Related Experiment Video

Updated: Jul 4, 2025

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
07:15

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

418

pNaKtide Inhibits Na/K-ATPase Signaling and Attenuates Obesity

Komal Sodhi1, Kyle Maxwell1, Yanling Yan1

  • 1Department of Medicine, Biomedical Science, and Surgery, Joan C. Edwards School of Medicine, Marshall University, Huntington, United States of America.

Journal of Clinical and Medical Sciences
|January 29, 2024
PubMed

Insights

This study shows that pNaKtide, a Na/K-ATPase inhibitor, reduces obesity and metabolic dysfunction by decreasing oxidative stress and improving insulin sensitivity in mice.

Area of Science:

  • Biochemistry
  • Metabolic Research
  • Oxidative Stress

Background:

  • Obesity is a global health issue linked to metabolic syndrome.
  • Oxidative stress plays a key role in obesity's pathophysiology.
  • Na/K-ATPase is known to amplify oxidative stress signaling.

Purpose of the Study:

  • To investigate the effect of inhibiting Na/K-ATPase signaling on obesity.
  • To evaluate the therapeutic potential of pNaKtide in obesity models.

Main Methods:

  • Experiments were conducted using murine preadipocytes and C57Bl6 mice on a high-fat diet.
  • The peptide antagonist pNaKtide was used to inhibit Na/K-ATPase.
  • Measurements included oxidant stress, lipid accumulation, body weight, systemic inflammation, and insulin sensitivity.

Main Results:

  • pNaKtide dose-dependently reduced oxidant stress and lipid accumulation in vitro.
  • In obese mice, pNaKtide significantly decreased body weight.
  • pNaKtide improved systemic oxidative and inflammatory markers and enhanced insulin sensitivity.

Conclusions:

  • Inhibition of Na/K-ATPase signaling with pNaKtide shows therapeutic potential for obesity.
  • pNaKtide effectively alleviates obesity and related metabolic comorbidities.
  • Targeting Na/K-ATPase oxidant amplification offers a novel strategy for obesity treatment.
Keywords:
Adipose tissueNa/K-ATPaseObesityOxidative stress

More Related Videos

Measuring the Rate of Lipolysis in Ex Vivo Murine Adipose Tissue and Primary Preadipocytes Differentiated In Vitro09:41

Measuring the Rate of Lipolysis in Ex Vivo Murine Adipose Tissue and Primary Preadipocytes Differentiated In Vitro

Published on: March 17, 2023

2.8K
An Adipocyte Cell Culture Model to Study the Impact of Protein and Micro-RNA Modulation on Adipocyte Function09:20

An Adipocyte Cell Culture Model to Study the Impact of Protein and Micro-RNA Modulation on Adipocyte Function

Published on: May 4, 2021

3.6K

Related Concept Videos

cAMP-dependent Protein Kinase Pathways01:25

cAMP-dependent Protein Kinase Pathways

Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
6.4K
Regulation of Food Intake01:30

Regulation of Food Intake

Short-term regulation of food intake primarily involves neural signals from the gastrointestinal (GI) tract, blood nutrient levels, and GI tract hormones. Communication between the gut and brain via vagal nerve fibers plays a significant role in evaluating the contents of the gut. Clinical studies have shown that protein ingestion produces a more prolonged response in these nerve fibers compared to an equivalent amount of glucose. Additionally, the activation of stretch receptors caused by GI...
232
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
3.6K
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
8.9K
GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of...
5.6K
Transducer Mechanism: Enzyme-Linked Receptors01:27

Transducer Mechanism: Enzyme-Linked Receptors

Enzyme-linked receptors are cell-surface receptors acting as an enzyme or associating with an enzyme intracellularly. They make excellent drug targets. Drugs can bind to the extracellular ligand-binding domain or directly affect their enzymatic domain and alter their activity.
Major types that are helpful drug targets include:
2.5K