Abstract
Both type 2 prediabetes/diabetes (T2DM) and new-onset prediabetes/diabetes after acute pancreatitis (NODAP) are characterized by impaired tissue sensitivity to insulin action. Although the outcomes of NODAP and T2DM are different, it is unknown whether drivers of insulin resistance are different in the two types of diabetes. This study aimed to investigate the associations between abdominal fat phenotypes and indices of insulin sensitivity in non-obese individuals with NODAP, T2DM, and healthy controls. Indices of insulin sensitivity (homeostasis model assessment of insulin sensitivity (HOMA-IS), Raynaud index, triglyceride and glucose (TyG) index, Matsuda index) were calculated in fasting and postprandial states. Fat phenotypes (intra-pancreatic fat, intra-hepatic fat, skeletal muscle fat, visceral fat, and subcutaneous fat) were determined using magnetic resonance imaging and spectroscopy. Linear regression and relative importance analyses were conducted. Age, sex, and glycated hemoglobin A1c were adjusted for. A total of 78 non-obese individuals (26 NODAP, 20 T2DM, and 32 healthy controls) were included. Intra-pancreatic fat was significantly associated with all the indices of insulin sensitivity in the NODAP group, consistently in both the unadjusted and adjusted models. Intra-pancreatic fat was not significantly associated with any index of insulin sensitivity in the T2DM and healthy controls groups. The variance in HOMA-IS was explained the most by intra-pancreatic fat (R2 = 29%) in the NODAP group and by visceral fat (R2 = 21%) in the T2DM group. The variance in the Raynaud index was explained the most by intra-pancreatic fat (R2 = 18%) in the NODAP group and by visceral fat (R2 = 15%) in the T2DM group. The variance in the TyG index was explained the most by visceral fat in both the NODAP group (R2 = 49%) and in the T2DM group (R2 = 25%). The variance in the Matsuda index was explained the most by intra-pancreatic fat (R2 = 48%) in the NODAP group and by visceral fat (R2 = 38%) in the T2DM group. The differing association between intra-pancreatic fat and insulin resistance can be used to differentiate NODAP from T2DM. Insulin resistance in NODAP appears to be predominantly driven by increased intra-pancreatic fat deposition.
Highlights
Acute pancreatitis (AP) is an inflammatory process in the pancreas that may remain localized, spread to nearby tissues, or lead to systemic inflammation
A long-established pathophysiological state linked to a spectrum of metabolic disorders, has mainly been investigated in populations with general obesity, and studies focusing on abdominal obesity have emerged only recently
The key finding is that IPFD was significantly associated with all the studied indices of insulin sensitivity in individuals with new-onset prediabetes or diabetes after AP (NODAP), consistently in both the unadjusted model and adjusted models
Summary
Acute pancreatitis (AP) is an inflammatory process in the pancreas that may remain localized, spread to nearby tissues, or lead to systemic inflammation. A 2020 case-control study (as part of the MENSA project) showed that both fasting and postprandial levels of oxyntomodulin—a gut hormone involved in the regulation of exocrine pancreatic function—were significantly lower in NODAP than T2DM [8]. There are several lines of epidemiological evidence that showed that outcomes of NODAP and T2DM are different. These include the risks of poor glycemic control [9], pancreatic cancer [10], mortality [11], and the risk–benefit ratio of common antidiabetic medications [12,13]. A thorough understanding of the mechanisms behind impaired glucose metabolism in patients after AP is critical with a view to improving clinical management and identifying potential novel targets for prevention and treatment
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