title: Second Giessen International Workshop on Interactions of Exocrine and Endocrine Pancreatic Diseases. Castle of Rauischholzhausen of the Justus-Liebig-university, Giessen (Rauischholzhausen), Germany. March 7-8, 2008.
abstract: The 'Second Giessen International Workshop on Interactions of Exocrine and Endocrine Pancreatic Diseases' was organized in order to reflect and discuss recent developments in the field, especially the progress that has been achieved since the first meeting in March 2005. About thirty international specialists were invited to share their experience and thoughts covering the main topics of: A) pancreatic diabetes (type 3c); B) chronic inflammation of the pancreas. The presentations of session A covered an overview about the frequency of exocrine dysfunction in diabetes mellitus, the relation between diabetes, celiac disease and the exocrine pancreas, the prevalence of type 3c diabetes, damage to the pancreas caused by genes, the role of incretins in type 2 and type 3 diabetes, the role of exocrine tissue in beta cell homeostasis, peculiarities in the treatment of type 3c diabetes and a lecture on incretins: from concept to treatment. Session B included presentations about the frequency of chronic inflammation of the pancreas and therapeutical implications, the role of ACE in the pancreas, genomics and the metabolic hypothesis of chronic pancreatitis, nutritional aspects of pancreatic diseases, the stellate cell concept, autoimmunity, genetic background of chronic pancreatitis and the hypothesis of chronic obstruction induced by gallstone disease. The meeting resulted in several new projects that will be started by the participants in the near future.
authors.affiliation: Department of Surgery, Karolinska University Hospital, Huddige, Sweden. ake.andren.sandberg@mail.chsa.se
authors.forename: Ake
authors.initials: A
authors.lastname: Andren-Sandberg
authors.forename: Philip D
authors.initials: PD
authors.lastname: Hardt
mesh_terms: D000368:Aged; D000428:Alcohol Drinking / Q000009:adverse effects / Q000453:epidemiology; D002454:Cell Differentiation; D002908:Chronic Disease; D015897:Comorbidity; D019005:Cystic Fibrosis Transmembrane Conductance Regulator / Q000235:genetics; D003920:Diabetes Mellitus / Q000145:classification / Q000453:epidemiology / Q000503:physiopathology*; D004035:Diet Therapy; D005260:Female; D020022:Genetic Predisposition to Disease; D005858:Germany; D051539:Hepatocyte Nuclear Factor 1-beta / Q000235:genetics; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D054795:Incretins / Q000097:blood / Q000502:physiology; D007515:Islets of Langerhans / Q000503:physiopathology*; D007564:Japan / Q000453:epidemiology; D008049:Lipase / Q000235:genetics; D008297:Male; D008875:Middle Aged; D009154:Mutation; D018529:Nutritional Support; D046790:Pancreas, Exocrine / Q000503:physiopathology*; D010182:Pancreatic Diseases / Q000453:epidemiology / Q000503:physiopathology* / Q000628:therapy; D015995:Prevalence; D012084:Renin-Angiotensin System; D012307:Risk Factors; D014481:United States / Q000453:epidemiology
chemical_list: C496495:HNF1B protein, human; D007004:Hypoglycemic Agents; D054795:Incretins; D019005:Cystic Fibrosis Transmembrane Conductance Regulator; D051539:Hepatocyte Nuclear Factor 1-beta; C054621:CEL protein, human; D008049:Lipase