Liver steatosis, the hallmark component of metabolic dysfunction-associated steatotic liver disease (MASLD), is particularly common among individuals with type 2 diabetes mellitus (T2DM). Shared mechanisms such as insulin resistance, oxidative stress, and chronic inflammation contribute to the coexistence of these conditions and accelerate disease progression, emphasizing the need for effective therapeutic strategies. In this 12-month, randomized, double-blind, placebo-controlled trial, 227 obese individuals with T2DM were assigned to receive either 1500 mg of curcumin daily or placebo. Curcumin significantly reduced liver fat content, liver stiffness, and glycated hemoglobin (HbA1c) compared with placebo (all p < 0.001). Improvements were also noted in inflammatory mediators, including interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) (all p < 0.001), reflecting curcumin’s anti-inflammatory effects. Antioxidant benefits were evident, as total antioxidant capacity (TAC), glutathione peroxidase (GPx), and superoxide dismutase (SOD) increased, while malondialdehyde levels decreased (all p < 0.001). Systematic safety assessments, including liver and kidney function tests, revealed no clinically significant abnormalities. Mild gastrointestinal discomfort was the most common non-serious adverse event. Overall, these findings support curcumin as a safe and effective adjunctive therapy for improving liver steatosis in obese patients with T2DM.

Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by insulin resistance and impaired insulin secretion, and curcumin—a polyphenolic compound derived from Curcuma longa—has shown potential anti-inflammatory and antioxidant effects. This randomized, double-blind, placebo-controlled trial evaluated the effects of 1500 mg/day curcumin supplementation for 12 months in 114 adults with T2DM, with assessments including fasting plasma glucose (FPG), glycated hemoglobin (HbA1c), insulin resistance (HOMA-IR), inflammatory cytokines (IL-6, IL-1β, TNF-α), high-sensitivity C-reactive protein (hs-CRP), neutrophil-to-lymphocyte ratio (NLR), antioxidant markers (SOD, GPx, TAS), and malondialdehyde (MDA). Curcumin supplementation was associated with significant reductions in pro-inflammatory cytokines (p < 0.001), hs-CRP and NLR (p < 0.05), and with improved antioxidant status as shown by increased TAS, SOD, and GPx together with reduced MDA levels (p < 0.001). Additionally, improvements in metabolic parameters were observed, including lower FPG (112.0 mg/dL vs. 134.5 mg/dL; p < 0.001), HbA1c (6.10% vs. 6.40%; p < 0.05), and HOMA-IR (4.88 vs. 6.71; p < 0.001). Overall, the findings suggest that long-term curcumin supplementation may contribute to improved inflammatory, antioxidant, and glycemic profiles in obese individuals with T2DM; however, further multi-center studies are needed to confirm these observations and clarify their clinical relevance.

Apolipoprotein C-III (APOC3) regulates triglyceride metabolism by inhibiting lipoprotein lipase activity and reducing the clearance of triglyceride-rich lipoproteins. We investigated the associations of APOC3 promoter polymorphisms (rs2854116 and rs2854117) with hypertriglyceridemia and metabolic dysfunction-associated steatotic liver disease (MASLD) in a Thai cohort. This cross-sectional study included 276 Thai adults from a MASLD case-control cohort. MASLD was defined using controlled attenuation parameter (CAP ≥ 248 dB/m) measured by transient elastography. APOC3 rs2854116 and rs2854117 were genotyped, and associations with hypertriglyceridemia and MASLD were evaluated using logistic regression under a prespecified additive genetic model. Sensitivity analyses stratified by and adjusted for MASLD status were performed. Exploratory haplotype analyses were also conducted. Under the additive model, rs2854116 was associated with hypertriglyceridemia in crude (OR 1.58 per T allele, 95% CI 1.08–2.33; p = 0.019) and adjusted analyses (OR 1.58, 95% CI 1.06–2.36; p = 0.025; FDR-adjusted p = 0.050), meeting the prespecified FDR threshold for the primary hypothesis family. The association remained significant after adjustment for MASLD status (OR 1.61, 95% CI 1.08–2.41; p = 0.020) and was consistent across MASLD strata (p for interaction = 0.61). The minor T allele was more frequent among participants with hypertriglyceridemia than among normotriglyceridemic controls (54.5% vs. 43.7%; OR 1.54, 95% CI 1.06–2.24; p = 0.022). Neither rs2854116 nor rs2854117 was associated with MASLD. Exploratory haplotype analyses likewise showed no consistent association with MASLD. APOC3 rs2854116 was associated with hypertriglyceridemia in this Thai cohort, supporting its role in triglyceride metabolism. In contrast, no clear evidence was found for an association between APOC3 variants and MASLD. Because the cohort was selected according to MASLD status, potential selection or collider bias cannot be excluded, and these findings require confirmation in larger, population-based Thai cohorts.