Fatty Liver Disease Patients Research Articles

Biomarkers for Assessing Non-Alcoholic Fatty Liver Disease in Patients with Type 2 Diabetes Mellitus on Sodium-Glucose Cotransporter 2 Inhibitor Therapy.

In the current modern era of unhealthy lifestyles, non-alcoholic fatty liver disease (NAFLD) is the most prevalent liver disease and has become a serious global health problem. To date, there is no approved pharmacotherapy for the treatment of NAFLD, and necessary lifestyle changes such as weight loss, diet, and exercise are usually not sufficient to manage this disease. Patients with type 2 diabetes mellitus (T2DM) have a significantly higher risk of developing NAFLD and vice versa. Sodium-glucose cotransporter 2 (SGLT2) inhibitors are antidiabetic agents that have recently been approved for two other indications: chronic kidney disease and heart failure in diabetics and non-diabetics. They are also emerging as promising new agents for NAFLD treatment, as they have shown beneficial effects on hepatic inflammation, steatosis, and fibrosis. Studies in animals have reported favorable effects of SGLT2 inhibitors, and studies in patients also found positive effects on body mass index (BMI), insulin resistance, glucose levels, liver enzymes, apoptosis, and transcription factors. There are some theories regarding how SGLT2 inhibitors affect the liver, but the exact mechanism is not yet fully understood. Therefore, biomarkers to evaluate underlying mechanisms of action of SGLT2 inhibitors on the liver have now been scrutinized to assess their potential as a future in-label therapy for NAFLD. In addition, finding suitable non-invasive biomarkers could be helpful in clinical practice for the early detection of NAFLD in patients. This is crucial for a positive disease outcome. The aim of this review is to provide an overview of the most recent findings on the effects of SGLT2 inhibitors on NAFLD biomarkers and the potential of SGLT2 inhibitors to successfully treat NAFLD.

S1338 Quality Improvement: Improving the Screening of Fatty Liver Disease in Patients with Type 2 Diabetes Mellitus

S1338 Quality Improvement: Improving the Screening of Fatty Liver Disease in Patients with Type 2 Diabetes Mellitus

Diagnosis and treatment of metabolic-associated fatty liver disease in patients with type 2 diabetes mellitus. Review

Metabolic‑associated fatty liver disease (MAFLD) is a new clinical definition of fatty liver disease that changes the definition of non‑alcoholic fatty liver disease (NAFLD) from a disease of exclusion to a disease of inclusion, in which the main pathogenic processes originate from metabolic dysfunction, primarily in type 2 diabetes mellitus (T2DM) and obesity. In recent years, MAFLD has become an epidemic and is closely associated with T2DM and a significant synergistic increase in the risk of cardiovascular disease. The presence of MAFLD significantly increases the risk of T2DM development, and the risk of new onset of T2DM in patients with MAFLD doubles. When managing patients with MAFLD and T2DM, the presence of fibrous nonalcoholic steatohepatitis (NASH) should be actively detected, for which non‑invasive indicators should first be used, such as FIB‑4 and FNI, which are available at the level of primary care. Despite evidence of utility in improving diagnosis, the effectiveness of many of the above non‑invasive tests for detecting fibrosis, particularly in unselected populations with advanced fibrosis, is low and generally remains uncertain at the primary care level. Modifications of lifestyle and diet have traditionally been considered the best therapeutic option for MAFLD in T2DM, with weight loss of ≥7% significantly improving steatosis, leading to reductions in NASH activity and glycemia. At the same time, only 40% of patients achieve this goal and reduce the activity of steatohepatitis, emphasizing the difficulty in treating MAFLD only by lifestyle changes. Nevertheless, mandatory dietary and lifestyle modification should still be recommended for patients with MAFLD, along with antidiabetic drugs that can reduce liver enzyme activity, inflammation, and fibrosis, such as PPARγ inhibitors, SGLT‑2i, GLP‑1 RA, as well as dual GIP and GLP‑1 RA agonists.

Approach to Fatty Liver Disease in Patients with Type 2 Diabetes

Type 2 diabetes is a major risk factor for development and progression of non-alcoholic fatty liver disease (NAFLD). Fatty liver is prevalent in people with type 2 diabetes, and overweight or obesity in these patients aggravates insulin resistance and steatohepatitis, which appear to be drivers for the disease progression. The goal of screening is not to identify steatosis itself, but rather to identify patients at risk for adverse hepatic outcomes such as cirrhosis, hepatocellular carcinoma, and death from liver disease. The most important risk factors for disease progression are liver fibrosis and its severity. There is a consensus that the FIB-4 (fibrosis-4 index) is the most cost-effective strategy for initial screening of hepatic fibrosis in a clinical setting. At present, there are no approved drugs for the treatment of NAFLD. Clinically significant improvements in NAFLD are achieved with weight loss. Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) and sodium glucose cotransporter 2 (SGLT2) inhibitors are effective for inducing weight loss in patients with type 2 diabetes, and some GLP-1 RAs and SGLT2 inhibitors have been shown to be effective for treating steatohepatitis. Therefore, GLP-1 RAs and SGLT2 inhibitors should be considered when choosing antidiabetic agents in patients with type 2 diabetes and NAFLD, especially in those who are overweight or obese.

