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1.
PeerJ ; 12: e17810, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-39099651

RESUMO

Background: Non-alcoholic fatty liver disease (NAFLD) is intricately linked with dietary patterns and metabolic homeostasis. Therefore, the present study focused to investigate the relation between dietary patterns and cardiometabolic risk factors related to fatty liver in NAFLD patients. Methods: This cross-sectional study included 117 individuals whose body mass index (BMI) threshold of 25 or above diagnosed with NAFLD by magnetic resonance imaging. The hospital database was used to review the patients' medical records such as lipid parameters, and fasting blood sugar. Anthropometric measurements and body composition were measured by researchers. Likewise, data from 24-h dietary recalls of individuals were collected to analyze their energy and nutrient intakes besides calculating dietary insulin index (DII), dietary insulin load (DIL), dietary glycemic index (DGI), and dietary glycemic load (DGL). Results: Participants consuming diets with distinct levels of DII, DIL, DGI, and DGL exhibited variations in dietary energy and nutrient intake. Specifically, differences were noted in carbohydrate intake across quartiles of DII, DIL, DGI, and DGL, while fructose consumption showed variability in DGL quartiles (p ≤ 0.05). Moreover, sucrose intake demonstrated distinctions in both DII and DGL quartiles (p ≤ 0.05). No statistical difference was found in biochemical parameters and the fatty liver index among different levels of DII, DIL, DGI, and DGL (p > 0.05). After adjusting for potential confounders, participants with a higher DGI had four times greater odds of developing metabolic syndrome compared to those in the bottom quartile (OR, 4.32; 95% CI [1.42-13.11]). Conclusion: This study provides initial evidence of the intricate association between dietary factors and NAFLD, emphasizing the necessity for further research including prospective designs with larger sample sizes, to garner additional insights.


Assuntos
Fatores de Risco Cardiometabólico , Dieta , Hepatopatia Gordurosa não Alcoólica , Humanos , Hepatopatia Gordurosa não Alcoólica/epidemiologia , Masculino , Feminino , Estudos Transversais , Pessoa de Meia-Idade , Adulto , Dieta/efeitos adversos , Índice Glicêmico , Índice de Massa Corporal , Carga Glicêmica , Fatores de Risco , Ingestão de Energia
2.
JHEP Rep ; 6(1): 100928, 2024 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-38089550

RESUMO

Background & Aims: Pathologists quantify liver steatosis as the fraction of lipid droplet-containing hepatocytes out of all hepatocytes, whereas the magnetic resonance-determined proton density fat fraction (PDFF) reflects the tissue triacylglycerol concentration. We investigated the linearity, agreement, and correspondence thresholds between histological steatosis and PDFF across the full clinical spectrum of liver fat content associated with non-alcoholic fatty liver disease. Methods: Using individual patient-level measurements, we conducted a systematic review and meta-analysis of studies comparing histological steatosis with PDFF determined by magnetic resonance spectroscopy or imaging in adults with suspected non-alcoholic fatty liver disease. Linearity was assessed by meta-analysis of correlation coefficients and by linear mixed modelling of pooled data, agreement by Bland-Altman analysis, and thresholds by receiver operating characteristic analysis. To explain observed differences between the methods, we used RNA-seq to determine the fraction of hepatocytes in human liver biopsies. Results: Eligible studies numbered 9 (N = 597). The relationship between PDFF and histology was predominantly linear (r = 0.85 [95% CI, 0.80-0.89]), and their values approximately coincided at 5% steatosis. Above 5% and towards higher levels of steatosis, absolute values of the methods diverged markedly, with histology exceeding PDFF by up to 3.4-fold. On average, 100% histological steatosis corresponded to a PDFF of 33.0% (29.5-36.7%). Targeting at a specificity of 90%, optimal PDFF thresholds to predict histological steatosis grades were ≥5.75% for ≥S1, ≥15.50% for ≥S2, and ≥21.35% for S3. Hepatocytes comprised 58 ± 5% of liver cells, which may partly explain the lower values of PDFF vs. histology. Conclusions: Histological steatosis and PDFF have non-perfect linearity and fundamentally different scales of measurement. Liver fat values obtained using these methods may be rendered comparable by conversion equations or threshold values. Impact and implications: Magnetic resonance-proton density fat fraction (PDFF) is increasingly being used to measure liver fat in place of the invasive liver biopsy. Understanding the relationship between PDFF and histological steatosis fraction is important for preventing misjudgement of clinical status or treatment effects in patient care. Our analysis revealed that histological steatosis fraction is often significantly higher than PDFF, and their association varies across the spectrum of fatty liver severity. These findings are particularly important for physicians and clinical researchers, who may use these data to interpret PDFF measurements in the context of histologically evaluated liver fat content.

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