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. 2013;8(1):e54944.
doi: 10.1371/journal.pone.0054944. Epub 2013 Jan 25.

Serum glucose and fructosamine in relation to risk of cancer

Affiliations

Serum glucose and fructosamine in relation to risk of cancer

Wahyu Wulaningsih et al. PLoS One. 2013.

Abstract

Background: Impaired glucose metabolism has been linked with increased cancer risk, but the association between serum glucose and cancer risk remains unclear. We used repeated measurements of glucose and fructosamine to get more insight into the association between the glucose metabolism and risk of cancer.

Methods: We selected 11,998 persons (>20 years old) with four prospectively collected serum glucose and fructosamine measurements from the Apolipoprotein Mortality Risk (AMORIS) study. Multivariate Cox proportional hazards regression was used to assess standardized log of overall mean glucose and fructosamine in relation to cancer risk. Similar analyses were performed for tertiles of glucose and fructosamine and for different types of cancer.

Results: A positive trend was observed between standardized log overall mean glucose and overall cancer risk (HR= 1.08; 95% CI: 1.02-1.14). Including standardized log fructosamine in the model resulted in a stronger association between glucose and cancer risk and aninverse association between fructosamine and cancer risk (HR = 1.17; 95% CI: 1.08-1.26 and HR: 0.89; 95% CI: 0.82-0.96, respectively). Cancer risks were highest among those in the highest tertile of glucose and lowest tertile of fructosamine. Similar findings were observed for prostate, lung, and colorectal cancer while none observed for breast cancer.

Conclusion: The contrasting effect between glucose, fructosamine, and cancer risk suggests the existence of distinct groups among those with impaired glucose metabolism, resulting in different cancer risks based on individual metabolic profiles. Further studies are needed to clarify whether glucose is a proxy of other lifestyle-related or metabolic factors.

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Conflict of interest statement

Competing Interests: Björn Zethelius is employed by the Medical Products Agency (MPA), Uppsala, Sweden and the views of the present study are his own and not necessarily any official views of the MPA. Niklas Hammar is employed by the AstraZeneca Sverige, Södertalje, Sweden and the views of the present study are his own and not necessarily any official views of the AstraZeneca Sverige. This does not alter the authors’ adherence to all the PLOS ONE policies on sharing data and materials.

Figures

Figure 1
Figure 1. Hazard ratios for overall cancer risk for standardized log fructosamine in different tertiles of glucose in fasting population.
The model was adjusted for age, sex, SES, fasting status, history of diabetes, lung and cardiovascular disease, serum albumin, total cholesterol and triglycerides.
Figure 2
Figure 2. Hazard ratios for overall cancer risk for groups of population based on tertiles of overall mean glucose and fructosamine.
All models were adjusted for age, sex, SES, fasting status, history of diabetes, lung and cardiovascular disease, serum albumin, total cholesterol and triglycerides. P-value for interaction was 0.77.
Figure 3
Figure 3. Hazard ratios for the risk of different types of cancer for groups of population based on tertiles of overall mean glucose and fructosamine.
All models were adjusted for age, SES, fasting status, history of diabetes, lung and cardiovascular disease, serum albumin, total cholesterol and triglycerides. Additional adjustment for sex was performed for colorectal and lung cancer, as well as for parity and age at first childbirth for breast cancer. P-values for interaction were 0.29, 0.93, 0.01, and 0.08 for prostate, breast, colorectal and lung cancer, respectively.

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References

    1. Danaei G, Vander Hoorn S, Lopez AD, Murray CJ, Ezzati M (2005) Causes of cancer in the world: comparative risk assessment of nine behavioural and environmental risk factors. Lancet 366: 1784–1793. - PubMed
    1. Ford ES, Zhao G, Li C (2010) Pre-diabetes and the risk for cardiovascular disease: a systematic review of the evidence. J Am Coll Cardiol 55: 1310–1317. - PubMed
    1. Ogunleye AA, Ogston SA, Morris AD, Evans JM (2009) A cohort study of the risk of cancer associated with type 2 diabetes. Br J Cancer 101: 1199–1201. - PMC - PubMed
    1. Rapp K, Schroeder J, Klenk J, Ulmer H, Concin H, et al. (2006) Fasting blood glucose and cancer risk in a cohort of more than 140,000 adults in Austria. Diabetologia 49: 945–952. - PubMed
    1. Giovannucci E, Harlan DM, Archer MC, Bergenstal RM, Gapstur SM, et al. (2010) Diabetes and cancer: a consensus report. CA Cancer J Clin 60: 207–221. - PubMed

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