'BEE WAX VENOM FORMULATION IMPROVES GLUCOSE AND LIPID METABOLISM VIA UPREGULATING PPAR-Γ IN HIGH-FAT DIET LOW DOSE STREPTOZOTOCIN INDUCED TYPE 2 DIABETIC RATS

Session Name
NEW MEDICATIONS FOR TREATMENT OF DIABETES
Session Type
E-POSTER VIEWING (EXHIBITION HOURS)
Date
20.02.2020, Thursday
Session Time
09:30 - 15:30
Channel
E-Poster Area
Lecture Time
09:42 - 09:43
Presenter
  • JAE KWON Lee, Korea, Republic of
Authors
  • Rangachari Balamurugan, Korea, Republic of
  • JAE KWON Lee, Korea, Republic of

Abstract

Background and Aims

Beeswax venom (BWV) formulation is composed of bee wax (BW) (98.29) and bee venom (BV) (1.71%) possesses various medicinally important molecule lead us to elucidate its antidiabetic property in high-fat diet (HFD) and low dose streptozotocin (STZ) induced type 2 diabetic rats.

Methods

Type 2 diabetes mellitus (T2DM) was induced by feeding HFD for 2 weeks followed by the injection of single dose of 35 mg/kg STZ. After 3 weeks of oral administration of BWV formulation (0.125, 0.250 and 0.500 mg/kg) and metformin (MET) 180mg/kg, the biochemical parameters such as serum glucose, serum insulin, lipid profile, liver marker enzymes was estimated. Furthermore, western blot analysis of liver peroxisome proliferator activated receptor-γ (PPAR-γ), CCAAT/enhancer binding protein (C/EBP- β) and CCAAT/enhancer binding protein-alpha (C/EBP-α) was performed. Histological analysis of pancreas was also studied.

Results

Oral administration of BWV formulation (0.125, 0.250 and 0.500 mg/kg) and metformin 180mg/kg significantly reduced the levels of serum glucose, total cholesterol (TC), triglycerides (TG), liver marker enzyme and significantly increased the serum insulin and body weight. Furthermore, BWV formulation treatment enhanced the liver PPAR-γ, C/EBP- β and C/EBP-α protein expression. At the same time histological analysis of pancreas showed significant amelioration of β-cell damage.

Conclusions

Our results suggest that BWV formulation regulated the abnormalities of glucose and lipid metabolism by its PPAR-γ agonist property in HFD low dose induced type 2 diabetic rats.

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