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Related Concept Videos

Diabetes Mellitus: Overview and Type I Subtype01:22

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Diabetes mellitus is a chronic metabolic disorder characterized by high blood glucose levels due to inadequate insulin production, insulin resistance, or both. The condition affects millions worldwide and can significantly impact their health and quality of life.
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Pathophysiology of Diabetes01:20

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Diabetes mellitus is a chronic metabolic disorder characterized by hyperglycemia. The four categories of diabetes are type 1 diabetes, type 2 diabetes, other specific types of diabetes, and gestational diabetes.
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Carbohydrates are polymers composed of molecules containing atoms of carbon, hydrogen and oxygen. One gram of carbohydrate can provide four kilo-calories of energy, which makes it the most efficient instant energy source.
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Type 2 diabetes, characterized by insulin resistance, arises when the insulin receptors on cells lose responsiveness to insulin, diminishing the cell's capacity to take up glucose, resulting in elevated blood glucose levels. To receive a diagnosis of Type 2 diabetes, a series of blood glucose tests are necessary to assess whether the blood glucose falls within normal parameters. If the result is out of the normal range, a patient may be diagnosed as prediabetic or diabetic, depending on the...
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The endoplasmic reticulum (ER) of pancreatic β-cells synthesizes preproinsulin, which consists of a signal peptide, A and B chains, and a C-peptide. Preproinsulin is then cleaved and folded into proinsulin, which translocates to the Golgi apparatus for sorting and packaging into secretory granules. In these granules, enzymatic clipping generates insulin and C-peptide.
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For most patients, experiencing several weeks of polyuria, polydipsia, fatigue, and significant weight loss may indicate the presence of diabetes. Furthermore, adults displaying the phenotypic appearance of type 2 diabetes (particularly those who are obese and not initially insulin-requiring), may have islet cell autoantibodies, suggesting autoimmune-mediated β cell destruction and a diagnosis of latent autoimmune diabetes of adults (LADA). The categorization of glucose homeostasis is...
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Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice
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Understanding type 1 diabetes through proteomics.

Inne Crèvecoeur1, Saurabh Vig1, Chantal Mathieu1

  • 1a Laboratory for Clinical and Experimental Endocrinology , KU Leuven , Leuven , Belgium.

Expert Review of Proteomics
|June 27, 2017
PubMed
Summary
This summary is machine-generated.

Proteomics reveals how the body attacks its own pancreatic beta-cells, causing type 1 diabetes (T1D). Understanding these mechanisms, including neo-antigen generation, is key to T1D pathogenesis and finding new biomarkers.

Keywords:
Type 1 diabetesautoantigenbeta-cellsbiomarkerisletspost translational modifications​​​

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Extraction of Tissue Antigens for Functional Assays
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Area of Science:

  • * Endocrinology and Immunology
  • * Molecular Biology and Proteomics

Background:

  • * Autoimmunity against pancreatic beta-cells causes insulin deficiency, leading to hyperglycemia and type 1 diabetes (T1D).
  • * Understanding beta-cell dysfunction and death is crucial for T1D research.

Purpose of the Study:

  • * To review proteomic discoveries shedding light on the beta-cell's role in T1D pathogenesis.
  • * To highlight how advanced proteomic techniques enhance insights into T1D mechanisms.

Main Methods:

  • * Utilized proteomic approaches like 2D-DIGE and MALDI imaging.
  • * Employed advanced sample preparation: laser capture microdissection and immunopeptidomics.
  • * Analyzed proteomic data from beta-cell lines, isolated islets (animal and human).

Main Results:

  • * Identified intracellular signaling pathways involved in beta-cell destruction.
  • * Discovered the generation of neo-antigens via post-translational modifications of beta-cell antigens.
  • * Found potential biomarkers for T1D disease progression.

Conclusions:

  • * Proteomics has uncovered beta-cell neo-autoantigen generation mechanisms (post-translational modifications, hybrid insulin peptides, defective ribosomal products).
  • * These findings revolutionize T1D pathogenesis understanding, emphasizing the beta-cell's role in its own destruction.