Risk of Diabetes Mellitus after First-Attack Acute Pancreatitis: A National Population-Based Study

Shen, Hsiu-Nien; Yang, Chengxu; Chang, Ya Hui; Lu, Chin-Li; Li, Chung‐Yi

doi:10.1038/ajg.2015.356

Cited by 106 publications

(99 citation statements)

References 35 publications

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“…An example of the translational importance of the latter is highlighted by the recent recognition that pancreatic islet β-cell failure may be seen as a late complication in 20%–30% of acute pancreatitis 77 . Differences in the microbiota, metabolism, diet, and regulation of inflammation can be substantial between human beings and rodents and affect disease mechanisms and phenotypes.…”

Section: General Mechanisms Values and Limitations Of Models And Stmentioning

confidence: 99%

Do Animal Models of Acute Pancreatitis Reproduce Human Disease?

Gorelick

Lerch

2017

Cellular and Molecular Gastroenterology and Hepatology

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Acute pancreatitis is currently the most common cause of hospital admission among all nonmalignant gastrointestinal diseases. To understand the pathophysiology of the disease and as a potential step toward developing targeted therapies, attempts to induce the disease experimentally began more than 100 years ago. Recent decades have seen progress in developing new experimental pancreatitis models as well as elucidating many underlying cell biological and pathophysiological disease mechanisms. Some models have been developed to reflect specific causes of acute pancreatitis in human beings. However, the paucity of data relating to the molecular mechanisms of human disease, the likelihood that multiple genetic and environmental factors affect the risk of disease development and its severity, and the limited information regarding the natural history of disease in human beings make it difficult to evaluate the value of disease models. Here, we provide an overview of key models and discuss our views on their strengths for characterizing cell biological disease mechanisms or for identifying potential therapeutic targets. We also acknowledge their limitations.

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Section: General Mechanisms Values and Limitations Of Models And Stmentioning

confidence: 99%

Do Animal Models of Acute Pancreatitis Reproduce Human Disease?

Gorelick

Lerch

2017

Cellular and Molecular Gastroenterology and Hepatology

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Section: Msmentioning

confidence: 99%

“…A recent comprehensive systematic review and meta-analysis of prospective clinical studies (11) showed that abnormal glucose metabolism (AGM) after an episode of AP is present in nearly 40% of patients without history of DM. Moreover, a large population-based study showed that patients after AP have a 2.5 times higher risk of developing newly diagnosed DM than individuals in the general population (32). Surveillance of high-risk patients with AP for prediabetes or diabetes would appear advisable (11,32).…”

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confidence: 99%

“…Moreover, a large population-based study showed that patients after AP have a 2.5 times higher risk of developing newly diagnosed DM than individuals in the general population (32). Surveillance of high-risk patients with AP for prediabetes or diabetes would appear advisable (11,32).The pathophysiology of DM after AP has been poorly investigated, and the present evidential base is largely extrapolated from studies of glucose homeostasis in patients with other major pancreatic diseases, such as chronic pancreatitis (CP) and pancreatic cancer (28a, 31a). Previous studies, most of which date back to the 1980s to 1990s, have suggested that the critical event in DM after CP and pancreatic cancer is insulin resistance (IR) and that it is related to pancreatic hormone abnormalities of not just insulin but also of glucagon and pancreatic polypeptide (4,14).…”

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confidence: 99%

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Relationship between pancreatic hormones and glucose metabolism: A cross-sectional study in patients after acute pancreatitis

