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A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis
Published on: October 26, 2020
Prorenin/renin and insulin resistance
Kazi Rafiq1, Yukiko Nagai, Daisuke Nakano
1Department of Pharmacology, Kagawa University Medical School, Kagawa, Japan.
Frontiers in Bioscience (Elite Edition)
|June 3, 2010
Summary
Fructose intake activates prorenin and angiotensin II in muscle, contributing to insulin resistance. Targeting the prorenin/(pro)renin receptor system may offer new therapeutic strategies for metabolic disorders.
Area of Science:
- Endocrinology
- Metabolic Research
- Renal Physiology
Background:
- Fructose consumption is linked to metabolic dysfunction, including insulin resistance.
- The prorenin/(pro)renin receptor system plays a role in cardiovascular and metabolic regulation.
- Previous studies indicated fructose-induced prorenin activation in skeletal muscle.
Purpose of the Study:
- To review the impact of the prorenin/(pro)renin receptor system on insulin resistance.
- To explore the therapeutic potential of targeting this system for metabolic diseases.
- To consolidate current knowledge on fructose's effects on muscle prorenin.
Main Methods:
- Literature review of studies investigating the prorenin/(pro)renin receptor system.
- Analysis of research on fructose-induced metabolic changes in animal models.
- Examination of pharmacological interventions targeting prorenin/(pro)renin receptor interactions.
Main Results:
- Fructose feeding in rats activates prorenin non-proteolytically, leading to angiotensin II production in skeletal muscle.
- Inhibition of prorenin/(pro)renin receptor interaction attenuated insulin resistance development.
- The inhibitor did not improve glucose intolerance in rats overexpressing the human renin gene.
Conclusions:
- The prorenin/(pro)renin receptor system is implicated in the development of insulin resistance.
- Targeting the prorenin/(pro)renin receptor pathway presents a potential therapeutic avenue for insulin resistance.
- Further research is needed to fully elucidate the role of this system in glucose metabolism.
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