RETRACTED: pNaKtide inhibits Na/K-ATPase reactive oxygen species amplification and attenuates adipogenesis

Komal Sodhi1, Kyle Maxwell1, Yanling Yan1

  • 1Departments of Medicine, Pharmacology, and Surgery, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV 25701, USA.

Science Advances
|November 25, 2015
PubMed

Insights

A novel peptide, pNaKtide, targeting the Na/K-ATPase pathway, effectively reduced obesity and improved insulin sensitivity in mice. This suggests inhibiting Na/K-ATPase amplification of oxidative stress may combat metabolic syndrome.

Area of Science:

  • Biochemistry
  • Physiology
  • Metabolic Research

Background:

  • Obesity is a global epidemic and a primary risk factor for metabolic syndrome.
  • Oxidative stress contributes to obesity development and maintenance.
  • Na/K-ATPase is identified as a pathway that amplifies oxidant signaling.

Purpose of the Study:

  • To investigate if pNaKtide, an inhibitor of Na/K-ATPase, can ameliorate obesity phenotypes.
  • To explore the potential of targeting Na/K-ATPase for treating obesity and related metabolic disorders.

Main Methods:

  • In vitro studies using isolated murine preadipocytes (3T3L1 cells).
  • In vivo studies using C57Bl6 mice fed a high-fat diet.
  • Administration of pNaKtide to assess its effects on oxidative stress, lipid accumulation, body weight, redox balance, inflammation, and insulin sensitivity.

Main Results:

  • pNaKtide dose-dependently attenuated oxidant stress and lipid accumulation in 3T3L1 cells.
  • In mice, pNaKtide administration reduced body weight gain.
  • pNaKtide restored systemic redox and inflammatory balance and improved insulin sensitivity.

Conclusions:

  • Inhibition of Na/K-ATPase amplification of oxidative stress is a potential therapeutic strategy.
  • pNaKtide demonstrates promise in combating obesity, insulin resistance, and metabolic syndrome.

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