Inflammation, oxidative stress, and metabolic diseases are intricately linked in a complex, self-reinforcing relationship. Inflammation can induce oxidative stress, while oxidative stress can trigger inflammatory responses, creating a cycle that contributes to the development and progression of metabolic disorders; in addition, these effects can be observed at systemic and local scales. Both processes lead to cellular damage, mitochondrial dysfunction, and insulin resistance, particularly affecting adipose tissue, the liver, muscles, and the gastrointestinal tract. This results in impaired metabolic function and energy production, contributing to conditions such as type 2 diabetes, obesity, and metabolic syndrome. Legumes are a good source of phenolic compounds and anthocyanins that exert an antioxidant effect—they directly neutralize reactive oxygen species and free radicals, reducing oxidative stress. In vivo, in vitro, and clinical trial studies demonstrate that these compounds can modulate key cellular signaling pathways involved in inflammation and metabolism, improving insulin sensitivity and regulating lipid and glucose metabolism. They also exert anti-inflammatory effects by inhibiting proinflammatory enzymes and cytokines. Additionally, anthocyanins and phenolics may positively influence the gut microbiome, indirectly affecting metabolism and inflammation.

Background/Objectives: Obesity in young adults is a major public health concern and a key contributor to cardiometabolic risk. Vitamin K2 (VK2) has been proposed as a potential adjuvant therapy; however, evidence from randomized controlled trials remains limited. This study evaluated the effect of VK2 supplementation on cardiometabolic risk factors in young adults with overweight or obesity. Methods: In this 12-week randomized, double-blind, placebo-controlled trial (NCT05995522), men and women aged 18–35 years with overweight or obesity (BMI 25–40 kg/m²) were assigned to receive VK2 (menaquinone-4, 100 µg/day) or placebo. Both groups received standardized nutritional counseling. Body composition, blood pressure, glucose homeostasis, lipid profile, and vitamin K-dependent proteins were assessed at baseline and post-intervention. Between-group differences were analyzed using ANCOVA adjusted for baseline values. Results: Forty-six participants completed the study (placebo n = 24; VK2 n = 22). VK2 supplementation significantly reduced total cholesterol (−10.64 mg/dL, p = 0.038) and LDL cholesterol (−6.12 mg/dL, p = 0.005) compared with placebo. A reduction in systolic blood pressure showed a trend toward significance (−5.56 mm Hg, p = 0.067). No significant effects were observed on body composition, glucose metabolism, or vitamin K-dependent proteins. Conclusions: VK2 supplementation resulted in improvements in total and LDL cholesterol levels, with no significant changes in vitamin K-dependent proteins, and may represent a safe and potentially beneficial adjunct to nutritional strategies aimed at early cardiometabolic risk modulation.