The present study specifically addresses the relationship betweenmicrocirculation and metabolic syndrome, a cluster of metabolic andcardiovascular modifications highly prevalent in the generalpopulation. The aim of the study was to assess skin microcirculationin a rat model of metabolic syndrome (fructose induced insulin resistance) and detect the effect of metformin treatment on various parameters of metabolic syndrome and microcirculation impairment.Thirty-six female rats were divided into three groups : Control group,fructose induced insulin resistance for 8 weeks and fructose inducedinsulin resistance group treated with metformin for two weeks. Serum levels of glucose, insulin, HOMA index, lipid profile, nitricoxide and inflammatory markers; high-sensitivity C-reactive protein(hs-CRP) and tumour necrosis factor,pressure, BMI and weight gain were measured. The skinmicrocirculation was assessed by measuring basal skin blood flow at30 ِC in perfusion units (P.U), the percent change between bloodflow at 30 ِC and blood flow after local heating of the skin to 44 ِcand the slope of this change in milleseconds. Also, frequency andpower of vasomotion were assessed. Our results proved theoccurrence of insulin resistance in fructose treated group. We alsodemonstrated a significant decrease in the percent change in bloodflow between blood flow at 30 ِC and 44 ِC, slope ofchange, vasomotion frequency 2 at 30C, frequency 2 and 3 at 44 ِCand power 1,2and3 at 44 ِC were decreased significantly in fructoseinduced insulin resistance group. Metformin treatment for 2 weeksimproved significantly the levels of serum glucose, serum insulin,insulin resistance, serum triglycerides, HDL-C, nitric oxide (NO),the inflammatory markers; high-sensitivity C reactive protein (hs-CRP) blood flow at 30 ِC and after local heating of the skin to 44 C, levels of vasomotion frequency3 at 30 ِC, levels of frequency1 and 2 at44 ِC, the levels of power 1 at 30 ِC and that of power3 at 44 ِC ascompared to fructose fed group. It can be claimed from our study thatuse of fructose in diet for at least 2 months could be a model forexperimentally studying the pathophysiological changes in themetabolic syndrome including the microvascular dysfunction whichmay be a potential factor explaining the clustering of severalcomponents of the metabolic syndrome. Our data also show that controls hyperglycemia, improveslipid profiles and restores the inflammatory markers. In addition to its insulin-sensitizing effects,metforminhas also been shown to have beneficial vascular effects. This supports the concept of the central role of metformin as a first-line of treatment in patients with metabolic syndrome in order toprotect against endothelial dysfunction associated with insulinresistance