Glycomacropeptide as an Efficient Agent to Fight Pathophysiological Mechanisms of Metabolic Syndrome.
Mathilde Foisy SauvéFrancis FeldmanAlain Théophile SanéMireille KoudoufioNatalie PateySchohraya SpahisJames ButcherHaonan DuanDaniel FigeysValérie MarcilAlain StintziEmile LevyPublished in: Nutrients (2024)
There is currently a growing interest in the use of nutraceuticals as a means of preventing the development of complex diseases. Given the considerable health potential of milk-derived peptides, the aim of this study was to investigate the protective effects of glycomacropeptide (GMP) on metabolic syndrome. Particular emphasis was placed on the potential mechanisms mitigating cardiometabolic disorders in high-fat, high-fructose diet-fed mice in the presence of GMP or Bipro, an isocaloric control. The administration of GMP for 12 weeks reduced obesity, hyperglycemia and hyperinsulinemia caused by a high-fat, high-fructose diet, resulting in a decline in insulin resistance. GMP also lessened systemic inflammation, as indicated by decreased circulating inflammatory cytokines. In the intestinal and hepatic tissues, GMP improved homeostasis by increasing insulin sensitivity and attenuating high-fat, high-fructose-induced inflammation, oxidative stress and endoplasmic reticulum stress. Biochemical and histological analyses revealed improved hepatic steatosis and fatty acid composition in the livers of high-fat, high-fructose diet-fed mice treated with GMP compared to Bipro. A trend toward a decrease in bile acids without any marked changes in intestinal microbiota composition characterized GMP-treated animals compared to those administered Bipro. GMP offers considerable potential for fighting metabolic syndrome-related components and complications given its beneficial effects on risk factors such as inflammation, oxidative stress and endoplasmic reticulum stress without involving the intestinal microbiota.
Keyphrases
- metabolic syndrome
- endoplasmic reticulum stress
- oxidative stress
- insulin resistance
- biofilm formation
- induced apoptosis
- high fat diet induced
- diabetic rats
- risk factors
- weight loss
- pseudomonas aeruginosa
- physical activity
- uric acid
- healthcare
- fatty acid
- candida albicans
- type diabetes
- dna damage
- escherichia coli
- adipose tissue
- human health
- ischemia reperfusion injury
- high fat diet
- skeletal muscle
- cardiovascular disease
- gene expression
- endothelial cells
- risk assessment
- cystic fibrosis
- high glucose
- heat shock
- heat shock protein