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Post-prandial hyperglycemia still remains a problem in the management of type 2 diabetes mellitus. Of all available anti-diabetic drugs, α-glucosidase inhibitors seem to be the most effective in reducing post-prandial hyperglycemia. We conducted a review analyzing the clinical efficacy and safety of α-glucosidase inhibitors, both alone and in combination with other anti-diabetic drugs, with respect to glycemic control, inflammation and atherosclerosis. α-Glucosidase inhibitors proved to be effective and safe both in monotherapy and as an add-on to other anti-diabetic drugs. Compared to miglitol and voglibose, acarbose seems to have some additive effects such as stabling carotid plaques, and reducing inflammation. Acarbose also proved to reverse impaired glucose tolerance to normal glucose tolerance.

Introduction The aim of this study was to compare the effects of mitiglinide/voglibose with those of glimepiride on glycemic variability and vascular endothelial function in patients with type 2 diabetes. Materials and Methods It was a multicenter, open‐label, randomized, crossover study. Hospitalized patients received either mitiglinide/voglibose (three times daily administration of 10 mg mitiglinide and 0.2 mg voglibose) or glimepiride (once‐daily 2 mg) in random order, each for 5 days. The reactive hyperemia index (RHI) and the mean amplitude of glycemic excursions (MAGE) were measured as co‐primary endpoints using reactive hyperemia peripheral arterial tonometry and continuous glucose monitoring. Results The analysis included 30 patients (15 in each group). The RHI was 1.670 ± 0.369 during treatment with mitiglinide/voglibose and 1.716 ± 0.492 during treatment with glimepiride, with no significant difference between the two. MAGE was significantly lower in the mitiglinide/voglibose group (47.6 ± 18.5 mg/dL) than in the glimepiride group (100.6 ± 32.2 mg/dL). Although the mean blood glucose levels over the entire 24 h period were comparable between the two groups, the use of mitiglinide/voglibose was associated with a lower standard deviation of mean glucose, coefficient of variation, and mean postprandial glucose excursion compared with glimepiride. The time below range (<70 mg/dL) and the time above range (>180, >200, and 250 mg/dL) were lower in the mitiglinide/voglibose group, while the time in range (70–180 mg/dL) was higher. Conclusions In our short‐duration randomized crossover study, although not impacting vascular endothelial function, mitiglinide/voglibose demonstrated potential benefits in reducing glycemic variability, postprandial hyperglycemia, and hypoglycemia in patients with type 2 diabetes.

A stability indicating UV spectrophotometric method has been developed and validated for the estimation of voglibose in pharmaceutical preperation. The proposed method utilized 0.1 N NaOH as solvent and detection was carried out at 214.5nm. Experiments were designed for determining linearity, limit of detection and quantitation, accuracy, precision and specificity of this analytical method. The stability studies of voglibose was carried out under acid, alkaline, thermal, oxidative and photolytic. The responses were linear in the concentration range of 5-25µg/ml with correlation coefficient of 0.9997. The % RSD for both inter-day and intra-day precision were less than 2%. The recovery of drug from sample was found to be 99.6-100.4%. Although the degradation products of stress condition had not been identified, the method had been able to detect the changes due to stress condition. The stated method can be used as stability indicating method with high degree of linearity, accuracy and precision for assay of voglibose in routine pharmaceutical analysis of tablet formulation. The method was found to be simple and cost effective. Hence this method can be successfully used to study stress degradation behavior of voglibose in small industry where high end instruments are not available.

Alzheimer’s disease (AD) is an age-dependent neurodegenerative disease hallmarked by Amyloid-β (Aβ) aggregation, cognitive impairment, and neuronal and synaptic loss. In this study, AD was induced in male Wistar rats ( n  = 6) by the administration of intracerebroventricular-streptozotocin (ICV-STZ-3 mg/kg/day), and Voglibose (Vog) was administered at various doses (10, 25, and 50 mg/kg), while Galantamine (3 mg/kg) acted as a reference standard drug. Behavioral alterations in both spatial and non-spatial memory functions were evaluated in the experimental rats. At the end of the study, all experimental rats were sacrificed, and their brain parts, the cortex and hippocampus, were subjected to biochemical, western blot, and histopathological analysis. In our study results, the statistically significant dose-dependent results from the behavioral tests show the Voglibose-treated groups significantly improved ( p  < 0.0001) spatial and non-spatial memory functions when compared with ICV-STZ-treated group. Meanwhile, when compared with ICV-STZ-treated rats, treatment with Voglibose (10, 25, and 50 mg/kg) showed the activities of both acetylcholinesterase (AChE) and malondialdehyde (MDA) were significantly attenuated ( p  < 0.0001), while the operation of antioxidant enzymes was considerably enhanced ( p  < 0.0001). The molecular estimation showed that it significantly attenuates ( p  < 0.0001) the TNF-α, IL-1β, and CRP activity, and the western blot results demonstrate the significantly attenuated Aβ aggregation. The histopathological results showed that the Voglibose treatment had an effective improvement in clear cytoplasm and healthy neuronal cells. In conclusion, our results suggest that Voglibose has potent neuroprotective effects against the ICV-STZ-induced AD model. Furthermore, these results support the possibility of Voglibose as a therapeutic approach to improving cognitive function, suggesting that controlling Aβ aggregation might be a novel target for the development of AD.

