology and pathophysiology of obesity in IBD, the influence of a Western diet on the course of Crohn’s disease and colitis in IBD patients and animal’s models, and the potential role of adipokines in these disorders. Since altered body composition, decrease of skeletal muscle mass, and development of pathologically changed mesenteric white adipose tissue are well-known features of IBD and especially of Crohn’s disease, we discuss the possible crosstalk between adipokines and myokines released from skeletal muscle during exercise with moderate or forced intensity. The emerging role of microbiota and the antioxidative and anti-inflammatory enzymes such as intestinal alkaline phosphatase is also discussed, in order to open new avenues for the therapy against intestinal perturbations associated with IBD.

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Voluntary exercise prevents colonic inflammation in high-fat diet-induced obese mice by up-regulating PPAR-γ activity

Cited by 38 publications

References 30 publications

Beneficial Effect of Voluntary Exercise on Experimental Colitis in Mice Fed a High-Fat Diet: The Role of Irisin, Adiponectin and Proinflammatory Biomarkers

Beneficial Effect of Voluntary Exercise on Experimental Colitis in Mice Fed a High-Fat Diet: The Role of Irisin, Adiponectin and Proinflammatory Biomarkers

Evaluation of hypocholesterolemic effect of oleuropein in cholesterol-fed rats

Role of Obesity, Mesenteric Adipose Tissue, and Adipokines in Inflammatory Bowel Diseases

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