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      Fasting serum insulin levels and insulin resistance are associated with colorectal adenoma in Koreans

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          Abstract

          Aims/Introduction

          Insulin has been associated with the risk of colorectal cancer ( CRC). However, few studies have evaluated the association between insulin and colorectal adenoma. We investigated the relationship between fasting serum insulin levels or homeostasis model assessment of insulin resistance ( HOMAIR) and colorectal adenoma.

          Materials and Methods

          We retrospectively enrolled 15,427 participants who underwent both fasting serum insulin measurement and colonoscopy for a routine health examination at Asan Medical Center from January 2007 to December 2008. Participants with a history of any cancer, previous colectomy or polypectomy, those taking antidiabetic medications, and inflammatory bowel disease, non‐specific colitis, non‐adenomatous polyps only or CRC on colonoscopic findings were excluded. Finally, 3,606 participants with histologically confirmed colorectal adenoma and 6,019 controls with no abnormal findings on colonoscopy were included. Participants were categorized into quartiles ( Q) based on fasting serum insulin levels and HOMAIR.

          Results

          Fasting serum insulin and HOMAIR were significantly higher in participants with colorectal adenomas compared with controls. Multivariate regression analysis adjusting for age, sex, smoking habits, drinking habits and family history of CRC showed that participants with higher quartiles of fasting serum insulin levels (odd ratio [ OR] 1.17 for 2nd Q, 1.19 for 3rd Q, and 1.42 for 4th Q, P < 0.05) or HOMAIR ( OR 1.18 for 2nd Q and 1.45 for 4th Q, P < 0.05) showed significantly increased ORs of colorectal adenoma compared with the lowest quartiles.

          Conclusions

          These findings showed that increased serum insulin levels and insulin resistance were significantly associated with the presence of colorectal adenoma.

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          Most cited references28

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          Metabolic syndrome, hyperinsulinemia, and colon cancer: a review.

          An impressive body of epidemiologic data collected over the past decade indicates that the risk of colon cancer is elevated in those with metabolic syndrome. This evidence includes studies that examined the risk of colon cancer or adenoma in relation to determinants of the metabolic syndrome (obesity, abdominal distribution of adiposity, and physical inactivity), clinical consequences of this syndrome (type 2 diabetes and hypertension), plasma or serum components of the definition of metabolic syndrome (hypertriglyceridemia, hyperglycemia, and low HDL cholesterol), and markers of hyperinsulinemia or insulin resistance (insulin and C-peptide), which is the underlying metabolic defect of the metabolic syndrome. The mechanism underlying these associations is unknown but may involve the influence of hyperinsulinemia in enhancing free or bioavailable concentrations of insulin-like growth factor-1. Future studies should also be based on better measurements of insulin resistance, beta-cell depletion, and insulin responses to better assess which aspects of insulin resistance are most closely related to the risk of colon neoplasia.
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            Insulin and colon cancer.

            Some factors related to Westernization or industrialization increase risk of colon cancer. It is believed widely that this increase in risk is related to the direct effects of dietary fat and fiber in the colonic lumen. However, the fat and fiber hypotheses, at least as originally formulated, do not explain adequately many emerging findings from recent epidemiologic studies. An alternative hypothesis, that hyperinsulinemia promotes colon carcinogenesis, is presented here. Insulin is an important growth factor of colonic epithelial cells and is a mitogen of tumor cell growth in vitro. Epidemiologic evidence supporting the insulin/colon-cancer hypothesis is largely indirect and based on the similarity of factors which produce elevated insulin levels with those related to colon cancer risk. Specifically, obesity--particularly central obesity, physical inactivity, and possibly a low dietary polyunsaturated fat to saturated fat ratio--are major determinants of insulin resistance and hyperinsulinemia, and appear related to colon cancer risk. Moreover, a diet high in refined carbohydrates and low in water-soluble fiber, which is associated with an increased risk of colon cancer, causes rapid intestinal absorption of glucose into the blood leading to postprandial hyperinsulinemia. The combination of insulin resistance and high glycemic load produces particularly high insulin levels. Thus, hyperinsulinemia may explain why obesity, physical inactivity, and a diet low in fruits and vegetables and high in red meat and extensively processed foods, all common in the West, increase colon cancer risk.
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              Major dietary patterns and the risk of colorectal cancer in women.

              Several foods and nutrients have been implicated in the development of colon and rectal cancers. In this study, we prospectively assessed the associations between major dietary patterns and the risks of these 2 cancers in women. Using dietary information collected in 1984, 1986, 1990, and 1994 from 76 402 women aged 38 to 63 years without a history of cancer in 1984, we conducted factor analysis and identified 2 major dietary patterns: "prudent" and "Western." We calculated factor scores for each participant and examined prospectively the associations between dietary patterns and colon and rectal cancer risks. The prudent pattern was characterized by higher intakes of fruits, vegetables, legumes, fish, poultry, and whole grains, while the Western pattern, by higher intakes of red and processed meats, sweets and desserts, french fries, and refined grains. During 12 years of follow-up, we identified 445 cases of colon cancer and 101 cases of rectal cancer. After adjusting for potential confounders, we observed a relative risk for colon cancer of 1.46 (95% confidence interval, 0.97-2.19) when comparing the highest with the lowest quintiles of the Western pattern (P value for trend across quintiles, .02). The prudent pattern had a nonsignificant inverse association with colon cancer (relative risk for fifth quintile compared with the first, 0.71; 95% confidence interval, 0.50-1.00; P for trend across quintiles, .31). We did not observe any significant association between dietary patterns and rectal cancer. We found a significant positive association between the Western dietary pattern and the risk of colon cancer.
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                Author and article information

                Journal
                J Diabetes Investig
                J Diabetes Investig
                10.1111/(ISSN)2040-1124
                JDI
                Journal of Diabetes Investigation
                Wiley-Blackwell
                2040-1116
                2040-1124
                05 December 2013
                04 May 2014
                : 5
                : 3 ( doiID: 10.1111/jdi.2014.5.issue-3 )
                : 297-304
                Affiliations
                [ 1 ]Health Screening and Promotion Center Asan Medical Center SeoulKorea
                [ 2 ] Division of Gastroenterology Department of Internal MedicineUniversity of Ulsan College of Medicine SeoulKorea
                [ 3 ] Division of Endocrinology & Metabolism Department of Internal MedicineUniversity of Ulsan College of Medicine SeoulKorea
                Author notes
                [*] [* ] Corresponding author. Hong‐Kyu Kim Tel.: +82‐2‐3010‐4802 Fax: +82‐2‐3010‐4964

                E‐mail address: hkkim0801@ 123456amc.seoul.kr

                Article
                JDI12178
                10.1111/jdi.12178
                4020334
                9a39dd2a-65bb-4995-b8bb-34ebb9727648
                Copyright © 2014 Asian Association for the Study of Diabetes and Wiley Publishing Asia Pty Ltd© 2013 The Authors. Journal of Diabetes Investigation published by Asian Association for the Study of Diabetes and Wiley Publishing Asia Pty Ltd

                This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

                History
                : 15 March 2013
                : 24 June 2013
                : 22 August 2013
                Page count
                Pages: 8
                Categories
                Original Article
                Articles
                Clinical Science and Care
                Custom metadata
                2.0
                jdi12178
                May 2014
                Converter:WILEY_ML3GV2_TO_NLM version:4.0.3 mode:remove_FC converted:04.05.2014

                insulin,insulin resistance,colorectal adenoma
                insulin, insulin resistance, colorectal adenoma

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