الفهرس 
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Abstract
Type-2 diabetes mellitus (T2DM) has developed in the last few decades into a chronic metabolic condition caused by combination of various hereditary and environmental variables. In most high- and middle-income nations, the incidence and prevalence of T2DM patients have even reached epidemic levels. The initiation and development of T2DM- related complications may be significantly influenced by genetic variables and genetic background.
Among the long-recognized results of phytochemicals, Consideration of these natural materials as a potential pool for the discovery of new anti-diabetic medication leads is motivated by their therapeutic potential for T2DM. The recent findings add to the descriptions of the anti-diabetic characteristics of plants utilised in conventional therapy. Cinnamon is expected to provide some anti-diabetic effectiveness without unfavourable side effects. One of the main components of cinnamon, cinnamonaldehyde, appears to lower plasma blood glucose concentration.
Autophagy is a system of intracellular breakdown that transports cytoplasmic elements to the lysosome. Autophagy is a cell-protection system that is triggered by damaged organelles, which promotes cell survival. Despite its simplicity, recent research has shown that autophagy performs a number of physiological and pathological roles, some of which are complex. Cinnamaldehyde has been shown to affect autophagy in T2D by either upregulating or downregulating the gene expression of certain autophagic biomarkers.
Additionally, elevated AT autophagy may be a factor in the inflammation of adipose tissue and the release of an inflammatory adipokine pattern. In addition, T2DM development is strongly correlated with obesity and inflammation. Type 2 diabetes has been demonstrated to be predicted by higher levels of IL1β.
The current study’s objective was to investigate int the impacts of cinnamaldehyde on the expression of some autophagy-regulated genes and some inflammatory genes components in adipose tissue in HFD/STZ-diabetic rats compared to metformin.
Cinnamaldehyde decreased the fasting blood glucose in the diabetic rats. It’s interesting to note that cinnamaldehyde therapy decreased autophagy in adipose tissue by upregulating mTORC1 gene expression and downregulating Beclin-1, LC3- II, and ATG5 gene expression. In addition, cinnamaldehyde could evidently reverse the increased production of IL-1β in adipose tissue. After all, utilizing cinnamaldehyde in conjunction with metformin has demonstrated superior improvement in lipid profile, inflammatory, and autophagic gene expression, as well as glucose homeostasis measures.
from the above-mentioned discussion, we can conclude that:
1. Cinnamaldehyde is a promising natural glucose and lipid lowering agent.
2. Cinnamaldehye decreases inflammation in adipose tissue.
3. Cinnamaldehyde inhibit autophagy in adipose tissue via upregulation of gene expression of mTORC1and downregulation of the expression of Beclin-1, LC3-II and ATG5.
4. Cinnamaldehyde may be used in conjunction with metformin as an adjuvant therapy to increase the effectiveness of the treatment and lessen side effects.
5. More research is required to determine the precise mechanism of action of cinnamaldehyde on the autophagic pathway in diabetes.