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- bmj.38415.708634.F7v1
- 330/7503/1304 most recent
- Josie M M Evans, lecturer in epidemiology (j.m.m.stansfield@dundee.ac.uk)1,
- Louise A Donnelly, statistician1,
- Alistair M Emslie-Smith, principal in general practice2,
- Dario R Alessi, principal investigator3,
- Andrew D Morris, professor of diabetic medicine4
- 1 Division of Community Health Sciences, Section of Public Health, University of Dundee, Dundee DD2 4BF
- 2 Mill Practice, Dundee
- 3 School of Life Sciences, University of Dundee
- 4 Division of Medicine, University of Dundee
- Correspondence to: J M M Evans
- Accepted 14 February 2005
Introduction
Metformin, widely given to patients with type 2 diabetes, works by targeting the enzyme AMPK (AMP activated protein kinase), which induces muscles to take up glucose from the blood. A recent breakthrough has found the upstream regulator of AMPK to be a protein kinase known as LKB1.1 2 LKB1 is a well recognised tumour suppressor. Activation of AMPK by metformin and exercise requires LKB1, and this would also explain why exercise is beneficial in the primary and secondary prevention of certain cancers.3 We hypothesise that metformin use in patients with type 2 diabetes may reduce their risk of cancer.
Participants, methods, and results
We tested this hypothesis using record linkage databases developed in Tayside, Scotland: a diabetes clinical information system (DARTS) and a database of dispensed prescriptions (MEMO).4 We did a pilot case-control study using previously validated methods.5
From 314 127 people who were resident (or died) in Tayside in …








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