Loading
Life sciences · Journal article
Cureus · October 25, 2026
No summary has been generated for this record yet. What follows is drawn from its source metadata only.
Journal article.
No findings were extractable from the material analysed.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
This record has not been graded across any dimension yet. Treat the label above as provisional and read the source.
What is missing. This record has no bottom line, key findings, reported figures, evidence dimensions. That is a gap in the analysis, not a judgement about the study.
BackgroundMetabolic dysfunction-associated steatotic liver disease (MASLD) is a common chronic liver disease associated with obesity, insulin resistance, dyslipidemia, oxidative stress, and chronic low-grade inflammation.Various proteins and gene variants are involved in the pathogenesis of MASLD; however, evidence regarding the role of DsbA-L in this disease is still limited.Therefore, this study evaluated the possible role of DsbA-L and its polymorphism at rs1917760 (-1308 G/T) in the pathogenesis of MASLD and attempted to address critical knowledge gaps regarding MASLD in the Indian population. MethodsThis was a hospital-based case-control study comprising 100 patients with MASLD and 100 healthy controls.Hepatic steatosis was assessed by abdominal USG.Blood samples were collected from the subjects, and serum was separated.Serum DsbA-L levels were quantified using a commercially available research-grade ELISA kit.DNA from MASLD cases was extracted using the QIAamp DNA Blood Mini Kit, whereas DNA from healthy controls was extracted using the phenol-chloroform method.DsbA-L rs1917760 was amplified using conventional PCR.All statistical analyses were conducted using R software and GraphPad Prism. ResultsThe mean DsbA-L level among cases was 130.86 ± 59.89 ng/mL, whereas that in the control group was 168.89 ± 60.84 ng/mL.The difference between these groups was statistically significant (p < 0.0001).Receiver operating characteristic (ROC) analysis indicated a modest discriminatory ability of DsbA-L (area under the curve (AUC) = 0.69).In univariable analysis, DsbA-L was significantly inversely associated with disease status; however, this association was no longer significant after adjusting for age, sex, and BMI (adjusted OR = 0.997, 95% CI: 0.991-1.003;p = 0.389).BMI remained independently associated with case status (adjusted OR = 1.761, 95% CI: 1.496-2.073;p < 0.001).The scatter plot demonstrated a statistically significant moderate inverse association between BMI and serum DsbA-L levels (Spearman's r = -0.43,p < 0.001).This indicates that individuals with higher BMI tended to have lower serum DsbA-L concentrations.The DsbA-L rs1917760 polymorphism exhibited the wild-type genotype (GG) in all subjects. ConclusionSerum DsbA-L levels were significantly lower in patients with MASLD and were inversely associated with BMI, suggesting a possible relationship between DsbA-L and MASLD.However, serum DsbA-L was not independently associated with the disease after adjustment for potential confounding factors.Furthermore, the DsbA-L rs1917760 polymorphism was monomorphic in our study population.