An Egg White-Derived Peptide Enhances Systemic Insulin Sensitivity and Modulates Markers of Non-Alcoholic Fatty Liver Disease in Obese, Insulin Resistant Mice.
Stepheny C de Campos ZaniRen WangHellen Veida-SilvaRobin D ClugstonJessica T Y YueMarcelo A MoriJianping WuCatherine B ChanPublished in: Metabolites (2023)
Non-alcoholic fatty liver disease (NAFLD), the hepatic manifestation of the metabolic syndrome, is a global health problem. Currently, no pharmacological treatment is approved for NAFLD. Natural health products, including bioactive peptides, are potential candidates to aid in the management of metabolic syndrome-related conditions, including insulin resistance and obesity. In this study, we hypothesized that an egg-white-derived bioactive peptide QAMPFRVTEQE (Peptide 2) would improve systemic and local white adipose tissue insulin sensitivity, thereby preventing high-fat diet-induced exacerbation of pathological features associated with NAFLD, such as lipid droplet size and number, inflammation, and hepatocyte hypertrophy in high-fat diet-fed mice. Similar to rosiglitazone, Peptide 2 supplementation improved systemic insulin resistance during the hyperinsulinemic-euglycemic clamp and enhanced insulin signalling in white adipose tissue, modulating ex vivo lipolysis. In the liver, compared with high-fat diet fed animals, Peptide 2 supplemented animals presented decreased hepatic cholesterol accumulation ( p < 0.05) and area of individual hepatic lipid droplet by around 50% ( p = 0.09) and reduced hepatic inflammatory infiltration ( p < 0.05) whereas rosiglitazone exacerbated steatosis. In conclusion, Peptide 2 supplementation improved insulin sensitivity and decreased hepatic steatosis, unlike the insulin-sensitizing drug rosiglitazone.
Keyphrases
- insulin resistance
- high fat diet induced
- high fat diet
- adipose tissue
- metabolic syndrome
- type diabetes
- glycemic control
- polycystic ovary syndrome
- skeletal muscle
- oxidative stress
- global health
- public health
- healthcare
- emergency department
- uric acid
- chronic obstructive pulmonary disease
- single cell
- cardiovascular risk factors
- high throughput
- signaling pathway