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Related Concept Videos

Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular uptake of...
Type II Diabetes II: Pathophysiology01:24

Type II Diabetes II: Pathophysiology

PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.
Dipeptidyl Peptidase 4 Inhibitors01:23

Dipeptidyl Peptidase 4 Inhibitors

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 significant...
Glucagon-like Receptor Agonists01:24

Glucagon-like Receptor Agonists

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 the...
Pathophysiology of Diabetes01:20

Pathophysiology of Diabetes

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.
Type 1 diabetes is characterized by autoimmune-mediated destruction of pancreatic β cells, with environmental factors potentially triggering this process in genetically susceptible individuals. Despite many not having a family history, certain genes increase susceptibility, suggesting a...
Nitric Oxide Signaling Pathway01:28

Nitric Oxide Signaling Pathway

Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure to...

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En Face Detection of Nitric Oxide and Superoxide in Endothelial Layer of Intact Arteries
08:58

En Face Detection of Nitric Oxide and Superoxide in Endothelial Layer of Intact Arteries

Published on: February 25, 2016

Inducible nitric oxide synthase-mediated decrease of intestinal P-glycoprotein expression under

Ayaka Nawa1, Wakako Fujita Hamabe, Shogo Tokuyama

  • 1Department of Clinical Pharmacy, Kobe Gakuin University Faculty of Pharmaceutical Sciences, 1-1-3 Minatojima, Chuo-ku, Kobe 650-8586, Japan.

Life Sciences
|January 26, 2010
PubMed
Summary

Diabetes reduces intestinal P-glycoprotein (P-gp) expression and function. This reduction is linked to increased nitric oxide (NO) production in the ileum, suggesting a novel mechanism in diabetic drug absorption.

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Area of Science:

  • Pharmacology
  • Gastroenterology
  • Endocrinology

Background:

  • P-glycoprotein (P-gp) is a key drug-efflux pump affected by pathological conditions.
  • Hyperglycemia may alter P-gp levels in the blood-brain barrier and kidneys, but intestinal effects are unclear.

Purpose of the Study:

  • To investigate changes in intestinal P-gp expression and function during diabetes development.
  • To elucidate the underlying mechanisms of these alterations.

Main Methods:

  • Type 1 diabetes induced in mice using streptozotocin (STZ).
  • Ileal P-gp expression analyzed by Western blot.
  • Ileal P-gp function assessed using an in situ closed loop method.

Main Results:

  • STZ administration significantly reduced ileal P-gp expression by day 9.
  • Ileal P-gp function decreased on days 3 and 9 post-STZ.
  • Increased nitric oxide synthase (NOS) activity observed on day 9.
  • NOS inhibition (L-NAME or aminoguanidine) prevented the reduction in P-gp expression.

Conclusions:

  • Increased nitric oxide (NO) production, likely via inducible NOS (iNOS), contributes to reduced ileal P-gp expression in STZ-induced diabetes.
  • This suggests a novel mechanism impacting intestinal drug transport in diabetic conditions.