Type-II diabetes mellitus is a chronic disorder that results from fluctuations in the glucose level leading to hyperglycemia with severe adverse effects increasing worldwide. Alpha-Amylase is the key enzyme involved in the mechanism of glucose formation therefore Alpha-Amylase inhibitors have become a therapeutic target in the development of new leads as they have the potential to suppress glucose levels. Existing drugs targeting Alpha-Amylase highlight major drawbacks in terms of poor absorption rate that causes several gastrointestinal issues. So, this research is aimed to develop novel inhibitors interacting with Alpha-Amylase’s active site using structural-based screening, binding pattern analysis, and molecular dynamic simulation. Hence, to search for a potential lead, we analyzed a total of 133 valiolamine derivatives and 535 desoxynojirimycin derivatives that exhibited drug-like properties screened through Lipinski filters. Virtual screening followed by binding interaction analysis we identified ten compounds that exhibited better binding energy scores compared to the standard drugs voglibose and miglitol, used in our study. The docking analysis, ADMET and metabolic site prediction estimated the best top two compounds with good drug profiles. Further, top compounds VG9 and VG15 were promoted to simulation study using the Biovia Discovery study to access the stability at a time interval of 100 ns. MD simulation results revealed that our compound VG9 possesses better conformational stability in the complex to the active site residues of Alpha-Amylase target protein than standard drug voglibose. Thus, our investigation revealed that compound VG9 also exhibits the best pharmacokinetic as well as binding affinity results and could act as a potential lead compound targeting Alpha-Amylase for Type II diabetes.

Voglibose is an α-glycosidase inhibitor that improves postprandial hyperglycemia and increases glucagon-like peptide-1 (GLP-1) secretion in patients with type 2 diabetes. Recently, there has been increasing interest in the anti-inflammatory effects of voglibose on the intestine, but the underlying mechanism is not clear. This study evaluated the effects and mechanisms of voglibose on glycemic control and intestinal inflammation. Type 2 diabetic KKAy mice were treated with voglibose (1 mg/kg) by oral gavage once daily. After 8 weeks, glucose metabolism, levels of short-chain fatty acids (SCFAs), systematic inflammatory factors, intestinal integrity and inflammation were evaluated using hematoxylin and eosin staining, immunohistochemistry, immunofluorescence and Western blot analysis. Voglibose ameliorated glucose metabolism by enhancing basal- and glucose-dependent GLP-1 secretion. Several beneficial SCFAs, such as acetic acid and propionic acid, were increased by voglibose in the fecal sample. Additionally, voglibose notably decreased the proportion of pro-inflammatory macrophages and the expression of nuclear factor kappa B but increased the expression of tight junction proteins in the ileum, thus markedly improving intestinal inflammatory damage and reducing the systematic inflammatory factors. Ileal genomics and protein validation suggested that voglibose attenuated inositol-requiring protein 1α-X-box binding protein 1-mediated endoplasmic reticulum stress (ERS). Together, these results showed that voglibose enhanced the secretion of GLP-1, which contributed to the glycemic control in KKAy mice at least in part by regulating intestinal inflammation and the expression of ERS factors.

Background/Objectives: Voglibose, an α-glucosidase inhibitor commonly prescribed to manage postprandial hyperglycemia in diabetes mellitus, demonstrates potential for repurposing as an anti-melanogenic agent. This study aims to explore the inhibitory effects of voglibose on melanogenesis and elucidate its molecular mechanisms, highlighting its possible applications in treating hyperpigmentation disorders. Methods: The anti-melanogenic effects of voglibose were investigated using B16F10 melanoma cells. Cell viability, melanin content, and tyrosinase activity were assessed following voglibose treatment. Western blot analysis was performed to examine changes in melanogenic proteins and transcription factors. The role of signaling pathways, including PKA/CREB, MAPK, PI3K/AKT, and GSK3β/β-Catenin, was analyzed. Primary human skin irritation tests were conducted to evaluate the topical safety of voglibose. Results: Voglibose significantly reduced melanin synthesis and tyrosinase activity in B16F10 cells in a dose-dependent manner. Western blot analysis revealed decreased expression of MITF, TRP-1, and TRP-2, indicating the inhibition of melanogenesis. Voglibose modulated key signaling pathways, including the suppression of PKA/CREB, MAPK, and AKT activation, while restoring GSK3β activity to inhibit β-catenin stabilization. Human skin irritation tests confirmed voglibose’s safety for topical application, showing no adverse reactions at 50 and 100 μM concentrations. Conclusions: Voglibose demonstrates anti-melanogenic properties through the modulation of multiple signaling pathways and the inhibition of melanin biosynthesis. Its safety profile and efficacy suggest its potential as a repurposed drug for managing hyperpigmentation and advancing cosmeceutical applications.

