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Related Concept Videos

Dipeptidyl Peptidase 4 Inhibitors01:23

Dipeptidyl Peptidase 4 Inhibitors

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Dipeptidyl peptidase 4 (DPP-4) is a serine protease widely distributed in the body. It's involved in the inactivation of GLP-1 and GIP hormones, which are crucial for insulin regulation. DPP-4 inhibitors, such as sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina), and vildagliptin (Galvus), help increase the proportion of active GLP-1, enhancing insulin secretion. These inhibitors work by competitively binding to DPP-4. This binding causes a...
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Glucagon-like Receptor Agonists01:24

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Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by...
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Insulin: Biosynthesis, Chemistry, and Preparation01:25

Insulin: Biosynthesis, Chemistry, and Preparation

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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.
Damage or functional impairment of β-cells inhibits insulin production, leading to diabetes. Diabetes treatment...
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Targeting PAD4: A Promising Strategy to Combat β-Cell Loss in Type 1 Diabetes.

Hsu Lin Kang1, András Szász1, Zsuzsanna Valkusz2

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Peptidylarginine deiminase 4 (PAD4) drives type 1 diabetes mellitus (T1DM) pathogenesis through neutrophil extracellular trap (NET) formation. Inhibiting PAD4 with Cl-amidine reduced NETosis, offering a potential therapeutic strategy for T1DM.

Keywords:
PAD4STZWistar rat

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Area of Science:

  • Biochemistry
  • Immunology
  • Endocrinology

Background:

  • Peptidylarginine deiminase 4 (PAD4) catalyzes protein citrullination, a process linked to type 1 diabetes mellitus (T1DM).
  • Understanding PAD4's role in pancreatic inflammation is crucial for T1DM research.

Purpose of the Study:

  • To investigate PAD4 expression and activity in a streptozotocin (STZ)-induced rat model of T1DM.
  • To evaluate the therapeutic potential of a PAD4 inhibitor, Cl-amidine, in mitigating T1DM-associated pancreatic inflammation.

Main Methods:

  • Assessed PAD4 mRNA and protein levels, citrullinated histone H3 (CitH3), calcium, and neutrophil elastase activity in STZ-induced diabetic Wistar rats.
  • Administered Cl-amidine, a pan-PAD inhibitor, to a subset of diabetic rats.
  • Compared findings between diabetic, non-diabetic, and treated groups.

Main Results:

  • Diabetic rats showed elevated PAD4 expression, CitH3 levels, and NETosis markers compared to controls.
  • Pancreatic calcium levels were reduced in diabetic rats, suggesting calcium consumption during PAD4 activation.
  • Cl-amidine treatment effectively attenuated NETosis in diabetic rats.

Conclusions:

  • PAD4 activation and subsequent NETosis are implicated in the pathogenesis of T1DM.
  • STZ-induced diabetic rats serve as a valuable model for studying PAD4's role in T1DM.
  • Cl-amidine demonstrates therapeutic promise for reducing pancreatic inflammation in T1DM.