Pear pomace ethanol extract improves insulin resistance through enhancement of insulin signaling pathway without lipid accumulation.
10.4162/nrp.2017.11.3.198
- Author:
Mi Kyoung YOU
1
;
Hwa Jin KIM
;
Jin RHYU
;
Hyeon A KIM
Author Information
1. Department of Food and Nutrition / Research Institute of Human Ecology, Mokpo National University, 1666, Yeongsan-ro, Cheonggye-myeon, Muan-gun, Jeonam 58554, Korea. kha@mokpo.ac.kr
- Publication Type:Original Article
- Keywords:
Insulin sensitivity;
glucose transporter;
lipid metabolism;
adipose tissue;
pyrus
- MeSH:
3T3-L1 Cells;
Adipose Tissue;
Animals;
Blotting, Western;
Body Weight;
Cell Survival;
Chemokine CCL2;
Diet, High-Fat;
Ethanol*;
Glucose;
Glucose Transport Proteins, Facilitative;
Glucose Transporter Type 4;
Homeostasis;
Insulin Receptor Substrate Proteins;
Insulin Resistance*;
Insulin*;
Lipid Metabolism;
Mice;
Obesity;
Pyrus*;
Triglycerides
- From:Nutrition Research and Practice
2017;11(3):198-205
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND/OBJECTIVES: The anti-diabetic activity of pear through inhibition of α-glucosidase has been demonstrated. However, little has been reported about the effect of pear on insulin signaling pathway in obesity. The aims of this study are to establish pear pomace 50% ethanol extract (PPE)-induced improvement of insulin sensitivity and characterize its action mechanism in 3T3-L1 cells and high-fat diet (HFD)-fed C57BL/6 mice. MATERIALS/METHODS: Lipid accumulation, monocyte chemoattractant protein-1 (MCP-1) secretion and glucose uptake were measure in 3T3-L1 cells. Mice were fed HFD (60% kcal from fat) and orally ingested PPE once daily for 8 weeks and body weight, homeostasis model assessment of insulin resistance (HOMA-IR), and serum lipids were measured. The expression of proteins involved in insulin signaling pathway was evaluated by western blot assay in 3T3-L1 cells and adipose tissue of mice. RESULTS: In 3T3-L1 cells, without affecting cell viability and lipid accumulation, PPE inhibited MCP-1 secretion, improved glucose uptake, and increased protein expression of phosphorylated insulin receptor substrate 1 [p-IRS-1, (Tyr⁶³²)], p-Akt, and glucose transporter type 4 (GLUT4). Additionally, in HFD-fed mice, PPE reduced body weight, HOMA-IR, and serum lipids including triglyceride and LDL-cholesterol. Furthermore, in adipose tissue, PPE up-regulated GLUT4 expression and expression ratio of p-IRS-1 (Tyr⁶³²)/IRS, whereas, down-regulated p-IRS-1 (Ser³⁰⁷)/IRS. CONCLUSIONS: Our results collectively show that PPE improves glucose uptake in 3T3-L1 cells and insulin sensitivity in mice fed a HFD through stimulation of the insulin signaling pathway. Furthermore, PPE-induced improvement of insulin sensitivity was not accompanied with lipid accumulation.
