## 1 Introduction  
Taste perception, an essential sensory function, significantly influences systemic health, nutritional status, and overall quality of life. It is known that factors such as aging, smoking, and certain medications can impair this sense [1]. Additionally, a variety of diseases can lead to gustatory disorders, detrimentally affecting patients' well-being. Among these conditions is diabetes mellitus (DM), a metabolic disorder that can bring about sensory deficits, including in taste perception [2, 3]. Recent research has highlighted the increasing association of DM with taste impairments [4]. Specifically, DM has been shown to negatively influence the perception of sweet, salty, and bitter tastes [5, 6]. Electrospstometric thresholds, for instance, tend to increase notably in patients with diabetes [3, 7]. Yet, despite the evident link between DM and taste disorders, the fundamental mechanisms at play are not entirely clear. A deeper exploration into the histological and histopathological aspects of taste buds can provide invaluable insights into the physiopathology of taste impairment in DM. Histologically, taste buds are complex structures housing specialized taste receptor cells (TRCs) that detect different taste qualities [8]. These TRCs are nestled within the epithelial cells in a well-organized manner, forming onion-like structures with a central taste pore opening to the oral cavity [9]. Each taste bud comprises approximately 50-100 TRCs [8] that are continuously renewed, with a lifespan of about 10-20 days [9]. The turnover of TRCs is a tightly regulated process, ensuring the integrity and functionality of taste buds [10]. Histopathologically, diabetes has been observed to induce changes in the structural and cellular integrity of taste buds [11]. Elevated glucose levels, characteristic of DM, can lead to oxidative stress and inflammatory responses within the taste buds, adversely affecting their morphology and function [11]. Such alterations include a reduction in the number of TRCs, changes in their ultrastructural appearance, and disruptions in the signaling pathways crucial for taste transduction [12]. Moreover, the supportive cells surrounding TRCs may also be compromised, further impairing taste perception. The resultant taste disorders could potentially exacerbate the dietary challenges faced by individuals with DM, underscoring the necessity of understanding and addressing the histopathological alterations in taste buds that are induced by DM [6; 13]. A closer look at the anatomy and physiology of taste perception reveals the significance of circumvallate papillae (CVP). Rats, interestingly, have only one CVP, positioned at the posterior midline of their tongues. This papilla is surrounded by a furrow, or trench, that contains a considerable number of taste buds [14]. A key process underpinning taste perception is apoptosis, the programmed death of cells. In taste buds, apoptosis is crucial for controlling the balance between the birth and death of taste cells, which inherently have a short lifespan. This balance is vital for the preservation of functional taste buds. If this equilibrium is disrupted, it could potentially result in taste disorders [15]. Although research has delved into apoptosis's role in taste biology, especially concerning age-related taste deterioration [1], the connection between apoptosis and taste dysfunctions in DM has not been extensively explored. Some initial research on diabetic rat models points to changes in the structure of vallate taste buds but stops short of probing into apoptosis [11; 16]. Enter 4-hexylresorcinol (4-HR), a plant-derived compound found in the extract of _Quercus cortex_, known for its diverse biological activities [17]. Current studies suggest that 4-HR can modulate cellular stress responses [18], boasting antioxidant properties [19; 20]. High glucose levels, a characteristic of DM, can induce oxidative stress, which may, in turn, initiate apoptosis in various tissues [21; 22].