## 4 Discussion
G1 subgroups, which might be due to the protective effect of OLE against STZ cytotoxicity in the beta cells (Figure 2). Furthermore, significant increases (\(p\) < 0.05) in insulin levels in the G2 subgroups treated with OLE were observed when compared with those in the D.W and Met. subgroups of the same group, thus indicating that OLE treatment was more effective than the Met. treatment in terms of enhancement of the insulin level. This enhancement might be due to the protective effect of OLE against STZ toxicity in the beta cells (Figure 2). A significant increase (\(p\) < 0.05) in insulin levels was observed in the G2 subgroups treated with OLE compared with those in the G3 subgroups. Alternatively, treatment with Met. did not lead to any significant enhancement in the insulin level in G2 compared with G3 (Figure 2). The induction of T1D in the rats was confirmed by the elevated levels of fasting plasma glucose and decreased levels of insulin. Similar results have been reported, wherein OLE was effective in increasing insulin sensitivity, reducing the fasting blood glucose level, and improving the glucose-induced release of insulin [14; 48]. Additionally, previous studies showed that metforminin increased hepatic insulin sensitivity and insulin dependence in the muscles and reduced blood glucose levels in humans [49; 50]. One study reported that metforminin was responsible for the release of insulin from beta cells [44], whereas another showed that it enhanced glucose uptake without any increase in insulin secretion [43]. Previous studies have shown that OLE reduces T.Ch., T.G, and LDL, and increase HDL in diabetic animals due to the antioxidant effect of phenolic compounds such as oleuropein, aglycone, and hydroxytyrosol [29; 32; 45; 51]. In the present study, OLE did not appear to alter the levels of T.Ch., T.G, HDL, and LDL; except increase in LDL in 1% OLE G3 and in 3% OLE G3 this may be due to the short duration of 5 weeks used in this study. Another explanation of LDL increase in G3 treated with 1% and 3% OLE could be treatment with OLE were after two weeks of streptozotocin injection not like G2 in which treatment with OLE was before streptozotocin injection, while G1 was control group without streptozotocin injection. The reason for the increase of LDL in G3 treated with 1% or 3% OLE is streptozotocin treatment, not OLE treatment, since G1 control without streptozotocin and treated with 1% and 3% OLE showing normal comparable LDL levels to control treated with distilled water in Figure 4. These results are supported by previous studies, which have been shown that streptozotocin treatment significantly increased LDL in rats [52; 53]. Long-term use of OLE or alcoholic extract with higher OLE concentrations has been reported to decrease the levels of cholesterol, triglyceride, and LDL, and increase the HDL level [29; 32; 51]. Nonetheless, consistent with the findings of previous studies [31; 54], Met. treatment did not appear to have any effect on the lipid profile. No significant changes in the expression of AMPK \(\alpha\)2 were observed in any of the groups, thus indicating that both OLE and Met. did not affect AMPK \(\alpha\)2 expression; additional studies are required to assess the long-term effects (Figure 5). One study reported an increase in AMPK \(\alpha\)2 expression after 10 weeks of Met. treatment, which may have caused an improvement in the glucose level [51; 54; 55]. Treatment with both OLE and Met. resulted in a significant decrease in AS160 levels in groups 2 and 3 when compared with their relative negative controls (D.W treatment;Table 4, Figure 6). This result agrees with a previous finding, wherein the knockdown or loss of AS160 increased the level of surface GLUT4 in adipocytes, whereas activation of AS160 led to the accumulation of GLUT4 in the cytosol [18]. Therefore, decreased phosphorylation or deactivation of AS120 is required for the increase in GLUT4 expression on the cell membrane. Another study showed that Met. stimulated the phosphorylation of AS160 [51]; alternatively, Met.