Hyperinsulinaemia and hyperglycaemia: possible risk factors of colorectal cancer among diabetic patients

被引:106
作者
Chang, CK
Ulrich, CM
机构
[1] Univ Washington, Sch Publ Hlth & Community Med, Dept Epidemiol, Seattle, WA 98195 USA
[2] Fred Hutchinson Canc Res Ctr, Program Epidemiol, Seattle, WA 98104 USA
关键词
diabetes mellitus; colorectal cancer; carcinogenesis; hyperglycaemia; hyperinsulinaemia; insulin resistance; IGF-1; epidemiology; review;
D O I
10.1007/s00125-003-1109-5
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Hyperinsulinaemia and hyperglycaemia are two possible risk factors for colorectal cancer, which constitutes the third leading cause of cancer death in Western countries. Molecular evidence as well as animal models provide support for these associations: Insulin has been shown to be an important growth factor for colonic carcinoma cells, and both insulin and insulin-like growth factor-1 receptors have been detected in colon cancer tissue. The insulin-signal transduction pathway is involved in the regulation of gene expression and apoptosis. The role of hyperglycaemia in carcinogenesis could include pathways via luminal factors (related to fecal bile acid concentrations, stool bulk, and prolonged transit time) or circulatory factors (via glucose as the only energy source for neoplastic cells). This review summarizes the epidemiologic literature with respect to hyperinsulinaemia and hyperglycaemia as risk factors for colorectal cancer, and aims to integrate the biological and epidemiological evidence. Epidemiologic findings to date indicate a slightly increased risk of colorectal cancer for diabetic patients; however, there are some inconsistencies. Possible explanations for these inconsistencies include inadequate information about patients' diabetic disease and treatment states. We suggest that future studies should take medical history, staging and treatment for hyperinsulinaemia and hyperglycaemia into account to further our understanding of the role of hyperglycaemia and hyperinsulinaemia in colorectal carcinogenesis.
引用
收藏
页码:595 / 607
页数:13
相关论文
共 95 条
[1]   GROWTH-FACTORS AND CANCER [J].
AARONSON, SA .
SCIENCE, 1991, 254 (5035) :1146-1153
[2]   CANCER RISK IN PATIENTS WITH DIABETES-MELLITUS [J].
ADAMI, HO ;
MCLAUGHLIN, J ;
EKBOM, A ;
BERNE, C ;
SILVERMAN, D ;
HACKER, D ;
PERSSON, I .
CANCER CAUSES & CONTROL, 1991, 2 (05) :307-314
[3]  
American Diabetes Association, 1998, DIABETES CARE, pS23
[4]  
[Anonymous], 2000, Diabetes Care, V23 Suppl 1, pS1
[5]  
[Anonymous], 1989, DIET HLTH IMPL RED C
[6]   A randomized trial of aspirin to prevent colorectal adenomas [J].
Baron, JA ;
Cole, BF ;
Sandler, RS ;
Haile, RW ;
Ahnen, D ;
Bresalier, R ;
McKeown-Eyssen, G ;
Summers, RW ;
Rothstein, R ;
Burke, CA ;
Snover, DC ;
Church, TR ;
Allen, JI ;
Beach, M ;
Beck, GJ ;
Bond, JH ;
Byers, T ;
Greenberg, ER ;
Mandel, JS ;
Marcon, N ;
Mott, LA ;
Pearson, L ;
Saibil, F ;
van Stolk, RU .
NEW ENGLAND JOURNAL OF MEDICINE, 2003, 348 (10) :891-899
[7]   GROWTH-REGULATORY EFFECTS OF SENSORY NEUROPEPTIDES, EPIDERMAL GROWTH-FACTOR, INSULIN, AND SOMATOSTATIN ON THE NONTRANSFORMED INTESTINAL EPITHELIAL-CELL LINE IEC-6 AND THE COLON-CANCER CELL-LINE HT-29 [J].
BJORK, J ;
NILSSON, J ;
HULTCRANTZ, R ;
JOHANSSON, C .
SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY, 1993, 28 (10) :879-884
[8]   GENETIC MECHANISMS IN TUMOR INITIATION AND PROGRESSION .10. THE RAS GENE FAMILY AND HUMAN CARCINOGENESIS [J].
BOS, JL .
MUTATION RESEARCH, 1988, 195 (03) :255-271
[9]   SUGAR, MEAT, AND FAT INTAKE, AND NONDIETARY RISK-FACTORS FOR COLON-CANCER INCIDENCE IN IOWA WOMEN (UNITED-STATES) [J].
BOSTICK, RM ;
POTTER, JD ;
KUSHI, LH ;
SELLERS, TA ;
STEINMETZ, KA ;
MCKENZIE, DR ;
GAPSTUR, SM ;
FOLSOM, AR .
CANCER CAUSES & CONTROL, 1994, 5 (01) :38-52
[10]   Pancreas and islet cell transplantation [J].
Bottino, R ;
Trucco, M ;
Balamurugan, AN ;
Starzl, TE .
BEST PRACTICE & RESEARCH CLINICAL GASTROENTEROLOGY, 2002, 16 (03) :457-474