Pendharkar

Asrani

Xiao

et al. 2016

American Journal of Physiology-Gastrointestinal and Liver Physi

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MS.Relationship between pancreatic hormones and glucose metabolism: A cross-sectional study in patients after acute pancreatitis. Am J Physiol Gastrointest Liver Physiol 311: G50 -G58, 2016. First published May 12, 2016 doi:10.1152/ajpgi.00074.2016.-Abnormal glucose metabolism is present in almost 40% of patients after acute pancreatitis, but its pathophysiology has been poorly investigated. Pancreatic hormone derangements have been sparingly studied to date, and their relationship with abnormal glucose metabolism is largely unknown. The aim was to investigate the associations between pancreatic hormones and glucose metabolism after acute pancreatitis, including the effect of potential confounders. This was a cross-sectional study of 83 adult patients after acute pancreatitis. Fasting venous blood was collected from all patients and used for analysis of insulin, glucagon, pancreatic polypeptide, amylin, somatostatin, C-peptide, glucose, and hemoglobin A1c. Statistical analyses were conducted using the modified Poisson regression, multivariable linear regression, and Spearman's correlation. Age, sex, body mass index, recurrence of acute pancreatitis, duration from first attack, severity, and etiology were adjusted for. Increased insulin was significantly associated with abnormal glucose metabolism after acute pancreatitis, in both unadjusted (P ϭ 0.038) and adjusted (P ϭ 0.001) analyses. Patients with abnormal glucose metabolism also had significantly decreased pancreatic polypeptide (P ϭ 0.001) and increased amylin (P ϭ 0.047) in adjusted analyses. Somatostatin, C-peptide, and glucagon were not changed significantly in both unadjusted and adjusted analyses. Increased insulin resistance and reduced insulin clearance may be important components of hyperinsulinemic compensation in patients after acute pancreatitis. Increased amylin and reduced pancreatic polypeptide fasting levels characterize impaired glucose homeostasis. Clinical studies investigating islet-cell hormonal responses to mixed-nutrient meal testing and euglycemichyperinsulinemic clamps are now warranted for further insights into the role of pancreatic hormones in glucose metabolism derangements secondary to pancreatic diseases. acute pancreatitis; glucose metabolism; insulin; amylin; pancreatic polypeptide THE PANCREAS, A DUAL GLAND with both endocrine and exocrine functions, plays a key role in the development of both diabetes and pancreatitis. Diabetes mellitus (DM) is one of the most prevalent chronic diseases and contributes significantly to allcause worldwide mortality, with one in 12 adult deaths attributed to it (15a, 16). Acute pancreatitis (AP) is the most common cause of gastrointestinal-related hospitalizations in the Western countries, with over 270,000 patients requiring hospitalization each year in the United States alone (19). A recent comprehensive systematic review and meta-analysis of prospective clinical studies (11) showed that abnormal glucose metabolism (AGM) after an episode of AP is present in nearly 40% of patients without h...

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“…While its statistics were, until recently, largely confined to chronic pancreatitis and pancreatic cancer (3,4), emerging large scale population-based studies show that more than 60% of all cases of diabetes of the exocrine pancreas are due to new-onset diabetes after acute pancreatitis (NODAP) (5)(6)(7), and that the risk of NODAP may not depend on severity of acute pancreatitis (8,9). However, the molecular mechanisms underlying the pathophysiology of NODAP remain unclear.…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2017

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Background: Calcitonin gene-related peptide (CGRP), a ubiquitous neuropeptide, plays a diverse and intricate role in chronic low-grade inflammation, including conditions such as obesity, type 2 diabetes, and diabetes of the exocrine pancreas. Diabetes of exocrine pancreas is characterised by chronic hyperglycemia and is associated with persistent low-grade inflammation and altered secretion of certain pancreatic and gut hormones. While CGRP may regulate glucose homeostasis and the secretion of pancreatic and gut hormones, its role in chronic hyperglycemia after acute pancreatitis (CHAP) is not known. The aim of this study was to investigate the association between CGRP and CHAP.Methods: Fasting blood samples were collected to measure insulin, HbA1c, CGRP, amylin, C-peptide, glucagon, pancreatic polypeptide (PP), somatostatin, gastric inhibitory peptide, glicentin, glucagon-like peptide-1 and 2, and oxyntomodulin. Modified Poisson regression analysis and linear regression analyses were conducted. Five statistical models were used to adjust for demographic, metabolic, and pancreatitisrelated risk factors.Results: A total of 83 patients were recruited. CGRP was significantly associated with CHAP in all five models (P-trend <0.005). Further, it was significantly associated with oxyntomodulin (P<0.005) and glucagon (P<0.030). Oxyntomodulin and glucagon independently contributed 9.7% and 7%, respectively, to circulating CGRP variance. Other pancreatic and gut hormones were not significantly associated with CGRP.Conclusions: CGRP is involved in regulation of blood glucose in individuals after acute pancreatitis. This may have translational implications in prevention and treatment of diabetes of the exocrine pancreas.

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Risk of Diabetes Mellitus after First-Attack Acute Pancreatitis: A National Population-Based Study

Cited by 106 publications

References 35 publications

Do Animal Models of Acute Pancreatitis Reproduce Human Disease?

Do Animal Models of Acute Pancreatitis Reproduce Human Disease?

Relationship between pancreatic hormones and glucose metabolism: A cross-sectional study in patients after acute pancreatitis

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

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