scholarly journals PPARγin Inflammatory Bowel Disease

PPAR Research ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Vito Annese ◽  
Francesca Rogai ◽  
Alessia Settesoldi ◽  
Siro Bagnoli
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Potential Role ◽  
Intestinal Inflammation ◽  
Experimental Colitis ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Beneficial Effects ◽  
Inflammatory Bowel

Peroxisome proliferator-activated receptor gamma (PPARγ) is member of a family of nuclear receptors that interacts with nuclear proteins acting as coactivators and corepressors. The colon is a major tissue which expresses PPARγin epithelial cells and, to a lesser degree, in macrophages and lymphocytes and plays a role in the regulation of intestinal inflammation. Indeed, both natural and synthetic PPARγligands have beneficial effects in different models of experimental colitis, with possible implication in the therapy of inflammatory bowel disease (IBD). This paper will specifically focus on potential role of PPARγin the predisposition and physiopathology of IBD and will analyze its possible role in medical therapy.

scholarly journals Role of peroxisome-proliferator-activated receptor β/δ (PPARβ/δ) in gastrointestinal tract function and disease

2008 ◽  
Vol 115 (4) ◽  
pp. 107-127 ◽  
Author(s):  
Jeffrey M. Peters ◽  
Holly E. Hollingshead ◽  
Frank J. Gonzalez
Keyword(s):  
Inflammatory Bowel Disease ◽  
Gastrointestinal Tract ◽  
Bowel Disease ◽  
Intestinal Cell ◽  
Null Mouse ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Ligand Activation ◽  
Inflammatory Bowel

PPARβ/δ (peroxisome-proliferator-activated receptor β/δ) is one of three PPARs in the nuclear hormone receptor superfamily that are collectively involved in the control of lipid homoeostasis among other functions. PPARβ/δ not only acts as a ligand-activated transcription factor, but also affects signal transduction by interacting with other transcription factors such as NF-κB (nuclear factor κB). Constitutive expression of PPARβ/δ in the gastrointestinal tract is very high compared with other tissues and its potential physiological roles in this tissue include homoeostatic regulation of intestinal cell proliferation/differentiation and modulation of inflammation associated with inflammatory bowel disease and colon cancer. Analysis of mouse epithelial cells in the intestine and colon has clearly demonstrated that ligand activation of PPARβ/δ induces terminal differentiation. The PPARβ/δ target genes mediating this effect are currently unknown. Emerging evidence suggests that PPARβ/δ can suppress inflammatory bowel disease through PPARβ/δ-dependent and ligand-independent down-regulation of inflammatory signalling. However, the role of PPARβ/δ in colon carcinogenesis remains controversial, as conflicting evidence suggests that ligand activation of PPARβ/δ can either potentiate or attenuate this disease. In the present review, we summarize the role of PPARβ/δ in gastrointestinal physiology and disease with an emphasis on findings in experimental models using both high-affinity ligands and null-mouse models.

The Role of Peroxisome Proliferator–Activated Receptor γ in Colon Cancer and Inflammatory Bowel Disease

2003 ◽  
Vol 127 (9) ◽  
pp. 1121-1123
Author(s):  
Arthur W. Bull
Keyword(s):  
Inflammatory Bowel Disease ◽  
Colon Cancer ◽  
Bowel Disease ◽  
Cell Function ◽  
Therapeutic Potential ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Ppar Γ ◽  
Inflammatory Bowel

Abstract Objective.—Review the role and therapeutic potential of peroxisome proliferator–activated receptor (PPAR) γ in colonic disorders. Data Sources.—Recent peer-reviewed scientific literature focusing on PPAR γ in the colon. Study Selection.—Research reports using animal models, cultured cell lines, and clinical material were examined for content related to the role of PPAR γ in normal colon cell function, colon cancer, and inflammatory bowel disease. Issues concerned with potential therapeutic use were also considered. Data Synthesis.—Key points pertaining to PPAR function and involvement in colon pathology were extracted and noted. Potential compromises to therapeutic utility are identified. Conclusions.—The emerging important role of PPAR γ in normal tissue homeostasis and pathologic outcomes suggests this receptor is a good candidate as a drug target. Several potential problems with this approach will require further investigation prior to widespread recommendations for modulation of PPAR as an efficacious therapy for cancer, chemoprevention of colon cancer, or treatment of inflammatory bowel disease. The widespread use of PPAR γ ligands for management of type 2 diabetes (such as the glitazone class of drugs including rosiglitazone and pioglitazone) may provide a fortuitous assessment of the efficacy of long-term PPAR modulation.

scholarly journals Mesalazine in Inflammatory Bowel Disease: A Trendy Topic Once Again?

