In our study, among diabetic patients with pancreatic cancer, there was a context of insulin resistance in only 50% of the cases; incidence of diabetes was two times higher than in control group (38% vs 19%). The frequency of diabetes in the control group was comparable to type 2 diabetes in general population (prevalence between 10 and 20% after 35 years). All diabetics Inhibitors,research,lifescience,medical in colo-rectal cancer group had an insulin-resistance, characteristic of “classic” type 2 diabetes. This observation suggests that in pancreatic cancer group, 50%

of mellitus diabetes was “classic”, and 50% of others types of diabetes, directly associated with pancreatic cancer and probably linked to insulin deficiency. Some weaknesses can be reported in our study. We have not included a healthy group. We have chosen

to compare two different tumour populations rather than using a control group of healthy subjects because we wanted to validate the divergent evolution of www.selleckchem.com/products/PF-2341066.html adiponectin rate during theses cancers. Because of the relatively small population in our study we could not possibly explore in detail Inhibitors,research,lifescience,medical the subgroup of diabetic patients and our odds ratio, have wide confidence Inhibitors,research,lifescience,medical intervals and are only informative. Our article is a transversal study that allows evaluation of adiponectin rate at the moment when cancer becomes symptomatic, so we can not evaluate the kinetics of adiponectin before apparition of neoplasia. At last, there isn’t a consensus Inhibitors,research,lifescience,medical between manufacturers of kits for the determination of adiponectin (positivity or increased

serum level). The case-controlled studies conducted in various cancers have showed variable rates. The rate of adiponectin was often less than 9 µg/L in cancer cases, and generally between 10 µg/L and 14 µg/L in the control group without cancer. In the study by Chang et al. comparing the rates of adiponectin in pancreatic cancer (14), in chronic pancreatitis and in healthy subjects, the averages were respectively 21.1, 13.7 and 5.8 µg/L. After the analysis of ROC curves, we have chosen 10 µg/L as the threshold of positivity, but this must be confirmed by further studies with Inhibitors,research,lifescience,medical a larger numbers of patients. Conclusion In summary, we demonstrate that adiponectin concentration is higher in PC than in CRC. Our results confirm indirectly that in CRC, adiponectin is often low and higher these in pancreatic cancer. We demonstrated that diabetes could be a factor for PC and differ in function of the natural in PC. Our data can speculate that we have two different mechanisms of natural history on PC. So, we hypothesize that an old diabetes mellitus could be an moderate risk factor of PC associated within an increase of IGF level and low adiponectin concentration and conversely an early diabetes with insulopenia and high level of adiponectin secondary and witness of an new PC. So, we think that other prospective studies must control our results and analyse the real key of adiponectin in these tumors. Footnotes No potential conflict of interest.