Supplementation with Vitis vinifera L. skin extract improves insulin resistance and prevents hepatic lipid accumulation and steatosis in high-fat diet–fed mice

Autor: Roberto Soares de Moura, Lenize Costa Reis Marins de Carvalho, Angela Castro Resende, Ana Paula Machado da Rocha, Cristiane Aguiar da Costa, Izabelle Barcellos Santos, Graziele Freitas de Bem, Viviane da Silva Cristino Cordeiro, Dayane Teixeira Ognibene, Gisele França da Costa
Rok vydání: 2017
Předmět:
Male
0301 basic medicine
medicine.medical_specialty
Endocrinology
Diabetes and Metabolism

Diet
High-Fat

Antioxidants
Mice
Phosphatidylinositol 3-Kinases
03 medical and health sciences
chemistry.chemical_compound
0302 clinical medicine
Endocrinology
Insulin resistance
Internal medicine
Nonalcoholic fatty liver disease
medicine
Hyperinsulinemia
Animals
Insulin
Vitis
Obesity
Triglycerides
Glucose Transporter Type 2
Nutrition and Dietetics
biology
Triglyceride
Plant Extracts
Lipogenesis
Polyphenols
medicine.disease
Cyclin-Dependent Kinases
Fatty Liver
Mice
Inbred C57BL

Oxidative Stress
Insulin receptor
Cholesterol
030104 developmental biology
Liver
chemistry
030220 oncology & carcinogenesis
Insulin Receptor Substrate Proteins
biology.protein
GLUT2
Insulin Resistance
Steatosis
Cyclin-Dependent Kinase-Activating Kinase
Zdroj: Nutrition Research. 43:69-81
ISSN: 0271-5317
DOI: 10.1016/j.nutres.2017.05.007
Popis: Nonalcoholic fatty liver disease is one of the most common complications of obesity. The Vitis vinifera L. grape skin extract (ACH09) is an important source of polyphenols, which are related to its antioxidant and antihyperglycemic activities. We hypothesized that ACH09 could also exert beneficial effects on metabolic disorders associated with obesity and evaluated ACH09's influence on high-fat (HF) diet-induced hepatic steatosis and insulin resistance in C57BL/6 mice. The animals were fed a standard diet (10% fat, control) or an HF diet (60% fat, HF) with or without ACH09 (200mg/[kg d]) for 12weeks. Our results showed that ACH09 reduced HF diet-induced body weight gain, prevented hepatic lipid accumulation and steatosis, and improved hyperglycemia and insulin resistance. The underlying mechanisms of these beneficial effects of ACH09 may involve the activation of hepatic insulin-signaling pathway because the expression of phosphorylated insulin receptor substrate-1, phosphatidylinositol 3-kinase, phosphorylated Akt serine/threonine kinase 1, and glucose transporter 2 was increased by ACH09 and correlated with improvement of hyperglycemia, hyperinsulinemia, and insulin resistance. ACH09 reduced the expression of the lipogenic factor sterol regulatory-element binding protein-1c in the liver and upregulated the lipolytic pathway (phosphorylated liver kinase B1/phosphorylated adenosine-monophosphate-activated protein kinase), which was associated with normal hepatic levels of triglyceride and cholesterol and prevention of steatosis. ACH09 prevented the hepatic oxidative damage in HF diet-fed mice probably by restoration of antioxidant activity. In conclusion, ACH09 protected mice from HF diet-induced obesity, insulin resistance, and hepatic steatosis. The regulation of hepatic insulin signaling pathway, lipogenesis, and oxidative stress may contribute to ACH09's protective effect.
Databáze: OpenAIRE