Associations between circulating levels of adipocytokines and abdominal adiposity in patients after acute pancreatitis

Abstract

Adipocytokines are strongly associated with abdominal adiposity during the course of acute pancreatitis (AP). This study investigated associations between a panel of adipocytokines and abdominal adiposity in AP patients after hospital discharge, as well as the effect of several covariates. Fasting venous blood samples were collected to measure adiponectin, interleukin 6, leptin, monocyte chemoattractant protein 1, tumour necrosis factor α (TNFα), resistin, and retinol-binding protein 4. Waist circumference (WC), waist-hip ratio, and waist-height ratio (WheightR) were used as measures of abdominal adiposity. Generalised linear models were built, adjusting for age, sex, ethnicity, diabetes status, aetiology, duration since admission for AP, recurrence, and severity of AP. A total of 93 patients were studied, on average at 22 months after AP. Interleukin 6, TNFα, and leptin were significantly associated with WC in both the unadjusted and all the three adjusted models. Also, they were significantly associated with WheightR in both the unadjusted and the three adjusted models. Other studied adipocytokines did not show a consistent association or were not significantly associated with the abdominal adiposity indices. The results suggest that excess abdominal adiposity favours pro-inflammatory milieu in AP patients after hospital discharge, independent of diabetes and effect of other covariates.

Comprehensive analysis of body composition and insulin traits associated with intra‐pancreatic fat deposition in healthy individuals and people with new‐onset prediabetes/diabetes after acute pancreatitis

“…Specifically, IFD exacerbates the inflammatory responses in AP, worsening its clinical course . It is now increasingly recognized that inflammation of the pancreas is not completely reversible and that chronic low‐grade inflammation persists in many individuals after AP . At least two out of five individuals develop new‐onset prediabetes and diabetes after AP (NODAP) .…”

“…At least two out of five individuals develop new‐onset prediabetes and diabetes after AP (NODAP) . Moreover, excess abdominal adiposity also contributes to low‐grade inflammation after AP . However, to the best of our knowledge, no study has investigated comprehensively the associations between IFD and body composition as well as indices of insulin secretion, indices of insulin sensitivity, incretins and related peptides in individuals with prediabetes and diabetes.…”

“…5 It is now increasingly recognized that inflammation of the pancreas is not completely reversible and that chronic low-grade inflammation persists in many individuals after AP. [6][7][8] At least two out of five individuals develop new-onset prediabetes and diabetes after AP (NODAP). 9 Moreover, excess abdominal adiposity also contributes to low-grade inflammation after AP.…”

“…9 Moreover, excess abdominal adiposity also contributes to low-grade inflammation after AP. 7,10 However, to the best of our knowledge, no study has investigated comprehensively the associations between IFD and body composition as well as indices of insulin secretion, indices of insulin sensitivity, incretins and related peptides in individuals with prediabetes and diabetes. The aim of the present study was to investigate body composition and insulin traits as biomarkers of IFD in NODAP and healthy individuals.…”

Calcitonin gene-related peptide: neuroendocrine communication between the pancreas, gut, and brain in regulation of blood glucose

“…Human adipose tissue depots have been identified as a major site of pro-calcitonin mRNA with recent studies reporting calcitonin secretion from adipocytes in obese individuals with associated insulin resistance (15,16). Increasing body of evidence shows that abdominal adiposity is also involved in metabolic dysregulations following an episode of acute pancreatitis (17)(18)(19). Further, elevated amylin levels have been reported in patients with chronic alcoholic pancreatitis and abnormal glucose metabolism (13), with similar findings reported in a study involving patients with acute pancreatitis that found a significant correlation between amylin and abnormal glucose metabolism (20,21).…”