2010 ◽  
Vol 24 (2) ◽  
pp. 127-133 ◽  
Author(s):  
Marietta Iacucci ◽  
Shanika de Silva ◽  
Subrata Ghosh
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Peroxisome Proliferator ◽  
Aminosalicylic Acid ◽  
Peroxisome Proliferator Activated Receptor ◽  
Inflammatory Bowel ◽  
Maintenance Of Remission ◽  
Near Future

5-aminosalicylic acid (5-ASA) preparations (eg, mesalazine, mesalamine) are well-established preparations used in the management of inflammatory bowel disease. These drugs are most useful for the treatment of mild to moderate flares of ulcerative colitis and, especially, for maintenance of remission. Although most gastroenterologists are very familiar with these drugs, the interest in these drugs has undergone a resurgence, with new preparations offering convenience and high dosage, while preserving their customary safety. New dosage regimens are likely to become standard practice in the near future. There is also considerable interest in chemoprevention of colorectal cancer in the context of inflammatory bowel disease, and the role of long-term maintenance therapy with 5-ASAs in achieving such chemoprevention. A mechanism of action for such chemoprevention has been provided by the agonism of the peroxisome proliferator-activated receptor-gamma by 5-ASA, which unifies its efficacy as an anti-inflammatory and chemopreventive agent. In the future, even more effective agents based on 5-ASA are expected, based on more powerful agonism of peroxisome proliferator-activated receptor-gamma; 5-ASA preparations have become ‘trendy’ again.

scholarly journals PPAR-αContributes to the Anti-Inflammatory Activity of Verbascoside in a Model of Inflammatory Bowel Disease in Mice

PPAR Research ◽  
2010 ◽  
Vol 2010 ◽  
pp. 1-10 ◽  
Author(s):  
Emanuela Esposito ◽  
Emanuela Mazzon ◽  
Irene Paterniti ◽  
Roberto Dal Toso ◽  
Giovanna Pressi ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Experimental Colitis ◽  
Inflammatory Activity ◽  
Radical Scavenger ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Dietary Polyphenols ◽  
Inflammatory Bowel ◽  
Anti Inflammatory

The previous results suggest that peroxisome proliferator-activated receptor-alpha (PPAR)-α, an intracellular transcription factor activated by fatty acids, plays a role in control of inflammation. There is persuasive epidemiological and experimental evidence that dietary polyphenols have anti-inflammatory activity. In this regard, it has been demonstrated that verbascoside (VB) functions as intracellular radical scavenger and reduces the microscopic and macroscopic signs of experimental colitis. With the aim to characterize the role of PPAR-αin VB-mediated anti-inflammatory activity, we tested the efficacy of VB in an experimental model of inflammatory bowel disease induced by dinitrobenzene sulfonic acid, comparing mice lacking PPAR-α(PPAR-αKO) with wild type (WT) mice. Results indicate that VB-mediated anti-inflammatory activity is weakened in PPAR-αKO mice, compared to WT controls, especially in the inhibition of neutrophil infiltration, intestinal permeability and colon injury. These results indicate that PPAR-αcan contribute to the anti-inflammatory activity of VB in inflammatory bowel disease.

scholarly journals Role of Peroxisome Proliferator Activated Receptor-gamma and its Ligands in Inflammatory Bowel Disease

1970 ◽  
Vol 1 (1) ◽  
pp. 33-38 ◽  
Author(s):  
Umid Kumar Shrestha ◽  
Bing Xia
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Peroxisome Proliferator ◽  
Aminosalicylic Acid ◽  
Peroxisome Proliferator Activated Receptor ◽  
Model Studies ◽  
Ppar Γ ◽  
Pubmed Search ◽  
Inflammatory Bowel

