The Study On Mechanism Of Radix Astragali Improvement Insulin Resistant Of Rat With High-fat-fed

[Objective] To investigate the mechanism by which radix astragali(RA) relieves insulin resistance(IR) in adipose tissue of rat with high-fat-fed(HF).[Methods] The S-D rats were divided into 4 groups randomly (1)HF, rats on high-fat diet ( fat 61% of total Kcal).(2) HF+RA, supplemented with radix astragali while on high-fat diet. (3) HF+TZD, administration of rosiglitazone with high-fat diet. (4)Control, normal diet. Each group was fed equicalorically for 4 weeks, then insulin sensitivity was measured with glucose-insulin tolerance test. Reverse transcription-polymerase chain reaction (RT-PCR) was used to determine the mRNA level of leptin, TNF-α and PPAR-γ in adipocyte. Sections of adipose tissue from rats were fixed with 100% ethanol and stained by the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) technique with a kit to detect apoptotic nuclei. [Results] (1)K values obtained from glucose-insulin tolerance test were significantly increased in HF+RA and HF+TZD group compared with that in HF group. (2)mRNA level of leptin and TNF-α were significantly decreased in HF+TZD group compared with that in HF group,but in HF+RA group there were no significant change in the leptin and TNF-αmRNA levels compared with that in HF group.(3)There was no significant change in the PPAR-γ mRNA levels with or without high-fat-fed,or with or without TZD or RA treatment.(4)The number of TUNEL-positive nuclei was much greater by TZD or RA treatment than in HF. [Conclusion] It is suggested that treatment with TZD can relieve insilin resistance of the rat with high-fat-fed through normalization of increased expression levels of leptin, TNF-α in adipose tissue. The mechanism which TZD can decrease the expression of leptin, TNF-α and improve IR would be closely related to increment of adipocyte apoptosis caused by TZD treatment. The treatment with RA can relieve insilin resistance of the rat with high-fat-fed and cause increment of adipocyte apoptosis but can't normalize the increased expression levels of leptin, TNF-α in adipose tissue. The mechanism which RA relieves IR in adipose tissue of rat with high-fat-fed is that it can increase adipocyte apoptosis.But the reason why RA treatment can increase adipocyte apoptosis is not clear.