Telmisartan attenuates the inflamed mesenteric adipose tissue in spontaneous colitis by mechanisms involving regulation of neurotensin/microRNA-155 pathway

Li, Yi; Zuo, Lugen; Zhu, Weiming; Gong, Jianfeng; Zhang, Wei; Guo, Zhen; Gu, Lili; Li, Jieshou

doi:10.1016/j.bcp.2014.12.020

Cited by 18 publications

(28 citation statements)

References 78 publications

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“…Telmisartan is shown to reduce the visceral adiposity due to attenuation of leptin and increasing APN expression in adipose tissue in addition to increasing APN serum levels [220,221]. In their study [215], the treatment with telmisartan has ameliorated spontaneous colitis and reduces the pathological changes in mWAT. This effect was associated with lower production of proinflammatory cytokines.…”

Section: Year Study Type Conclusionmentioning

confidence: 91%

“…Li et al [215] investigated the effect of the role of telmisartan on pathologically altered mWAT in IL-10 −/− mice with spontaneous colitis, with a major aim to analyze the inflammatory response and adipokine production. Telmisartan acts as the antagonist of receptor angiotensin II type 1 and also as a partial agonist of peroxisome proliferator-activated receptor γ (PPAR-γ) [216].…”

Section: Year Study Type Conclusionmentioning

confidence: 99%

“…This effect was associated with lower production of proinflammatory cytokines. Additionally, mice receiving telmisartan have reduced leptin and increased adiponectin mRNA expression in mWAT [215]. Interestingly, both bariatric surgery and, particularly, the duodenojejunal bypass have ameliorated the severity of colitis in chemically induced IBD [222].…”

Section: Year Study Type Conclusionmentioning

confidence: 99%

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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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Section: Year Study Type Conclusionmentioning

confidence: 91%

Section: Year Study Type Conclusionmentioning

confidence: 99%

Section: Year Study Type Conclusionmentioning

confidence: 99%

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

et al. 2019

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“…This notion is supported by our recent study in which the regulation of the abnormal immune response in MAT attenuated experimental colitis. 205 As a hallmark for CD, hypertrophy of MAT is involved in the pathogenesis and disease course in CD. Decision making during the surgery for CD has involved the depth (margin of mesentery) and length of resection.…”

Section: Mesenteric Fat In the Disease Course Of CDmentioning

confidence: 99%

The Role of the Mesentery in Crohnʼs Disease

Zhu

Zuo

et al. 2016

Inflammatory Bowel Diseases

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Crohn's disease (CD) is a complex gastrointestinal disorder involving multiple levels of cross talk between the immunological, neural, vascular, and endocrine systems. The current dominant theory in CD is based on the unidirectional axis of dysbiosis-innate immunity-adaptive immunity-mesentery-body system. Emerging clinical evidence strongly suggests that the axis be bidirectional. The morphologic and/or functional abnormalities in the mesenteric structures likely contribute to the disease progression of CD, to a less extent the disease initiation. In addition to adipocytes, mesentery contains nerves, blood vessels, lymphatics, stromal cells, and fibroblasts. By the secretion of adipokines that have endocrine functions, the mesenteric fat tissue exerts its activity in immunomodulation mainly through response to afferent signals, neuropeptides, and functional cytokines. Mesenteric nerves are involved in the pathogenesis and prognosis of CD mainly through neuropeptides. In addition to angiogenesis observed in CD, lymphatic obstruction, remodeling, and impaired contraction maybe a cause and consequence of CD. Lymphangiogenesis and angiogenesis play a concomitant role in the progress of chronic intestinal inflammation. Finally, the interaction between neuropeptides, adipokines, and vascular and lymphatic endothelia leads to adipose tissue remodeling, which makes the mesentery an active participator, not a bystander, in the disease initiation and precipitation CD. The identification of the role of mesentery, including the structure and function of mesenteric nerves, vessels, lymphatics, and fat, in the intestinal inflammation in CD has important implications in understanding its pathogenesis and clinical management.

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“…All of these beneficial effects could be explained by decreased TNF-α and increased production of IL-10, together with downregulation of receptor activator of NF-κB (RANK) and receptor activator of NF-κB ligand (RANKL; Guerra et al, 2015). Li, Zuo, et al (2015) showed that treatment with telmisartan not only ameliorated the severity of colitis in IL-10 knockout mice but also attenuated mesenteric adipose tissue alteration, at least in part, through suppressing the neuro- were significantly decreased with ARB therapy (Okawada et al, 2011). Taken together, these findings support the beneficial effects of ARBs in colitis through modulation of inflammation, oxidative stress, and apoptosis.…”

Section: Arbs In the Treatment Of Colitismentioning

confidence: 99%

The potential therapeutic use of renin–angiotensin system inhibitors in the treatment of inflammatory diseases

Ranjbar

Shafiee

Hesari

et al. 2018

Journal Cellular Physiology

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Inflammation is a normal part of the immune response to injury or infection but its dysregulation promotes the development of inflammatory diseases, which cause considerable human suffering. Nonsteroidal anti-inflammatory agents are the most commonly prescribed agents for the treatment of inflammatory diseases, but they are accompanied by a broad range of side effects, including gastrointestinal and cardiovascular events. The renin-angiotensin system (RAS) is traditionally known for its role in blood pressure regulation. However, there is increasing evidence that RAS signaling is also involved in the inflammatory response associated with several disease states. Angiotensin II increases blood pressure by binding to angiotensin type 1 (AT ) receptor, and direct renin inhibitors, angiotensin-converting enzyme (ACE) inhibitors and AT receptor blockers (ARBs) are clinically used as antihypertensive agents. Recent data suggest that these drugs also have anti-inflammatory effects. Therefore, this review summarizes these recent findings for the efficacy of two of the most widely used antihypertensive drug classes, ACE inhibitors and ARBs, to reduce or treat inflammatory diseases such as atherosclerosis, arthritis, steatohepatitis, colitis, pancreatitis, and nephritis.

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Telmisartan attenuates the inflamed mesenteric adipose tissue in spontaneous colitis by mechanisms involving regulation of neurotensin/microRNA-155 pathway

Cited by 18 publications

References 78 publications

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

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

The Role of the Mesentery in Crohnʼs Disease

The potential therapeutic use of renin–angiotensin system inhibitors in the treatment of inflammatory diseases

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