Journal List > Korean J Gastroenterol > v.59(1) > 1006950

Kim and Han: Obesity and Pancreatic Diseases

Abstract

Obesity is defined as BMI (calculated as weight in kg divided by height in m2) more than 30, and overweight is defined as BMI of 25-29.9. Obesity has been considered as a risk factor for pancreatic diseases, including pancreatitis and pancreatic cancer. Severe acute pancreatitis is significantly more frequent in obese patients. Furthermore, obese patients develop systemic and local complications of acute pancreatitis more frequently. The underlying mechanisms are increased inflammation and necrosis from increased amount of intra- and peri-pancreatic fat. In addition, obesity is a poor prognostic factor in acute pancreatitis, and overweight before disease onset appears to be a risk factor for chronic pancreatitis. Overweight and/or obesity are associated with greater risk of pancreatic cancer and younger age of onset. Physical activity appears to decrease the risk of pancreatic cancer, especially among those who are overweight. Long-standing diabetes increases the risk of pancreatic cancer. The pathogenic mechanism is that obesity and physical inactivity increase insulin resistance. In a state of hypersinulinemia, increased circulating level of insulin-like growth factor-1 induces cellular proliferation of pancreatic cancer. Obesity is associated with negative prognostic factor and increased mortality in pancreatic cancer. However, there are controversies regarding the effects of obesity on long-term post-operative results in the patient with pancreatic cancer.

Figures and Tables

Fig. 1
Hypothetical concept of the role of adipose tissue in acute pancreatitis (modified from Fig. 2 of reference 16). Peripancreatic and pancreatic necrosis in acute pancreatitis cause a release of highly active cytokines and adipokines from adipose tissue. Released cytokines and adipokines are responsible to multiorgan failure, insulin resistance, and metabolic alteration, which determine the morbidity and mortality of acute pancreatitis. IL-1, interleukin-1; IL-6, interleukin-6; TNF, tumor necrosis factor.
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Fig. 2
The influence of obesity and inactive activity to pancreatic cancer (modified from Fig. 1 of reference 22). Obesity, inactive physical activity and abdominal adiposity increase the secretion of insulin through insulin resistance. Hyperinsulinemia and decreased insulin- like growth factor binding protein-1 (IGFBP-1) induces the secretion of insulin-like growth factor-1 (IGF-1), which stimulates proliferation of pancreatic cancer cells.
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Notes

Financial support: None.

Conflict of interest: None.

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