Glucose Counter-regulation After Acute Pancreatitis. Issue 5 (May 2019)

• Record Type: Journal Article
• Authors: Bharmal, Sakina H.; Pendharkar, Sayali; Singh, Ruma G.; Cho, Jaelim; Petrov, Maxim S.
• Is Part Of: Pancreas. Volume 48:Issue 5(2019)
• Publication Date: 2019-05
• Subjects: acute pancreatitis -- counter-regulatory hormones -- diabetes -- gut peptides -- proinflammatory cytokines; Pancreas -- Diseases -- Periodicals; Pancreas -- Periodicals; Neuroendocrine tumors -- Periodicals; 616.37005
• DOI: 10.1097/MPA.0000000000001318
• Languages: English
• ISSNs: 0885-3177

Abstract

Abstract : Objectives: Persistent hyperglycemia is a common sequela of acute pancreatitis (AP). The role of counter-regulatory hormones in maintaining glucose homeostasis has been largely studied during the course of AP, but not after clinical resolution of the disease. The objectives of this study were to investigate the associations between circulating levels of glucagon, cortisol, and human growth hormone and glucose homeostasis after AP as well as their associations with a comprehensive panel of pancreatic hormones, gut peptides, and proinflammatory cytokines. Methods: Participants with no history of pre-existing prediabetes or diabetes were categorized into hyperglycemia and normoglycemia after AP groups. Binary logistic regression and linear regression analyses were conducted. Results: Eighty-three individuals were included, of whom 19 had hyperglycemia. Glucagon, cortisol, and human growth hormone did not differ significantly between the groups. Glucagon explained up to 86% of the variance in glucagon-like peptide 1, whereas cortisol explained up to 89% of the variance in interleukin 6 in hyperglycemia after AP. Conclusions: Counter-regulatory hormones do not appear to play a direct role in the mechanisms underlying hyperglycemia after AP. However, significant associations between glucagon and glucagon-like peptide 1, as well as between cortisol and interleukin 6, suggest that that these hormones may be involved indirectly in the pathophysiology of hyperglycemia after AP. Abstract : Supplemental digital content is available in the text.