Different studies in experimental diabetes models suggest that zinc oxide nanoparticles (ZnONPs) are useful as antidiabetic agents. However, this evidence was performed and measured in long-term treatments and with repeated doses of ZnONPs. This work aimed to evaluate the ZnONPs acute effects on glycemia during the next six h after an oral or intraperitoneal administration of the treatment in healthy and diabetic rats. In this study, the streptozotocin-nicotinamide intraperitoneal administration in male Wistar rats were used as a diabetes model. 10 mg/kg ZnONPs did not modify the baseline glucose in any group. Nevertheless, the ZnONPs short-term administration (100 mg/kg) induced a hyperglycemic response in a dose and route-dependent administration in healthy (130 ± 2 and 165 ± 10 mg/dL with oral and intraperitoneal, respectively) and diabetic rats (155 ± 2 and 240 ± 20 mg/dL with oral, and intraperitoneal, respectively). The diabetic rats were 1.5 fold more sensitive to ZnONPs effect by the intraperitoneal route. In conclusion, this study provides new information about the acute response of ZnONPs on fasting glycemia in diabetic and healthy rat models; these data are essential for possible future clinical approaches.

ZnO nanoparticles (ZnONPs) have been shown to have therapeutic potential in some diseases such as diabetes and cancer. However, concentration-dependent adverse effects have also been reported. Studies which evaluate the effects of ZnONPs on the cardiovascular system are scarce. This study aimed to evaluate the cardiovascular effects of a low dose of ZnONPs administered chronically in healthy rats. Changes in dyslipidemia biomarkers, blood pressure, aortic wall structure, vascular contractility, and expression of cannabinoid receptors in the aorta wall were evaluated. Healthy rats were divided into two groups: control or treated (one, two, and three months). The treated rats received an oral dose of 10 mg/kg/day. The results showed that treatment with ZnONPs induced dyslipidemia from the first month, increasing atherosclerosis risk, which was confirmed by presence of atherosclerotic alterations revealed by aorta histological analysis. In in vitro assays, ZnONPs modified the aorta contractile activity in response to the activation of cannabinoid receptors (CB₁ and CB₂). The expression of CB₁ and CB₂ was modified as well. Moreover, ZnONPs elicited an increase in blood pressure. In conclusion, long-time oral administration of ZnONPs induce dyslipidemia and atherosclerosis eliciting alterations in aorta contractility, CB₁ and CB₂ receptors expression, and an increase in blood pressure in healthy rats.

Background: In recent years, the role of neurotrophins and their receptors in peripheral tissues has been of great interest. At a metabolic level, the brain-derived neurotrophic factor (BDNF) and its receptor trkB have been reported to participate in insulin secretion from the pancreas in response to increases in circulating blood glucose. Objetive: To determines the role of the BDNF-trkB pathway in insulin secretion and pancreatic morphology in rats fed a cafeteria-style diet for 16 weeks. Methods: For the study, male rats of the Wistar strain were divided into three groups as follows: (1) control group (standard diet), (2) CAF group (cafeteria-style diet) and (3) CAF group treated with ANA-12 (TrkB receptor antagonist). After 4 months of intervention, the glucose and insulin tolerance curves, serum insulin levels, body fat and hematoxylin-eosin staining pancreas were evaluated. Results: The results showed that the cafeteria-style diet induced an increase in the amount of body fat, alterations in the glucose tolerance curve, increased insulin circulation levels, increased HOMA indices and increased pancreatic islet size. The antagonism of the trkB receptor in the rats fed a cafeteria-style diet enhanced some effects such as the accumulation of body fat and insulin secretion and induced a greater increase in the pancreas islet size. Conclusions: Under conditions of cafeteria-style diet-induced obesity, the antagonism of the BDNF-trkB pathway had no enhanced effect on the increase in insulin secretion or pancreatic islet size.

Background/Objectives: To better understand the mechanisms involved in atherosclerosis, different models have been developed, but these fail when studying the progression of this disease. The purpose of this study was to standardize a new model of atherosclerosis progression in rats using Paigen-type modified atherogenic diet. Methods: The design included a control group (n = 16) and 64 rats with atherogenic Paigen-type diet subdivided into four subgroups with different doses (Athero 1, Athero 2, Athero 3, and Athero 4). The atherogenic diet was supplemented orally in sequential stages: 1) Hypervitaminic (1.5 mL/kg/day for 12 days) and 2) Hyperlipidic (48 days ad libitum). Blood pressure, heart rate, aortic histopathology, inflammatory biomarkers, and biochemical lipid and liver profiles were measured in all groups on days 30 and 60. Results: All Athero 1 rats were sacrificed due to a poisoning for vitamin D2 excess. Athero 2 rats were sacrificed at day 30 showing severe atherosclerotic lesions (grades V–VIII). Athero 3 rats showed mild lesions (I–IV) at day 30 and severe lesions (V–VIII) at day 60. Athero 4 rats showed mild lesions (I–IV) at days 30 and 60. Diet-dependent changes in blood pressure and heart rate were observed. Furthermore, glycemia, dyslipidemia, and liver profile were associated with the degree of atherosclerotic lesion. Conclusions: “Athero 3” atherogenic diet generates a stable model to study the progress of atherosclerosis in rats.