Background Type 2 Diabetes Mellitus (T2DM) is a progressive metabolic disorder marked by insulin resistance and chronic hyperglycemia. Although voglibose, an alpha-glucosidase inhibitor, is used in T2DM management, its efficacy is limited, particularly when used alone. This study aimed to investigate whether combining voglibose with ubiquinone and tempol—agents known for their antioxidant, anti-inflammatory, and insulin-sensitizing properties—could enhance therapeutic outcomes. Methods A total of 62 male Wistar Albino rats were allocated into eight experimental groups, including healthy, diabetic, and various treatment combinations. Glucose metabolism, insulin sensitivity, inflammatory markers, oxidative stress parameters, and the expression levels of GLUT4, IRS1, PIK3R1 genes, as well as histopathological alterations were systematically evaluated for over a 7-week experimental period. Results The combinations of voglibose + ubiquinone and voglibose + tempol + ubiquinone significantly enhanced insulin secretion, decreased blood glucose and HbA1c levels, and mitigated inflammatory and degenerative tissue alterations, demonstrating superior efficacy compared to voglibose alone and, in some parameters, even to the voglibose + glibenclamide combination. These combinations also restored GLUT4 and PIK3R1 gene expression in muscle tissue. Conclusion The findings support that supplementing voglibose therapy with ubiquinone and tempol enhances its antidiabetic potential and may serve as a safer and more effective strategy, particularly for patients with advanced or treatment-resistant T2DM. Further clinical research is warranted to confirm translational applicability.

Background: The strict glycaemic control postpones all the microvascular and macrovascular complications. In type 2 diabetes the initiation of metformin is the cornerstone in reducing blood sugar. The next option is either insulin or oral hypoglycaemic agents. The DPP-4 inhibitors like gliptins have the advantages of less incidence of hypoglycaemia, good safety profile and can be combined to any oral hypoglycaemics. The meta-analysis showed that teneligliptin has less adverse profile in number of Japanese and Korean studies. It was proved that the fasting glucose and postprandial glucose substantially reduced with a potential benefit of reducing cholesterol, thereby reducing the risk of cardiovascular diseases. The advantage of using this drug as is does not worsen the hepatic and renal status. Voglibose an α-glycosidase inhibitors delay the glucose absorption from GIT hence effective in reducing postprandial hyperglycaemia. Methods: This prospective randomized controlled study was designed to compare the efficacy of teneligliptin and voglibose as an add on therapy on patients with uncontrolled blood sugar in addition to metformin 500mg BD and glimepiride 2 mg OD. Totally 80 patients were included between the age groups of 40 to 70 years. Patients were divided into two groups 40 patients each, group A were given teneligliptin and group B patients were given voglibose for a period of 6 months. At the end of 3rd month and 6th month investigations were done for FBS, PPBS and HbA1c.Statisticalmethods: Data were tabulated and results were analysed by using Analysis of Variance. AP value of <0.05 was considered as statistically significant. Results: At the end ofsix months group II showed significant reduction in fasting blood sugar and post-prandial blood sugar level. A significant reduction in FBS, PPBS, HbA1c is seen in both the groups, where teneligliptin has a favourable glucose reduction along with voglibose. Conclusions: Our study concludes that teneligliptin is better than voglibose as the 2nd line add on therapy to sulphonylureas, metformin or insulin.

Peyer’s patches (PPs) are specialized gut-associated lymphoid tissues that initiate follicular helper T (Tfh)-mediated immunoglobulin A (IgA) response to luminal antigens derived from commensal symbionts, pathobionts, and dietary sources. IgA-producing B cells migrate from PPs to the small intestinal lamina propria and secrete IgA across the epithelium, modulating the ecological balance of the commensal microbiota and neutralizing pathogenic microorganisms. α-glucosidase inhibitors (α-GIs) are antidiabetic drugs that inhibit carbohydrate digestion in the small intestinal epithelium, leading to alterations in the commensal microbiota composition and metabolic activity. The commensal microbiota and IgA responses exhibit bidirectional interactions that modulate intestinal homeostasis and immunity. However, the effect of α-GIs on the intestinal IgA response remains unclear. We investigated whether α-GIs affect IgA responses by administering voglibose and acarbose to mice via drinking water. We analyzed Tfh cells, germinal center (GC) B cells, and IgA-producing B cells in PPs by flow cytometry. We also assessed pathogen-specific IgA responses. We discovered that voglibose and acarbose induced Tfh cells, GCB cells, and IgA-producing B cells in the PPs of the proximal small intestine in mice. This effect was attributed to the modification of the microbiota rather than a shortage of monosaccharides. Furthermore, voglibose enhanced secretory IgA (S-IgA) production against attenuated Salmonella Typhimurium. Our findings reveal a novel mechanism by which α-GIs augment antigen-specific IgA responses by stimulating Tfh-GCB responses in PPs, and suggest a potential therapeutic application as an adjuvant for augmenting mucosal vaccines.