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Related Concept Videos

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...
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...
Insulin: The Receptor and Signaling Pathways01:28

Insulin: The Receptor and Signaling Pathways

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 this inhibition is released...
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.
Oral Hypoglycemic Agents: α-Glucosidase Inhibitors01:19

Oral Hypoglycemic Agents: α-Glucosidase Inhibitors

α-glucosidase inhibitors, including acarbose (Precose), miglitol (Glyset), and voglibose (Voglib) (primarily available in Asia), are drugs that control blood sugar levels by delaying the digestion of starch and disaccharides. They achieve this by inhibiting α-glucosidase enzymes in the intestine, which slow the absorption of carbohydrates in the intestine, which in turn leads to a prolonged release of the glucoregulatory hormone GLP-1 from intestinal L-cells.
Acarbose and miglitol are typically...

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Updated: Jun 21, 2026

Antagonistic Effect of Jiawei Shengjiang San on a Rat Model of Diabetic Nephropathy: Related to EGFR/MAPK3/1 Signaling Pathway
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Antagonistic Effect of Jiawei Shengjiang San on a Rat Model of Diabetic Nephropathy: Related to EGFR/MAPK3/1 Signaling Pathway

Published on: May 10, 2024

Ginsenoside Rd ameliorates glucose metabolism by regulating GLP-1/ MAPK/ NF-κB signaling pathway in db/db mice.

Wenbin Wu, Yujin Guo1,2, Qingsong Xia1,2

  • 1Tongji Hospital of Tongji Medical College of Huazhong University of Science and Technology Department of Hematology, Department of Integrated Traditional Chinese and Western Medicine, Hubei, China, Wuhan.

Planta Medica
|June 19, 2026
PubMed
Summary
This summary is machine-generated.

Ginsenoside Rd improves type 2 diabetes (T2DM) in mice by reducing inflammation and enhancing GLP-1 secretion. This study explores its mechanism involving the GLP-1/MAPK/NF-κB pathway.

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Last Updated: Jun 21, 2026

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Published on: May 10, 2024

Area of Science:

  • Pharmacology
  • Endocrinology
  • Molecular Biology

Background:

  • Ginsenoside Rd demonstrates therapeutic potential for type 2 diabetes mellitus (T2DM).
  • The precise molecular mechanisms underlying Ginsenoside Rd's effects on T2DM remain largely unelucidated.
  • This study investigates the role of inflammation in the pancreas and intestine in mediating Ginsenoside Rd's T2DM-ameliorating effects.

Purpose of the Study:

  • To elucidate the mechanism of action of Ginsenoside Rd in T2DM.
  • To investigate the modulation of the GLP-1/MAPK/NF-κB signaling pathway by Ginsenoside Rd.
  • To assess the impact of Ginsenoside Rd on inflammatory responses in the pancreas and intestine.

Main Methods:

  • Metabolic indicators of T2DM were monitored in db/db mice.
  • GLP-1 and GLP-1R levels were assessed using immunohistochemistry, Western blotting, and PCR.
  • Inflammatory markers (AMPK, Sirt1, MAPK, NF-κB) were analyzed via ELISA, transcriptomics, Western blot, and PCR.
  • In vitro experiments were conducted to further investigate the GLP-1 signaling pathway.

Main Results:

  • Ginsenoside Rd treatment led to decreased blood glucose and improved insulin resistance in db/db mice.
  • Expression of GLP-1 and GLP-1R was significantly upregulated post-treatment.
  • Transcriptome analysis revealed alterations in inflammatory response pathways.
  • Increased AMPK phosphorylation and decreased MAPK phosphorylation were observed, consistent with in vitro findings.

Conclusions:

  • Ginsenoside Rd shows promise in ameliorating T2DM in a mouse model.
  • The therapeutic effects may involve the inhibition of pancreatic and intestinal inflammation.
  • Promotion of GLP-1 secretion appears to be a key mechanism mediating Ginsenoside Rd's action.