## 4 Discussion
This was accomplished with BGL decreases in group V, which was treated with honey extract, compared to the significant increases in untreated group III. The results also revealed a significant reduction in hepatic glycogen levels (4.6 \(\pm\) 0.18) in the diabetes-induced mice in group III (Table 1). The administration of honey extract appears to have the potential to improve insulin levels or sensitivity, as evidenced by the improvement in glycogen content to 6.86 \(\pm\) 0.13 in the treated group V, as shown in Table 2. Cellular damage may result from oxidant stress, a crucial element in the pathogenesis of diabetes [40]. The body creates more free radicals when hyperglycemic, which might lead to an increase in oxidative stress and an increase in the likelihood of vascular problems [41]. The current study examined the effects of honey extract in mice with T1 DM more closely by assessing the antioxidant activity. In our experiment, the administration of 2 mg/kg/b.wt honey extract to group V significantly increased the SOD, GSH, and CAT activities in the T1 DM mice after 24 days, which were significantly decreased in the diabetic group III (Table 3). The amelioration of the activities of those enzymes can efficiently reduce oxidative stress, indicating that the utilization of honey extract enhanced the power of scavenging ROS. In addition, honey extract has significant antioxidant properties and is high in polyphenols, which are thought to be one of the potential mechanisms for protecting enzyme activity. However, in the current study, the diabetes-induced mice in group V treated with honey extract expressed higher SOD, GSH, and CAT activities. Moreover, other studies have reported similar results [42; 43]. The findings of the present study showed significantly increased serum MMP-9 levels in mice with diabetes compared to those in normal mice in group I, mainly due to the triggering of more ROS production by hyperglycemia, which then activates the pathway that increases the expression of MMP-9. Although research has shown that hyperglycemia can affect many intracellular signaling processes, whether these changes are related to vascular disease is still unknown. In T1 DM animal models, serum MMP-9 activity was assessed. Therefore, plasma MMP-9 levels could serve as a reasonable indicator of the intensity and stability of diabetic plaques, considering the growing evidence for their involvement in the development of atherogenesis. This is in agreement with [PERSON] et al. who discovered that diabetes patients' plasma had much higher levels of MMP-9 than in the normal group [44]. In the present study, the administration of 2 mg/kg/b.wt honey extract to group V significantly reduced serum MMP-9 activity, either directly or through the improvement of BGLs or antioxidant enzyme activities. Cardiovascular diseases are the primary cause of mortality globally; thus, mechanism may significantly reduce the frequently occurring cardiovascular complications associated with diabetes. TIMPs regulate MMPS activation and have a stronger affinity for MMP-9 than any other MMP [45]. TIMP-1 level estimation is a marker for identifying the aberrant regulation of tissue remodeling (TIMP-1a) [46]. In our study, T1 DM, either directly or indirectly through oxidation or inflammatory changes, significantly decreased serum TIMP-1 levels. This finding is supported by [PERSON], who found that the gene expression of TIMP-1 in the retina was reduced by about 35% compared with the results of control rats [47]. However, [PERSON] et al. noted that plasma TIMP-1 concentrations were noticeably increased in people with diabetics compared to controls. Treatment with honey extract helped slow down this reduction, although it was still noticeably lower than in normal mice [48]. In the current study, pancreas histopathology in group I and treated honey extract only in group II revealed normal-sized, distributed, and numbered islets of Langerhans with pale, rounded, and avoid \(\beta\)-cells in the center (Figures 1A,B and 2A,B).