ArticleOdontology2026
Estrogen deficiency due to type 2 diabetes induced hyposalivation in female mice by promoting inflammation in the salivary glands.
Article in Odontology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Estrogen deficiency is related to salivary gland dysfunction, and the prevalence of hyposalivation in women with type 2 diabetes (T2D) is higher than the general population; nevertheless, the contribution of estrogen to hyposalivation in T2D is unclear. Four-week-old female C57BL/6 mice were divided into four groups (n = 6): control, ovariectomized (OVx), T2D, and OVx-T2D. T2D was induced by a combination of a high-carbohydrate diet and low-dose streptozotocin. Estrogen deficiency was induced at 8 weeks of age by OVx. At 20 weeks of age, stimulated saliva secretion and quality, blood glucose, and serum 17β-estradiol levels were determined, and the parotid and submandibular glands were obtained, histologically processed, and analyzed for histomorphometry; fibrosis development; and the expression of interleukin (IL)-1, IL-6, IL-10, IL-17, tumor necrosis factor (TNF)-α, and α-amylase. Compared with the control group we found a decrease in the 17β-estradiol concentration, an increase in body weight, a decrease in saliva secretion with alterations in its quality, a decrease in parotid and submandibular glands number of acini and α-amylase, acinar hypertrophy and fibrosis and increase in expression of IL-1, IL-6, IL-17, and TNF-α with a decrease in IL-10 in OVx, T2D, and OVx-T2D groups. In conclusion, T2D reduces 17β-estradiol levels comparable to OVx, and loss of estradiol results in hyposalivation and histological alterations through the establishment of a proinflammatory microenvironment in female mice parotid and submandibular glands.
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