Journal
BIOMEDICINES
Volume 10, Issue 6, Pages -Publisher
MDPI
DOI: 10.3390/biomedicines10061235
Keywords
ACE; bioactive peptides; IRW; insulin resistance; obesity
Categories
Funding
- Natural Sciences and Engineering Research Council of Canada [CRDPJ 532150-18]
- Egg Farmers of Canada
- Global Egg Corporation
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IRW has beneficial effects on body composition and glucose metabolism in HFD mice, improving glucose tolerance, reducing weight gain, and promoting glucose uptake in skeletal muscle through multiple signaling pathways.
IRW (Isoleucine-Arginine-Tryptophan), has antihypertensive and anti-inflammatory properties in cells and animal models and prevents angiotensin-II- and tumor necrosis factor (TNF)-alpha-induced insulin resistance (IR) in vitro. We investigated the effects of IRW on body composition, glucose homeostasis and insulin sensitivity in a high-fat diet (HFD) induced insulin resistant (IR) model. C57BL/6 mice were fed HFD for 6 weeks, after which IRW was incorporated into the diet (45 or 15 mg/kg body weight (BW)) until week 14. IRW45 (at a dose of 45 mg/kg BW) reduced BW (p = 0.0327), fat mass gain (p = 0.0085), and preserved lean mass of HFD mice (p = 0.0065), concomitant with enhanced glucose tolerance and reduced fasting glucose (p < 0.001). In skeletal muscle, IRW45 increased insulin-stimulated protein kinase B (AKT) phosphorylation (p = 0.0132) and glucose transporter 4 (GLUT4) translocation (p < 0.001). Angiotensin 2 receptor (AT2R) (p = 0.0024), phosphorylated 5'-AMP-activated protein kinase (AMPK alpha) (p < 0.0124) and peroxisome proliferator-activated receptor gamma (PPAR gamma) (p < 0.001) were enhanced in skeletal muscle of IRW45-treated mice, as was the expression of genes involved in myogenesis. Plasma angiotensin converting enzyme-2 (ACE2) activity was increased (p = 0.0016). Uncoupling protein-1 in white adipose tissue (WAT) was partially restored after IRW supplementation. IRW improves glucose tolerance and body composition in HFD-fed mice and promotes glucose uptake in skeletal muscle via multiple signaling pathways, independent of angiotensin converting enzyme (ACE) inhibition.
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