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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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Peripheral Artery Disease I: Introduction01:30

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Peripheral artery disease (PAD) predominantly results from atherosclerosis, which involves the accumulation of fatty deposits, or plaques, within the walls of arteries. This causes them to narrow and harden, significantly reducing blood flow. PAD predominantly affects the legs, particularly the arteries supplying the thighs and calves. In rare cases, it may involve other arteries, including those in the arms.Etiology of PAD:The principal cause of PAD is atherosclerosis, which results from fatty...
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Insulin: The Receptor and Signaling Pathways01:28

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Insulin action is mediated through a receptor tyrosine kinase, akin to the IGF-1 receptor. The number of receptors per cell varies significantly, from 40 on erythrocytes to 300,000 on adipocytes and hepatocytes. The insulin receptor consists of linked α/β subunit dimers, forming a heterotetramer glycoprotein with two extracellular α subunits and two β subunits spanning the membrane. The α subunits inhibit the inherent tyrosine kinase activity of the β subunits, but...
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Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

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The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
Insulin and C-peptide are...
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Insulin Secretory Vesicles01:05

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Insulin secretory vesicles release insulin to stimulate blood glucose uptake and regulate carbohydrate metabolism. When the blood glucose levels increase, glucose enters the pancreatic β-islet cells through glucose transporters. Once inside, glucose is metabolized through glycolysis, the citric acid cycle, and the electron transport chain, producing ATP. This increase in ATP concentration closes ATP-sensitive potassium channels, leading to depolarization of the membrane and the opening of...
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Pathophysiology of Diabetes01:20

Pathophysiology of Diabetes

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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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Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance
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DPP4 Activity, Hyperinsulinemia, and Atherosclerosis.

Kaitlin M Love1, Zhenqi Liu1

  • 1Division of Endocrinology and Metabolism, Department of Medicine, University of Virginia Health System, Charlottesville, VA, USA.

The Journal of Clinical Endocrinology and Metabolism
|February 11, 2021
PubMed
Summary
This summary is machine-generated.

Dipeptidyl peptidase-4 (DPP4) links obesity and insulin resistance to atherosclerosis. While DPP4 inhibition shows promise in preclinical models, its cardiovascular benefits in type 2 diabetes require further investigation.

Keywords:
DPP4atherosclerosisdiabeteshyperinsulinemiainsulin resistanceoxidative stress

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Area of Science:

  • Endocrinology
  • Cardiovascular Science
  • Metabolic Disease

Background:

  • Obesity and type 2 diabetes are linked to hyperinsulinemia, elevated dipeptidyl peptidase-4 (DPP4), and atherosclerosis.
  • Hyperinsulinemia promotes vascular inflammation, smooth muscle cell growth, dyslipidemia, and hypertension, contributing to atherosclerosis.

Purpose of the Study:

  • To investigate the role of DPP4 in linking insulin resistance and atherosclerosis.
  • To review preclinical and clinical evidence on DPP4 inhibition for cardiovascular outcomes.

Main Methods:

  • Literature review of PubMed searches using terms related to insulin, atherosclerosis, hyperinsulinemia, cardiovascular outcomes, and DPP4.
  • Analysis of preclinical studies (rodent models) and clinical trials involving DPP4 inhibitors.

Main Results:

  • DPP4 activity is elevated in obesity and mirrors atherogenic effects of hyperinsulinemia.
  • Genetic DPP4 deletion protects rodents from insulin resistance and improves cardiovascular outcomes.
  • DPP4 inhibition reduces inflammation, oxidative stress, and atherosclerosis in preclinical models, with some positive effects on endothelial function and arterial stiffness in small clinical studies.

Conclusions:

  • DPP4 may be a critical link between obesity, insulin resistance, and atherosclerosis.
  • Discrepancies between preclinical and clinical findings on cardiovascular outcomes warrant further research into DPP4 function and inhibition.