Evaluation of Biochemical Markers  Serum Amylase and Serum Lipase for  the Assessment of Pancreatic Exocrine  Function in Diabetes Mellitus

Madole, Mahesh Basavaraj; Iyer, C M; Madivalar, Mamatha Thimmanna; Wadde, Satish K; Howale, Deepak S.

doi:10.7860/jcdr/2016/23787.8900

Cited by 22 publications

(31 citation statements)

References 26 publications

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“…In a seminal report by Coppetiers et al, in situ HLA-tetramer staining revealed CD8 + T cells specific for islet antigens -insulin, IGRP and IA-2 -within insulitic lesions, though the persistence of β-cell mass and number of islet antigen-reactive T cell specificities varied across donors in accordance with disease duration [56]. Similarly, CD4 + T cells isolated from the islets of organ donors with recent-onset T1D exhibited reactivity to multiple GAD65 epitopes, as well as proinsulin [76][77][78][79][80][81][82][83][84][85][86][87][88][89][90] and IA-2 545-562 , measured by antigen-stimulated IFNγ secretion [57]. Moreover, islet-infiltrating CD4 + T cell clones, when reconstructed to express T cell receptors (TCRs) as transductants, have been identified to respond to proinsulin, C-peptide amino acids 19-35 (C:19-35), and insulin B:9-23 [48].…”

Section: Immunological Determinants Of Human T1dmentioning

confidence: 99%

“…result in the generation and presentation of neoantigens [67]. Indeed, T cells reactive to post-translationally modified proteins such as a citrullinated form of GRP78 292-305 and islet amyloid polypeptide (IAPP) [65][66][67][68][69][70][71][72][73][74][75][76][77][78][79][80][81][82][83][84] , as well as defective ribosomal insulin gene products (DRiPs) and peptides formed from the fusion of insulin C-peptide fragments with chromogranin A or IAPP (termed hybrid insulin peptides, HIPs) have been isolated from the islets of T1D donors [57,68]. Thus, β-cells may play a role in their own destruction through stress-induced protein processing defects, which may serve to induce a critical break in tolerance or to exacerbate existing pathology by expanding the β-cell antigenic repertoire.…”

Section: Immunology Of Diabetes Society Review Series: Insights Into mentioning

confidence: 99%

“…Deficits in exocrine pancreas mass and function have been identified in subjects with and at-risk for T1D. Indeed, reduced secretion of pancreatic enzymes, such as trypsinogen [82], amylase, and lipase [83], as well as a smaller pancreas organ as measured by weight or volume [40,41], are potentially reflective of exocrine damage accompanying T1D pathology. Increased complement deposition was also observed on the vascular endothelium and extracellular matrix (ECM) surrounding vessels and ducts within the exocrine pancreas tissue in T1D versus control donors [84], indicating localized inflammation.…”

Section: The Contributions Of Pancreas Architecture To T1d Pathologymentioning

confidence: 99%

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Islet–immune interactions in type 1 diabetes: the nexus of beta cell destruction

Peters

Posgai

2019

Clinical and Experimental Immunology

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Recent studies in Type 1 Diabetes (T1D) support an emerging model of disease pathogenesis that involves intrinsic β-cell fragility combined with defects in both innate and adaptive immune cell regulation. This combination of defects induces systematic changes leading to organ-level atrophy and dysfunction of both the endocrine and exocrine portions of the pancreas, ultimately culminating in insulin deficiency and β-cell destruction. In this review, we discuss the animal model data and human tissue studies that have informed our current understanding of the cross-talk that occurs between β-cells, the resident stroma, and immune cells that potentiate T1D. Specifically, we will review the cellular and molecular signatures emerging from studies on tissues derived from organ procurement programs, focusing on in situ defects occurring within the T1D islet microenvironment, many of which are not yet detectable by standard peripheral blood biomarkers. In addition to improved access to organ donor tissues, various methodological advances, including immune receptor repertoire sequencing and single-cell molecular profiling, are poised to improve our understanding of antigen-specific autoimmunity during disease development. Collectively, the knowledge gains from these studies at the islet-immune interface are enhancing our understanding of T1D heterogeneity, likely to be an essential component for instructing future efforts to develop targeted interventions to restore immune tolerance and preserve β-cell mass and function.