Peroxisome proliferator-activated receptor-gamma (PPAR-γ), a nuclear receptor, is highly expressed in the colonic epithelium in contrast to its impaired expression in the patients with ulcerative colitis (UC). Several natural and synthetic ligands of PPAR-γ with some effects in the colon have been identified. The aim of this review is to provide an overview of the role of PPAR-γ and its ligands in inflammatory bowel disease (IBD). Review of article was done using a PubMed search. Animal model studies have revealed that PPAR-γ is the key receptor for 5-aminosalicylic acid that mediates its main effects in the colon. Moreover, the clinical trials have shown that the PPAR-γ agonist rosiglitazone is effective in the treatment of mild to moderately active UC. PPAR-γ gene therapy, used as an adjunct intervention, may be effective in suppressing inflammation in colitis. Some commensal bacteria and natural ligands present in food may induce PPAR-γ expression and activation in the colon which suggest the possibility of associating a natural regulator and a synthetic ligand of PPAR-γ as drug therapy for IBD patients. Further studies are required for the development of unique and effective therapies with PPAR-γ agonists in IBD patients. DOI: http://dx.doi.org/10.3126/jaim.v1i1.5838 Journal of Advances in Internal Medicine. 2012; 1(1): 33-38

Obesity and inflammatory bowel disease

2021 ◽  
Vol 75 (1) ◽  
pp. 20-28
Author(s):  
Vladimír Teplan ◽  
Milan Lukáš
Keyword(s):  
Inflammatory Bowel Disease ◽  
Adipose Tissue ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Perioperative Complications ◽  
Overweight And Obesity ◽  
Special Role ◽  
Low Concentrations ◽  
Inflammatory Bowel

The incidence and prevalence of overweight and obesity has dramatically increased in the last decades and is generally considered to be global pandemics. The incidence of inflammatory bowel disease (IBD) is rising parallel with overweight and obesity. Contrary to a conventional believe, about 15–40% patients with IBD are obese, which can contribute to the development and course of IBD, especially in Crohn’s disease. Although the findings of some cohort studies are still conflicting, recent results indicate a special role of visceral adipose tissue and particularly mesenteric adipose tissue known as creeping fat, leading to intestinal inflammation. The involvement of altered adipocyte function and deregulated production of adipokines such as leptin and adiponectin has been suggested in the pathogenesis of IBD. The emerging role of Western diet and microbiota can also open new possibilities in IBD management. The effect of obesity on the IBD-related therapy remains to be studied. The finding that obesity results in suboptimal response to the therapy, potentially promoting rapid clearance of biologic agents and thus leading to their low concentrations, has a great importance. Obesity also makes IBD colorectal surgery technically challenging and might increase a risk of perioperative complications.

scholarly journals Thymus leukemia antigen controls intraepithelial lymphocyte function and inflammatory bowel disease

2008 ◽  
Vol 105 (46) ◽  
pp. 17931-17936 ◽  
Author(s):  
Danyvid Olivares-Villagómez ◽  
Yanice V. Mendez-Fernandez ◽  
Vrajesh V. Parekh ◽  
Saif Lalani ◽  
Tiffaney L. Vincent ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Genetic Model ◽  
Critical Role ◽  
Intraepithelial Lymphocytes ◽  
Lymphocyte Function ◽  
Intestinal Epithelial ◽  
Inflammatory Bowel

Intestinal intraepithelial lymphocytes (IEL) bear a partially activated phenotype that permits them to rapidly respond to antigenic insults. However, this phenotype also implies that IEL must be highly controlled to prevent misdirected immune reactions. It has been suggested that IEL are regulated through the interaction of the CD8αα homodimer with the thymus leukemia (TL) antigen expressed by intestinal epithelial cells. We have generated and characterized mice genetically-deficient in TL expression. Our findings show that TL expression has a critical role in maintaining IEL effector functions. Also, TL deficiency accelerated colitis in a genetic model of inflammatory bowel disease. These findings reveal an important regulatory role of TL in controlling IEL function and intestinal inflammation.

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