期刊
DIABETOLOGIA
卷 54, 期 12, 页码 3037-3046出版社
SPRINGER
DOI: 10.1007/s00125-011-2316-0
关键词
C-peptide; HbA(1c); Cohort study; Diabetes; EPIC; Pancreatic cancer
资金
- German Research Foundation [Graduiertenkolleg 793]
- WCRF-UK
- WCRF International [2009/39]
- European Commission
- International Agency for Research on Cancer
- Danish Cancer Society (Denmark)
- Ligue Contre le Cancer
- Institut Gustave Roussy
- Mutuelle Generale de l'Education Nationale
- Institut National de la Sante et de la Recherche Medicale (Inserm) (France)
- Deutsche Krebshilfe
- Deutsches Krebsforschungszentrum
- Federal Ministry of Education and Research (Germany)
- Hellenic Health Foundation
- Stavros Niarchos Foundation
- Hellenic Ministry of Health and Social Solidarity (Greece)
- Italian Association for Research on Cancer (AIRC)
- National Research Council (Italy)
- Dutch Ministry of Public Health, Welfare and Sports (VWS)
- Netherlands Cancer Registry (NKR)
- LK Research Funds
- Dutch Prevention Funds
- Dutch ZON (Zorg Onderzoek Nederland)
- World Cancer Research Fund (WCRF)
- Statistics Netherlands (the Netherlands)
- Nordforsk, Nordic Centre of Excellence programme on Food, Nutrition and Health (Norway)
- Health Research Fund (FIS)
- Regional Government of Andalucia
- Regional Government of Asturias
- Regional Government of Basque Country
- Regional Government of Murcia
- Regional Government of Navarra
- ISCIII RETIC (Spain) [RD06/0020]
- Swedish Cancer Society
- Swedish Scientific Council
- Regional Government of Skane and Vasterbotten (Sweden)
- Cancer Research UK
- Medical Research Council
- Stroke Association
- British Heart Foundation
- Department of Health
- Food Standards Agency
- Wellcome Trust (UK)
- [ERC-2009-AdG 232997]
- Medical Research Council [G0401527, G0801056B, MC_U106179471, G1000143] Funding Source: researchfish
Aims/hypothesis There has been long-standing debate about whether diabetes is a causal risk factor for pancreatic cancer or a consequence of tumour development. Prospective epidemiological studies have shown variable relationships between pancreatic cancer risk and blood markers of glucose and insulin metabolism, overall and as a function of lag times between marker measurements (blood donation) and date of tumour diagnosis. Methods Pre-diagnostic levels of HbA(1c) and C-peptide were measured for 466 participants with pancreatic cancer and 466 individually matched controls within the European Prospective Investigation into Cancer and Nutrition. Conditional logistic regression models were used to estimate ORs for pancreatic cancer. Results Pancreatic cancer risk gradually increased with increasing pre-diagnostic HbA(1c) levels up to an OR of 2.42 (95% CI 1.33, 4.39 highest [>= 6.5%, 48 mmol/mol] vs lowest [<= 5.4%, 36 mmol/mol] category), even for individuals with HbA(1c) levels within the non-diabetic range. C-peptide levels showed no significant relationship with pancreatic cancer risk, irrespective of fasting status. Analyses showed no clear trends towards increasing hyperglycaemia (as marked by HbA(1c) levels) or reduced pancreatic beta cell responsiveness (as marked by C-peptide levels) with decreasing time intervals from blood donation to cancer diagnosis. Conclusions/interpretation Our data on HbA(1c) show that individuals who develop exocrine pancreatic cancer tend to have moderate increases in HbA(1c) levels, relatively independently of obesity and insulin resistance-the classic and major risk factors for type 2 diabetes. While there is no strong difference by lag time, more data are needed on this in order to reach a firm conclusion.
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