Insulin, leptin, and adiponectin receptors in colon

regulation relative to differing body adiposity independent of diet and in response to dimethylhydrazine

Janice Drew, Andrew Farquharson, Sara Padidar, Garry G. Duthie, Julian Mercer, John R. Arthur, Philip C. Morrice, Lawrence N. Barrera

Research output: Contribution to journalArticle

37 Citations (Scopus)

Abstract

Insulin, leptin, and adiponectin receptors in colon: regulation relative to differing body adiposity independent of diet and in response to dimethylhydrazine. Am J Physiol Gastrointest Liver Physiol 293: G682-G691, 2007. First published July 26, 2007; doi:10.1152/ajpgi.00231.2007.-Obesity has recently become a focus of research to elucidate diet and lifestyle factors as important risk factors for colon cancer. Altered levels of insulin, leptin, and adiponectin have been identified as potential candidates increasing colon cancer risk within the prevailing obesogenic environment. There has been considerable research to characterize signaling via these hormones in the brain, liver, and adipose tissue; however, very little is known of their emerging role in peripheral signaling, particularly in epithelial tissues. This study profiles insulin, leptin, and adipokine receptors in the rat colon, revealing novel microanatomical location of these receptors and thereby supporting a potential role in regulating colonic tissue. Potential involvement of insulin, leptin, and adiponectin receptors in increased risk of colon cancer was investigated using Sprague-Dawley rats, either resistant or susceptible to diet-induced obesity. Regulation of insulin, leptin, and adiponectin receptors as a consequence of differing levels of adiposity was assessed regionally in the colon in response to treatment with the chemical carcinogen 1,2-dimethylhydrazine (DMH). However, significantly increased fat mass, increased levels of plasma insulin, leptin, and triglycerides, previously associated with an increased risk of colon cancer, were not associated with promotion of precancerous lesions in the experimental rats or deregulation of insulin, leptin, or adiponectin receptors. These findings do not support a direct link between the deregulation of insulin and adipokine levels observed in obese rats and an increased risk of colon carcinogenesis.

Original languageEnglish
Pages (from-to)G682-G691
Number of pages10
JournalAmerican journal of physiology. Gastrointestinal and liver physiology
Volume293
Issue number4
DOIs
Publication statusPublished - Oct 2007

Keywords

  • obesity
  • colon cancer
  • adipokine
  • hormone receptors
  • in situ hybridization
  • real-time PCR
  • inflammatory-bowel-disease
  • azoxymethane-treated rats
  • epithelial-cells
  • growth-factor
  • colorectal-cancer
  • resistant rats
  • emerging role
  • kappa-B
  • carcinogenesis

Cite this

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title = "Insulin, leptin, and adiponectin receptors in colon: regulation relative to differing body adiposity independent of diet and in response to dimethylhydrazine",
abstract = "Insulin, leptin, and adiponectin receptors in colon: regulation relative to differing body adiposity independent of diet and in response to dimethylhydrazine. Am J Physiol Gastrointest Liver Physiol 293: G682-G691, 2007. First published July 26, 2007; doi:10.1152/ajpgi.00231.2007.-Obesity has recently become a focus of research to elucidate diet and lifestyle factors as important risk factors for colon cancer. Altered levels of insulin, leptin, and adiponectin have been identified as potential candidates increasing colon cancer risk within the prevailing obesogenic environment. There has been considerable research to characterize signaling via these hormones in the brain, liver, and adipose tissue; however, very little is known of their emerging role in peripheral signaling, particularly in epithelial tissues. This study profiles insulin, leptin, and adipokine receptors in the rat colon, revealing novel microanatomical location of these receptors and thereby supporting a potential role in regulating colonic tissue. Potential involvement of insulin, leptin, and adiponectin receptors in increased risk of colon cancer was investigated using Sprague-Dawley rats, either resistant or susceptible to diet-induced obesity. Regulation of insulin, leptin, and adiponectin receptors as a consequence of differing levels of adiposity was assessed regionally in the colon in response to treatment with the chemical carcinogen 1,2-dimethylhydrazine (DMH). However, significantly increased fat mass, increased levels of plasma insulin, leptin, and triglycerides, previously associated with an increased risk of colon cancer, were not associated with promotion of precancerous lesions in the experimental rats or deregulation of insulin, leptin, or adiponectin receptors. These findings do not support a direct link between the deregulation of insulin and adipokine levels observed in obese rats and an increased risk of colon carcinogenesis.",
keywords = "obesity, colon cancer, adipokine, hormone receptors, in situ hybridization, real-time PCR, inflammatory-bowel-disease, azoxymethane-treated rats, epithelial-cells, growth-factor, colorectal-cancer, resistant rats, emerging role, kappa-B, carcinogenesis",
author = "Janice Drew and Andrew Farquharson and Sara Padidar and Duthie, {Garry G.} and Julian Mercer and Arthur, {John R.} and Morrice, {Philip C.} and Barrera, {Lawrence N.}",
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AU - Drew, Janice

AU - Farquharson, Andrew

AU - Padidar, Sara

AU - Duthie, Garry G.

AU - Mercer, Julian

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AB - Insulin, leptin, and adiponectin receptors in colon: regulation relative to differing body adiposity independent of diet and in response to dimethylhydrazine. Am J Physiol Gastrointest Liver Physiol 293: G682-G691, 2007. First published July 26, 2007; doi:10.1152/ajpgi.00231.2007.-Obesity has recently become a focus of research to elucidate diet and lifestyle factors as important risk factors for colon cancer. Altered levels of insulin, leptin, and adiponectin have been identified as potential candidates increasing colon cancer risk within the prevailing obesogenic environment. There has been considerable research to characterize signaling via these hormones in the brain, liver, and adipose tissue; however, very little is known of their emerging role in peripheral signaling, particularly in epithelial tissues. This study profiles insulin, leptin, and adipokine receptors in the rat colon, revealing novel microanatomical location of these receptors and thereby supporting a potential role in regulating colonic tissue. Potential involvement of insulin, leptin, and adiponectin receptors in increased risk of colon cancer was investigated using Sprague-Dawley rats, either resistant or susceptible to diet-induced obesity. Regulation of insulin, leptin, and adiponectin receptors as a consequence of differing levels of adiposity was assessed regionally in the colon in response to treatment with the chemical carcinogen 1,2-dimethylhydrazine (DMH). However, significantly increased fat mass, increased levels of plasma insulin, leptin, and triglycerides, previously associated with an increased risk of colon cancer, were not associated with promotion of precancerous lesions in the experimental rats or deregulation of insulin, leptin, or adiponectin receptors. These findings do not support a direct link between the deregulation of insulin and adipokine levels observed in obese rats and an increased risk of colon carcinogenesis.

KW - obesity

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KW - adipokine

KW - hormone receptors

KW - in situ hybridization

KW - real-time PCR

KW - inflammatory-bowel-disease

KW - azoxymethane-treated rats

KW - epithelial-cells

KW - growth-factor

KW - colorectal-cancer

KW - resistant rats

KW - emerging role

KW - kappa-B

KW - carcinogenesis

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DO - 10.1152/ajpgi.00231.2007

M3 - Article

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SP - G682-G691

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JF - American journal of physiology. Gastrointestinal and liver physiology

SN - 1522-1547

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