Special Issue "Drug Candidates for the Treatment of Metabolic Syndrome"

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Pharmacology".

Deadline for manuscript submissions: 31 January 2023 | Viewed by 502

Special Issue Editor

Dr. Seong-Hee Maria Ko
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Guest Editor
Department of Microbiology, College of Medicine, Gachon University, Incheon, Korea
Interests: lipid metabolism; metabolic disorder of post-menopausal women; free radical research; diabetes; obesity

Special Issue Information

Dear Colleagues, 

Metabolic syndrome is defined as a cluster of conditions characterized by impaired glucose metabolism, hypertension, central obesity, low LDL-C, and high triglyceride levels. It also promotes glucose intolerance and chronic systemic inflammatory conditions characterized by immune cell infiltration, and this immune system activation increases the risk of serious disease following viral infection. In addition, studies have been reported to increase diseases associated with various metabolic disorders, such as nonalcoholic fatty liver, psoriasis, and IBD. Metabolic disease tends to progress quietly and gradually rather than with acute symptoms. Due to the recent COVID-19 pandemic, increased processed food and salt intake, surplus energy accumulation, sedentary lifestyle, and reduced physical activity are thought to be risk factors for an increase in metabolic disease. Therefore, the discovery of drugs related to metabolic diseases and metabolic disorder has an important meaning in this difficult period. I hope that this Special Issue will provide an opportunity to help all patients and bring about the development of the scientific community. In order to do this, the cooperation of all our valuable colleagues, including yourself, is essential.

We are pleased to welcome papers reviewing the most recent research on this topic in the present thematic issue. 

We look forward to your contribution.

Dr. Seong-Hee Maria Ko
Guest Editor

Manuscript Submission Information

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Keywords

  • metabolic disorder
  • IBD
  • diabetes
  • hypertension
  • obesity

Published Papers (1 paper)

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Research

Article
Partial Synthetic PPARƳ Derivative Ameliorates Aorta Injury in Experimental Diabetic Rats Mediated by Activation of miR-126-5p Pi3k/AKT/PDK 1/mTOR Expression
Pharmaceuticals 2022, 15(10), 1175; https://doi.org/10.3390/ph15101175 - 22 Sep 2022
Viewed by 315
Abstract
Type 2 diabetes mellitus (T2D) is a world wild health care issue marked by insulin resistance, a risk factor for the metabolic disorder that exaggerates endothelial dysfunction, increasing the risk of cardiovascular complications. Peroxisome proliferator-activated receptor PPAR) agonists have therapeutically mitigated hyperlipidemia and [...] Read more.
Type 2 diabetes mellitus (T2D) is a world wild health care issue marked by insulin resistance, a risk factor for the metabolic disorder that exaggerates endothelial dysfunction, increasing the risk of cardiovascular complications. Peroxisome proliferator-activated receptor PPAR) agonists have therapeutically mitigated hyperlipidemia and hyperglycemia in T2D patients. Therefore, we aimed to experimentally investigate the efficacy of newly designed synthetic PPARα/Ƴ partial agonists on a High-Fat Diet (HFD)/streptozotocin (STZ)-induced T2D. Female Wistar rats (200 ± 25 g body weight) were divided into four groups. The experimental groups were fed the HFD for three consecutive weeks before STZ injection (45 mg/kg/i.p) to induce T2D. Standard reference PPARƳ agonist pioglitazone and the partial synthetic PPARƳ (PIO; 20 mg/kg/BW, orally) were administered orally for 2 weeks after 72 h of STZ injection. The aorta tissue was isolated for biological ELISA, qRT-PCR, and Western blotting investigations for vascular inflammatory endothelial mediators endothelin-1 (ET-1), intracellular adhesion molecule 1 (ICAM-1), E-selectin, and anti-inflammatory vasoactive intestinal polypeptide (VIP), as well as microRNA126-5p and p-AKT/p-Pi3k/p-PDK-1/p-mTOR, endothelial Nitric Oxide Synthase (eNOS) immunohistochemical staining all are coupled with and histopathological examination. Our results revealed that HFD/STZ-induced T2D increased fasting blood glucose, ET-1, ICAM-1, E-selectin, and VIP levels, while decreasing the expression of both microRNA126-5p and p-AKT/p-Pi3k/p-PDK-1/p-mTOR phosphorylation. In contrast, the partial synthetic PPARƳ derivative evidenced a vascular alteration significantly more than reference PIO via decreasing (ET-1), ICAM-1, E-selectin, and VIP, along with increased expression of microRNA126-5p and p-AKT/p-Pi3k/p-PDK-1/p-mTOR. In conclusion, the partial synthetic PPARƳ derivative significantly affected HFD/STZ-induced T2D with vascular complications in the rat aorta. Full article
(This article belongs to the Special Issue Drug Candidates for the Treatment of Metabolic Syndrome)
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