Biomolecules

Diabetic nephropathy (DN) is associated with inflammatory dysregulation and altered lipid mediators. We investigated inflammatory markers, fatty acids, and plasma pre-miR-29c in controls and type 2 diabetes mellitus (T2DM) patients stratified by albuminuria severity. This cross-sectional study included 120 T2DM patients (albumin-to-creatinine ratio, ACR: <30, 30–300, and >300 mg/g; n = 40 each) and 40 controls. TNF-α, IL-6, and lipoxin A₄ (LXA₄) were measured by ELISA; EPA, DHA, AA, and DGLA by LC–MS/MS; and plasma pre-miR-29c by semi-quantitative endpoint RT-PCR. TNF-α was higher in all T2DM groups compared with controls. LXA₄ was lower in the ACR <30 and >300 mg/g groups, while IL-6 showed no significant difference. Compared with controls, EPA was lower in both albuminuric groups, DHA was lower, and AA was higher in all T2DM groups, while DGLA remained unchanged. Plasma pre-miR-29c increased with albuminuria severity and correlated strongly with the ACR (ρ = 0.852; FDR-adjusted p < 0.001). In the final Firth model, log₂-transformed pre-miR-29c was the only variable that remained statistically associated with DN (OR = 170.692, 95% CI: 22.319–23,827.669; p < 0.001); the wide confidence interval reflects near-complete separation. These exploratory findings suggest that pre-miR-29c may serve as a candidate marker of albuminuria severity, requiring confirmation by quantitative PCR with validated normalisation in longitudinal cohorts.

Vitamin D deficiency (VDD) is highly prevalent worldwide and has been associated with chronic inflammatory and cardiovascular diseases (CVD). However, its relationship with coordinated inflammatory and cardiometabolic networks remains unclear. We studied 1075 participants classified as VDD (25(OH)D < 25 nmol/L; n = 304) or in the ≥25 nmol/L group (n = 771) based on circulating 25(OH)D levels. Body composition and plasma levels of IL-17, IL-34, activin A, follistatin, and FSTL1 were assessed; the follistatin/FSTL1 ratio (FOFS) and C-reactive protein–triglyceride–glucose index (CTI) were calculated. Detectable IL-17 and IL-34 concentrations were available for 195 and 247 participants, respectively. VDD participants exhibited higher levels of inflammatory biomarkers and a higher prevalence of hypertension (HTN), hyperlipidemia (HLD), and CVD. Multivariable analysis revealed a particularly strong independent association between IL-17 and VDD (OR = 8.36, 95% CI: 3.72–18.80). Structural equation modeling (SEM) supported an interconnected inflammatory–cardiometabolic association network, characterized by a strong association between VDD and IL-17 (β = 0.689) and significant interrelationships among IL-17, IL-34, FOFS, CTI, and cardiometabolic comorbidities. These findings identify IL-17 as a prominent inflammatory correlate of VDD and suggest that FOFS may represent a link between inflammatory activation and cardiometabolic morbidity associated with VDD.

Astragalus polysaccharides (APS) have potential as functional feed additives, but their effects on physiological and intestinal responses in geese remain incompletely characterized. A total of 432 one-day-old Taihu goslings were assigned to diets containing 0, 100, or 200 mg/kg APS, with six replicates per treatment and 24 geese per replicate. Organ indices, serum biochemical and intestinal barrier-related parameters, and intestinal length were evaluated using six independent experimental replicates per treatment (n = 6), whereas intestinal histomorphology and cecal microbiota were assessed using four biological replicates per treatment (n = 4) at each sampling age. Samples were collected at 30, 60, and 90 d, with intestinal metabolites analyzed using four biological replicates per treatment (n = 4) and jejunal mucosal metabolic indicators evaluated using six experimental replicates per treatment (n = 6) at 90 d. Compared with the control, 200 mg/kg APS increased thymus index at 30 d, serum superoxide dismutase activity at 30 and 60 d (p = 0.038 and 0.020, respectively), and jejunal and ileal villus height at 30, 60, and 90 d. APS reduced serum diamine oxidase activity at 30 d (p = 0.001), and the 200 mg/kg group remained lower at 90 d. Cecal microbial community structure differed among treatments at 30 and 60 d (PERMANOVA p = 0.047 and 0.006, respectively), whereas Shannon diversity was unchanged. At 90 d, APS altered jejunal and cecal organic acid profiles with selected responses remaining significant after Benjamini–Hochberg false discovery rate correction (q < 0.05) and increased jejunal mucosal citric acid content at 200 mg/kg. APS affected selected physiological and intestinal outcomes, with additional changes in cecal microbial community structure and intestinal metabolism, while 200 mg/kg produced the clearest changes in serum superoxide dismutase activity and intestinal morphology.