Key result
Empagliflozin preserves skin microvascular reactivity ~22% over untreated controls in high-fat diet rats.
Why the study?
The increasing prevalence of obesity and metabolic disorders necessitates finding methods to prevent associated cardiovascular complications. This study experimentally evaluated the potential protective effect of the SGLT2 blocker empagliflozin on the morphofunctional state of skin microvessels in rats fed a high-fat diet.
Does empagliflozin protect the morphofunctional state of skin microvessels and prevent endothelial dysfunction in rats fed a high-fat diet?
Does empagliflozin protect the morphofunctional state of skin microvessels and prevent endothelial dysfunction in rats fed a high-fat diet?
In a rat model of high-fat diet-induced metabolic load, daily empagliflozin attenuated endothelial dysfunction and prevented microvascular wall thickening and fibrosis in skin microvessels.
Empagliflozin may preserve microvessel morphology in obese rats; leaves open human translation for metabolic CV prevention.
Introduction . The increasing prevalence of obesity and metabolic disorders in humans necessitates the search for methods to prevent cardiovascular complications that are characteristic of diseases associated with metabolic disorders. The objective of this study was to experimentally evaluate the potential protective effect of the sodium-glucose cotransporter 2 (SGLT2) blocker empagliflozin (EMPA) on the morphofunctional state of skin microvessels in rats fed a high-fat diet. Materials and Methods . Rats in the high-fat diet (HFD) and EMPA groups (n=12 each) were maintained on the HFD (50 % fat) for 8 weeks. Rats in the EMPA group also received 1 mg/kg EMPA daily. Rats in the standard diet (SD) group (n=15), fed a standard diet (15 % fat), served as controls. After measuring blood pressure in rats by the cuff method, blood flow in the skin of the back was studied using laser Doppler flowmetry, the baseline microcirculation index and the amplitude of its fluctuations in the endothelial, neurogenic, and myogenic ranges was evaluated and the corresponding tone was calculated. The reactivity of the skin microvascular bed was assessed based on the increase in the microcirculation index after iontophoresis of acetylcholine (ACh) and sodium nitroprusside compared to the baseline. The blood levels of triglycerides, high-density and low-density lipoproteins were determined, and the visceral fat mass index was calculated. Quantitative morphometry of skin microvessels was performed using the Video Test-Morphology 5.2 program. Results . In rats on the HFD, the average baseline microcirculation index decreased, and the tone increased in all ranges, while the tone decreased when EMPA was applied. EMPA prevented the suppression of the reactivity of the skin microvascular bed: the microcirculation index in response to ACh was 9.94±0.20 p. u. in the EMPA group compared to the HFD group (8.12±0.18 p. u.), but it was lower than in the SD group (10.65±0.22 p. u.). The dilation response to sodium nitroprusside was similar to that of the HFD group and lower than that of the SD group. EMPA prevented an increase in microvessel wall thickness and prevented the development of fibrosis, which is typical for HFD. Conclusion . EMPA application weakens endothelial dysfunction of the skin microvessels in rats with excessive consumption of fats, preventing a decrease in dilation. EMPA reduces remodeling of the microvascular network of the skin in HFD.
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Ivanova et al. (2026) studied High-fat diet-induced skin microvascular dysfunction and remodeling in rats (n=39). Empagliflozin vs. High-fat diet alone (50% fat) and standard diet control (15% fat) was evaluated on Skin microvascular reactivity (microcirculation index in response to acetylcholine iontophoresis). Empagliflozin (1 mg/kg/day) preserved acetylcholine-induced skin microvascular reactivity in high-fat diet-fed rats compared to untreated high-fat controls (9.94±0.20 vs 8.12±0.18 p.u.).
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