Background/Objectives: Estrogen deficiency is associated with metabolic disturbances and impaired glucose homeostasis. Morin, a natural flavonol, has shown promising hypoglycemic and antioxidant properties, but its effects under hypoestrogenic diabetic conditions remain poorly understood. The aim of this study was to evaluate the effects of morin on body weight, fasting blood glucose, glucose tolerance, and selected serum biochemical markers in an experimental model of diabetes under estrogen-deficient conditions (ovariectomized diabetic female mice). Methods: Female CD1 mice underwent sham surgery or ovariectomy (OVX), and each surgical condition was further divided into non-diabetic and diabetic subgroups treated with vehicle, glibenclamide (10 mg/kg), or morin (30 mg/kg). Body weight and fasting blood glucose were monitored over a 15-day treatment period. Oral glucose tolerance was assessed on day 15, and serum biochemical markers, including glucose, cholesterol, triglycerides, uric acid, blood urea nitrogen, creatinine, ALT, and AST, were measured thereafter. Results: Ovariectomy aggravated diabetes-associated hyperglycemia, impaired glucose tolerance, and triglyceride elevation. Morin treatment reduced fasting blood glucose and improved glucose tolerance in diabetic mice, including ovariectomized animals. Morin also attenuated the increase in serum triglycerides and blood urea nitrogen in ovariectomized diabetic mice, although it did not significantly improve cholesterol, uric acid, creatinine, ALT, or AST levels. Compared with glibenclamide, morin showed relevant glucose-lowering activity but had a more limited effect on the overall biochemical profile. Conclusions: These findings suggest that morin may partially improve glycemic control and selected metabolic alterations in experimental diabetes associated with estrogen deficiency. Further studies are required to clarify its mechanisms of action, long-term efficacy, and translational relevance.

The polypharmacology of statins includes indirect interactions with the serotonergic system, particularly with the 5-HT1A and 5-HT7 receptors. Statins influence both the expression and function of these receptors, which may affect the regulation of anxiety. The main objective of this study was to examine the effects of subchronic treatment with atorvastatin (STA) and acute treatment with serotonergic drugs on anxiety-like behavior, as well as their possible relationship to changes in the expression of 5-HT1AR and 5-HT7R in different brain regions of mice. In the first phase, the effect of STA (10, 20, or 30 mg/kg daily for 21 days) on anxiety-related exploratory behavior was assessed in male CD1 mice using the avoidance exploratory behavior test. Concurrently, receptor expression levels were measured in the prefrontal cortex, hippocampus, and striatum following STA administration. In the second phase, the effect of serotonergic drugs (0.5 or 1 mg/kg of 8-OH-DPAT, a 5-HT1A/5-HT7 receptor agonist, or WAY100635, a 5-HT1A receptor antagonist) on anxiety-related behaviors was studied in separate groups of animals, stratified by dose, that had previously been treated with or without STA. The persistence of the anxiogenic effect following serotonergic drug administration in mice previously treated with STA may be related to the increased mRNA expression of 5-HT1AR and 5-HT7R observed in the hippocampus, striatum, and prefrontal cortex, although confirmation at the protein level is needed in future studies.