Nutrients

Vitamin D₃ is a fat-soluble steroid essential for bone metabolism, immune modulation, and inflammation control, all critical for periodontal health. Its active form, 1,25-dihydroxyvitamin D₃, binds to the vitamin D receptor (VDR) in periodontal cells, including periodontal ligament stromal cells, fibroblasts, osteoblasts, and macrophages, enhancing osteogenesis, antimicrobial defenses, and anti-inflammatory responses. Clinical and experimental evidence demonstrates that adequate systemic vitamin D₃ levels and local activation in gingival tissues improve outcomes of nonsurgical and surgical periodontal therapies, reducing probing pocket depth (PPD), clinical attachment loss (CAL), and gingival inflammation. Dose-dependent supplementation shows greater clinical efficacy, and emerging evidence supports potential topical applications. This review integrates molecular mechanisms with clinical findings, highlighting the therapeutic potential of vitamin D₃ in periodontal disease management.

Background/Objectives: Conventional pharmacotherapy for the most prevalent human diseases still has limited efficacy. Natural medicines are recognized for their therapeutic efficacy and low side effects. Tamarindus indica is a tropical tree of the Fabaceae family, valued for its multiple uses and the nutritional properties of its fruits. The purpose of this review is to provide an overview of the nutraceutical value of T. indica, focusing on its phytochemical composition and main health benefits. Methods: For this purpose, a bibliography search was performed in PubMed, Scopus, and ScienceDirect databases, including all articles published between 2000 and December 2025. Results: The T. indica fruit contains different phytochemical compounds, such as flavonoids, tannins, alkaloids, and saponins, with therapeutic potential. These compounds exert free radical scavenging activity, improve antioxidant and detoxification enzyme activities, exert antimicrobial effects, attenuate the activation of pro-inflammatory mediators, and regulate the expression of lipid metabolism genes. Conclusions: This article presents an integrated analysis summarizing the phytochemical characteristics, mode of action, medical utility, and safe use of T. indica, thereby contributing to a greater understanding of its potential health benefits.

Objective: This study investigated the effects of different doses and timing of sulforaphane (SFN) supplementation on reducing obesity induced by a high-glycemic-index diet (HGID) and on correcting poor glycemic control and dyslipidemia in C57BL/6 mice. Method: For 15 weeks, mice were administered a control diet (control), HGID, HGID + oral 5 mg/kg/day SFN (HGID + LSFN), or HGID + 20 mg/kg/day SFN (HGID + HSFN), and following 15 weeks of HGID, mice were treated with 5 mg/kg/day SFN (PO-HGID + LSFN) or 20 mg/kg/day SFN (PO-HGID + HSFN) for 5 weeks. Results: SFN reduced body weight gain and serum glucose. The lowest levels of HbA1c were observed in the control and HGID + LSFN groups. Mice in the HGID group exhibited impaired glucose clearance and were less sensitive to insulin compared to the control. A remarkable improvement in glucose and insulin tolerance was observed in both PO-HGID + SFN and HGID + SFN groups. Lipid profile parameters and serum insulin levels were found to be lower in the control and HGID + SFN groups compared to the HGID group. SFN increased serum adiponectin levels when administered concurrently with HGID. IRS1 and IRS2 levels were highest in the control and HGID + LSFN groups, and high-dose SFN supplementation suppressed IRS1 independently of timing. Exposure to HGID downregulated the expression of PGC-1α and sirtuins. SIRT1 and SIRT3 gene expressions showed a significant increase at both doses, whereas SIRT2 gene expression increased significantly only at 5 mg/kg/day SFN. FASN expression was upregulated in all HGID-fed groups with or without SFN intervention. Conclusions: SFN may reverse the adverse effects of HGID in a time- and dose-dependent manner by regulating postprandial insulin, inhibiting gluconeogenesis, and enhancing fatty acid oxidation through the activation of sirtuins and PGC-1α.