Type 2 Diabetes Mellitus and Its Association with the Risk of Pancreatic Carcinogenesis: A Review / 대한소화기학회지
The Korean Journal of Gastroenterology
;
: 168-177, 2016.
Artigo
em Inglês
| WPRIM
| ID: wpr-165886
ABSTRACT
The prevalence of diabetes mellitus (DM) and associated diseases such as cancers are substantially increasing worldwide. About 80% of the patients with pancreatic cancer have glucose metabolism alterations. This suggests an association between type 2 DM and pancreatic cancer risk and progression. There are hypotheses that show metabolic links between the diseases, due to insulin resistance, hyperglycemia, hyperinsulinemia, low grade chronic inflammation, and alteration in the insulin-insulin-like growth factor axis. The use of diabetes medications can influence the extent of carcinogenesis of the pancreas. This study briefly reviews recent literature on investigation of metabolic link of type 2 DM, risk of carcinogenesis of the pancreas and their association, as well as the current understanding of metabolic pathways implicated in metabolism and cellular growth. The main finding of this review, although there are discrepancies, is that according to most research long-term DM does not raise the risk of pancreatic cancer. The longest duration of DM may reflect hypoinsulinemia due to treatment for hyperglycemia, but recent onset diabetes was associated with increased risk for pancreatic cancer due to hyperinsulinemia and hyperglycemia. In conclusion, the review demonstrates that type 2 DM and the duration of diabetes pose a risk for pancreatic carcinogenesis, and that there is biological link between the diseases.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Neoplasias Pancreáticas
/
Resistência à Insulina
/
Fator de Crescimento Insulin-Like I
/
Fatores de Risco
/
Diabetes Mellitus Tipo 2
/
Hiperglicemia
/
Insulina
Tipo de estudo:
Estudo de etiologia
/
Fatores de risco
Limite:
Humanos
Idioma:
Inglês
Revista:
The Korean Journal of Gastroenterology
Ano de publicação:
2016
Tipo de documento:
Artigo
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