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Section: Immunological Determinants Of Human T1dmentioning

confidence: 99%

Section: Immunology Of Diabetes Society Review Series: Insights Into mentioning

confidence: 99%

Section: The Contributions Of Pancreas Architecture To T1d Pathologymentioning

confidence: 99%

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Islet–immune interactions in type 1 diabetes: the nexus of beta cell destruction

Peters

Posgai

2019

Clinical and Experimental Immunology

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“…Moreover, serum amylase activity is linked to the islet β cell function in type 2 diabetes patients . In fact, serum amylase has been regarded as a biochemical marker to assess pancreatic exocrine function in patients with diabetes mellitus …”

Section: Introductionmentioning

confidence: 99%

“…3 In fact, serum amylase has been regarded as a biochemical marker to assess pancreatic exocrine function in patients with diabetes mellitus. 4 The ABO blood type antigens (A, B, and H determinants) are glycoproteins presenting human blood types and are widely distributed on red blood cell surface and normal tissue throughout the body. 5 Several studies have found that inherited blood group antigens were associated with disease risk such as cardiovascular disease, thrombotic vascular disease and stroke.…”

Section: Introductionmentioning

confidence: 99%

Serum amylase activity altered by the ABO blood group system in Chinese subjects

Peng

Goyal

Lin

et al. 2019

Clinical Laboratory Analysis

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ObjectiveThe underlying interactions between ABO blood group antigens and pancreatic exocrine tissue have been demonstrated, and serum amylase was synthesized by pancreatic ductal cells. Thus, we investigated the link between ABO blood type and serum amylase activity in Chinese subjects.MethodsOur study included 343 relatively healthy Chinese individuals, and the data were retrieved from electronic medical record database.ResultsA increased trend was observed for serum amylase activity in ABO blood type distribution, and we found that serum amylase activity was remarkable increased in subjects with O blood type compared to those with non‐O blood type (P = 0.013). Logistic regression analysis indicated that serum amylase was independently associated with individuals with O blood group (adjusted odds ratio 1.574; 95% CI, 1.022‐2.425, P = 0.039).ConclusionsThe present evidence suggests a significant link between serum amylase activity and ABO blood type in the study population, indicating ABO blood type may be associated with the susceptibility of pancreatic disease.

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Exocrine pancreas function is impaired in adult relatives of patients with type 1 diabetes

et al. 2021

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Aims Alterations of the exocrine pancreas have been reported in type 1 diabetes, but their contribution to the pathogenesis of the disease is poorly understood. Here, we investigated markers of exocrine pancreas dysfunction in individuals at-risk of developing type 1 diabetes. Methods Serum P-amylase and lipase levels were assessed in samples obtained from healthy controls, patients with new onset type 1 diabetes, relatives participating to the TrialNet Pathway to Prevention who were, at blood collection, autoantibody negative or positive for a single autoantibody (low-risk individuals), and positive for multiple autoantibodies (high-risk individuals). Linear mixed models were adopted to estimate variation of pancreatic enzymes among the groups and to evaluate the influence of high-risk HLA genotypes and residual beta cell function on exocrine pancreas function. Results In adults, but not children, reduced levels of P-amylase and lipase were shown in at-risk individuals, including (for P-amylase levels only) those at low-risk, and in T1Dnew. Furthermore, while high-risk HLA genotypes negatively affected P-amylase levels in autoantibody negative adult individuals, fasting C-peptide levels did not correlate with pancreatic enzyme levels. Conclusions Exocrine pancreas dysfunction precedes the onset of type 1 diabetes in adult at-risk individuals and may be unrelated to fasting C-peptide levels.

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Evaluation of Biochemical Markers Serum Amylase and Serum Lipase for the Assessment of Pancreatic Exocrine Function in Diabetes Mellitus

Cited by 22 publications

References 26 publications

Islet–immune interactions in type 1 diabetes: the nexus of beta cell destruction

Islet–immune interactions in type 1 diabetes: the nexus of beta cell destruction

Serum amylase activity altered by the ABO blood group system in Chinese subjects

Exocrine pancreas function is impaired in adult relatives of patients with type 1 diabetes

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