| [ Summary ] |
Recent advances in the understanding of obesity reveal that obesity can directly or indirectly be a risk factor for the pathogenesis and pathophysiology of a wide range of digestive organs including the pancreas. Previous studies have shown a higher incidence of acute pancreatitis, development of more severe clinical conditions, and a higher incidence of pancreatic cancer in obese patients. Fat tissue is now recognized as an endocrine organ for its capacity to produce and secrete various humoral factors named adipocytokines. In obese patients, anti‒inflammatory cytokines called adiponectins show decreased production and secretion whereas leptin, a well‒known pro‒inflammatory adipocytokine, is excessively produced and secreted, thus causing a sustained local and/or systemic inflammatory condition in the body. Increased fat tissue, especially visceral fat, is known to correlate with the severity of acute pancreatitis and the risk of pancreatic cancer. This chapter discusses the clinical evidence for the influence of obesity on the pathogenesis and clinical course of pancreatic diseases and the molecular mechanisms which link the two pathological conditions. |