Abstract
Until recently, fat was considered a relatively inactive tissue serving only as a depot for the storage of excess lipid around the body. Over the last decade, however, several studies have established fat as a metabolically active endocrine organ able to affect human pathophysiology at multiple levels. During this time adipose tissue has been shown to produce a number of hormones and inflammatory mediators collectively termed as adipokines. These molecules have been shown to be involved in the etiology of a number of inflammation- associated pathological conditions ranging from atherosclerosis and hypertension to diabetes and cancer. Despite the close physical association of abdominal fat and the intestine in the visceral cavity and the significant paracrine functions now attributed to adipose tissue, very little is known on the potential interactions between these tissues as they may relate to intestinal homeostasis. Considering the dramatic alterations in mesenteric fat depot size and placement during at least one intestinal disease, Crohn's disease, the potential involvement of fat tissue in the development as well as the progression of this and other pathological conditions should be considered. In this review we discuss the latest knowledge on neuropeptide-adipose tissue communication and the potential changes such interaction may induce in intra-abdominal fat tissue physiology. Finally we will discuss evidence on the potential pathways by which such changes in fat physiology may affect the development and progress of intestinal pathological conditions such as inflammatory bowel disease.
Keywords: Neuropeptides, IBD, Obesity, Adipose tissue, Adipokines, pathophysiology, homeostasis, Crohn's disease, diabetes, hypertension, atherosclerosis, endocrine, proangiogenic, hypertrophy, creeping fat, radiographic
Current Pharmaceutical Design
Title: Neuropeptide - Adipose Tissue Communication and Intestinal Pathophysiology
Volume: 17 Issue: 16
Author(s): Iordanes Karagiannides, Kyriaki Bakirtzi and Charalabos Pothoulakis
Affiliation:
Keywords: Neuropeptides, IBD, Obesity, Adipose tissue, Adipokines, pathophysiology, homeostasis, Crohn's disease, diabetes, hypertension, atherosclerosis, endocrine, proangiogenic, hypertrophy, creeping fat, radiographic
Abstract: Until recently, fat was considered a relatively inactive tissue serving only as a depot for the storage of excess lipid around the body. Over the last decade, however, several studies have established fat as a metabolically active endocrine organ able to affect human pathophysiology at multiple levels. During this time adipose tissue has been shown to produce a number of hormones and inflammatory mediators collectively termed as adipokines. These molecules have been shown to be involved in the etiology of a number of inflammation- associated pathological conditions ranging from atherosclerosis and hypertension to diabetes and cancer. Despite the close physical association of abdominal fat and the intestine in the visceral cavity and the significant paracrine functions now attributed to adipose tissue, very little is known on the potential interactions between these tissues as they may relate to intestinal homeostasis. Considering the dramatic alterations in mesenteric fat depot size and placement during at least one intestinal disease, Crohn's disease, the potential involvement of fat tissue in the development as well as the progression of this and other pathological conditions should be considered. In this review we discuss the latest knowledge on neuropeptide-adipose tissue communication and the potential changes such interaction may induce in intra-abdominal fat tissue physiology. Finally we will discuss evidence on the potential pathways by which such changes in fat physiology may affect the development and progress of intestinal pathological conditions such as inflammatory bowel disease.
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Cite this article as:
Karagiannides Iordanes, Bakirtzi Kyriaki and Pothoulakis Charalabos, Neuropeptide - Adipose Tissue Communication and Intestinal Pathophysiology, Current Pharmaceutical Design 2011; 17 (16) . https://dx.doi.org/10.2174/138161211796196981
DOI https://dx.doi.org/10.2174/138161211796196981 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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