Keywords [eng] |
Keywords: Acute pancreatitis, inflammation, hypertriglyceridemia, trypsinogen, calcium, necrosis, monocytes, mitochondria, tissue damage, necrotizing pancreatitis, diabetes, prediabetes, metabolic syndrome, insulin resistance, high blood pressure, hypertriglyceridemia, HDL levels, obesity, hyperglycaemia, lipopolysaccharides. |
Abstract [eng] |
Abstract: Both the acute pancreatitis and the metabolic syndrome are currently not only of global importance, but indeed their incidence is increasing world-wide; interestingly this development is taking place parallel for both. In addition to this the therapeutic access to both diseases turns out to be difficult due to many things we do not yet know about as to the exact pathophysiological mechanisms. However, important details have been detected about principal mechanisms running their course like the calcium dysregulation with its fatal consequence of destructing the mitochondrial power in acute pancreatitis or the dysregulation largely - but not only - concerning the three main substance classes of carbohydrates, proteins, and lipids, all this happening via abundance of food plus lack of physical exercise in metabolic syndrome. The immensely high costs for the health systems in all countries concerned with acute pancreatitis and the metabolic syndrome as well as the status of inflammation plus the role of the microbiome as important players in both diseases and furthermore the suspicion that metabolic syndrome worsens the severity of the course of the acute pancreatitis suggest the necessity to put effort into their common research. The findings then may serve as a starting point for both further research and therapeutical access. |