Iordanes Karagiannides1, Charalabos Pothoulakis. 1. Inflammatory Bowel Disease Center, Division of Digestive Diseases, David Geffen School of Medicine at UCLA, Los Angeles, California 90095-7019, USA.
Abstract
PURPOSE OF REVIEW: The purpose of this review is to present recent data on the effects of substance P on the development of two common pathological conditions, namely obesity and gut inflammation, and elucidate the role of this neuropeptide as a potential regulator between increased adiposity and exacerbated inflammatory responses during inflammatory bowel disease. RECENT FINDINGS: We present data that demonstrate a role for substance P in both obesity and inflammatory bowel disease and investigate potential effects on fat tissue that may influence the progression of intestinal inflammation. More specifically, we discuss new evidence for direct effects of substance P on fat tissue that determine fat depot size and overall weight in mice and analyze some of the potential mechanisms. Furthermore, we present data that describe changes in the intestinal sensory innervation, in particular substance P-positive innervation, during gut inflammation and new direct evidence of the effects of preestablished obesity in the outcome of experimental inflammation of the colon in mice. In the end we propose a link between the role of substance P in the promotion of obesity and the potential consequences on inflammatory bowel disease. SUMMARY: We propose that substance P may promote fat tissue expansion either centrally or peripherally and thus create a proinflammatory environment (as is the case with obesity) which may in turn affect the progression (exacerbate) of gut inflammation. Further studies are required on the effects of 'creeping fat' in inflammatory bowel disease in order to decipher the role of this type of fat-depot expansion in the development of the disease.
PURPOSE OF REVIEW: The purpose of this review is to present recent data on the effects of substance P on the development of two common pathological conditions, namely obesity and gut inflammation, and elucidate the role of this neuropeptide as a potential regulator between increased adiposity and exacerbated inflammatory responses during inflammatory bowel disease. RECENT FINDINGS: We present data that demonstrate a role for substance P in both obesity and inflammatory bowel disease and investigate potential effects on fat tissue that may influence the progression of intestinal inflammation. More specifically, we discuss new evidence for direct effects of substance P on fat tissue that determine fat depot size and overall weight in mice and analyze some of the potential mechanisms. Furthermore, we present data that describe changes in the intestinal sensory innervation, in particular substance P-positive innervation, during gut inflammation and new direct evidence of the effects of preestablished obesity in the outcome of experimentalinflammation of the colon in mice. In the end we propose a link between the role of substance P in the promotion of obesity and the potential consequences on inflammatory bowel disease. SUMMARY: We propose that substance P may promote fat tissue expansion either centrally or peripherally and thus create a proinflammatory environment (as is the case with obesity) which may in turn affect the progression (exacerbate) of gut inflammation. Further studies are required on the effects of 'creeping fat' in inflammatory bowel disease in order to decipher the role of this type of fat-depot expansion in the development of the disease.
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