Objective: To study the mechanisms by which APS ameliorates insulin resistance

we examined whether treatment with APS improves insulin sensitivity in insulin-resistant rats and whether this is associated with an increase of adiponectin and reduction of tumor necrosis alpha(TNF-α) and free fatty acides(FFA) in serum. Method: Seventy male SD rats were randomly divided into two groups:normal control group(NC group

n=12) and high fat-diet-induced model group(HFM group

n=60).Rats in NC group were fed with ordinary diet while those in HFM group were fed with high fat diet for six weeks.Then the rats in HFM group were randomly divided into five groups:high fat-diet-induced control group(HFC group)

pioglitazone group(Pio group)

low APS group(Laps group)

medium APS group(Maps group) and high APS group(Haps group)

with 12 rats in each.Normal saline

20 mg ·kg-1 ·d-1 pioglitazone and APS of different dosages (200

400

800 mg ·kg-1 ·d-1)were lavaged respectively for eight weeks.Changes of fasting blood glucose(FBG)

fasting insulin(FINS)

adiponectin

TNF-α and FFA in one half rats of each group were routinely measured

meanwhile glucose infusion rate(GIR) of another half was evaluated by hyperinsulinaemic-euglycaemic clamp technique. Result: Compared with those in NC group

the FFA

FINS and TNF-α of the rats in HFC group were significantly higher(P<0.05)

while adiponectin and GIR significantly lower(P<0.05).Compared with those in HFC group

the above mentioned indexes in the low and medium APS groups were improved significantly(P<0.05). Conclusion: These results indicate that moderate APS can regulate part of the insulin signaling in insulin-resistant serum and that APS could be a potential insulin sensitizer for the treatment of insulin resistance.