Approximately 25–50% of the population worldwide exhibits serum triglycerides (TG) (≥150 mg/dL) which are associated with an increased level of highly atherogenic remnant-like particles, non-alcoholic fatty liver disease, and pancreatitis risk. High serum TG levels could be related to cardiovascular disease, which is the most prevalent cause of mortality in Western countries. The etiology of hypertriglyceridemia (HTG) is multifactorial and can be classified as primary and secondary causes. Among the primary causes are genetic disorders. On the other hand, secondary causes of HTG comprise lifestyle factors, medical conditions, and drugs. Among lifestyle changes, adequate diets and nutrition are the initial steps to treat and prevent serum lipid alterations. Dietary intervention for HTG is recommended in order to modify the amount of macronutrients. Macronutrient distribution changes such as fat or protein, low-carbohydrate diets, and caloric restriction seem to be effective strategies in reducing TG levels. Particularly, the Mediterranean diet is the dietary pattern with the most consistent evidence for efficacy in HTG while the use of omega-3 supplements consumption is the dietary component with the highest number of randomized clinical trials (RCT) carried out with effective results on reducing TG. The aim of this review was to provide a better comprehension between human nutrition and lipid metabolism.

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.

Rheumatoid arthritis (RA) is characterized by chronic inflammation mediated by the JAK/STAT pathway. Variants in STAT4 have been associated with autoimmune susceptibility, but their functional role in RA remains unclear. The aim of this study was to genetically and functionally characterize STAT4 in RA patients with varying disease activity by analyzing two variants, mRNA expression, phosphorylated STAT4 (pSTAT4), and inflammatory cytokines (IL-12, IL-23, and IFN-γ). Sixty-three Mexican patients with RA were stratified into remission/low and moderate/high activity groups. Genotyping, STAT4 mRNA expression, pSTAT4 quantification, cytokine profiling, and treatment analyses were conducted. Patients receiving methotrexate, hydroxychloroquine, and sulfasalazine had higher IL-12 concentrations compared with those on other regimens. In remission/low activity patients, GC/GC carriers exhibited increased IL-12, PBMC levels, and anti-CCP antibodies, while GC/TT carriers in the moderate/high activity group showed distinct ESR values. Secondary analyses revealed that TT/TT carriers with STAT4 overexpression exhibited higher IFN-γ and IL-23 levels. IL-12 differences persisted among GC/GC carriers regardless of STAT4 expression status. In conclusion, these exploratory findings suggest potential interactions among STAT4 haplotypes, expression status, and treatment regimens influencing cytokine and inflammatory profiles in RA. However, due to the small subgroup sizes, the observed associations should be interpreted with caution and considered hypothesis-generating until validated in larger cohorts.