Assessment of Non-Alcoholic Fatty Liver Disease as Risk Factor for Cardiovascular Disease

Objectives: Non-alcoholic fatty liver disease (NAFLD) is increasing in prevalence during present obesity pandemic. More than 25% of persons globally are believed to have non-alcoholic fatty liver disease. Many reports claim that there is an increased risk of atherosclerotic cardiovascular disease (ASCVD) among patients with non-alcoholic fatty liver disease. NAFLD is a silent disease in initial stages but progress to severe hepatic disease and increases cardiovascular morbidity in later stages, so identification and management of NAFLD are of paramount importance in preventive aspect of cardiovascular disease (CVD). Hence, the aim of this present study is to assess the risk of CVD in patients with non-alcoholic fatty liver disease in patients with and without diabetes and to evaluate usefulness of non-alcoholic fatty liver disease as a risk factor for CVD. Materials and Methods: The present study is a single-center observational study and it included 81 patients with non-alcoholic fatty liver disease. Results: In these patients, cardiovascular risk is assessed by ASCVD score, PROCAM score, QRISK 3 score, and atherogenic index of plasma and compared between diabetic and non-diabetic population. The difference has been found between diabetic and non-diabetic in Procom_score, ASCVD_score, and Q-risk_score but not found in AIP_score. Conclusion: The outcome of this study is that there is an increased risk of cardio vascular disease in patients with non-alcoholic fatty liver disease and risk is further increased in patients with coexisting diabetes mellitus and NAFLD.

The Effects of Ginger (Zingiber Officinale Roscoe) on Non-Alcoholic Fatty Liver Disease in Patients with Type 2 Diabetes Mellitus: A Randomized Double-Blinded Placebo-Controlled Clinical Trial

Nonalcoholic fatty liver disease (NAFLD) is a prominent etiological factor for liver cirrhosis worldwide. It is frequently associated with obesity, diabetes, dyslipidemia, and hypertension. The objective of this study is to assess the efficacy and safety of ginger (Zingiber officinale Roscoe) supplementation in patients with type 2 diabetes mellitus (T2DM) who have NAFLD. In a two-arm, double-blind, placebo-controlled clinical trial, seventy-six patients diagnosed with both T2DM and NAFLD were randomly assigned to receive either ginger powder capsules (1000 mg, twice daily) or placebo capsules (administered in the same manner) for a period of three months. Anthropometric measurements, blood pressure readings, biochemical profiles, and imaging parameters were assessed before and after the intervention. Safety measures were also evaluated. In both the ginger and placebo groups, there was a significant reduction in mean body mass index (BMI), waist and hip circumferences, as well as liver transaminase levels. Moreover, significant improvements in mean systolic and diastolic blood pressures were observed in the ginger group (p = 0.02 and < 0.0001, respectively). Within the ginger group, there was a decrease in serum insulin levels and insulin resistance (HOMA-IR) (p = 0.002 and 0.004, respectively). Furthermore, the ginger group exhibited an improvement in serum HDL-cholesterol level (p = 0.01). However, there were no significant changes in the assessed inflammatory markers or the indices obtained from fibroscan imaging, including steatosis percent and controlled attenuation parameter. This study demonstrates that ginger supplementation can significantly improve mean systolic and diastolic blood pressures. However, it does not have a significant impact on inflammatory markers or fibroscan imaging indices. Nonetheless, the three-month use of ginger improves serum insulin level, insulin resistance (HOMA-IR), and HDL-cholesterol level compared to baseline values. Further investigations with longer durations and larger sample sizes are recommended.

Hepatic T-cell senescence and exhaustion are implicated in the progression of fatty liver disease in patients with type 2 diabetes and mouse model with nonalcoholic steatohepatitis

Immunosenescence and exhaustion are involved in the development and progression of type 2 diabetes (T2D) and metabolic liver diseases, including fatty liver, fibrosis, and cirrhosis, in humans. However, the relationships of the senescence and exhaustion of T cells with insulin resistance-associated liver diseases remain incompletely understood. To better define the relationship of T2D with nonalcoholic fatty liver disease, 59 patients (mean age 58.7 ± 11.0 years; 47.5% male) with T2D were studied. To characterize their systemic immunophenotypes, peripheral blood mononuclear cells were analyzed using flow cytometry. Magnetic resonance imaging (MRI)-based proton density fat fraction and MRI-based elastography were performed using an open-bore, vertical-field 3.0 T scanner to quantify liver fat and fibrosis, respectively. The participants with insulin resistance had a significantly larger population of CD28 − CD57+ senescent T cells among the CD4+ and CD8 + T cells than those with lower Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) values. The abundances of senescent CD4+ and CD8 + T cells and the HOMA-IR positively correlated with the severity of liver fibrosis, assessed using MRI-based elastography. Interleukin 15 from hepatic monocytes was found to be an inducer of bystander activation of T cells, which is associated with progression of liver disease in the participants with T2D. Furthermore, high expression of genes related to senescence and exhaustion was identified in CD4+ and CD8 + T cells from the participants with nonalcoholic steatohepatitis or liver cirrhosis. Finally, we have also demonstrated that hepatic T-cell senescence and exhaustion are induced in a diet or chemical-induced mouse model with nonalcoholic steatohepatitis. In conclusion, we have shown that T-cell senescence is associated with insulin resistance and metabolic liver disease in patients with T2D.

Association between the Triglyceride–Glucose Index and Non-Alcoholic Fatty Liver Disease in patients with Atrial Fibrillation

BackgroundThe triglyceride and glucose index (TyG), as a surrogate of insulin resistance (IR), is closely associated with non-alcoholic fatty liver disease (NAFLD). However, the association between the TyG index and NAFLD in atrial fibrillation (AF) is unknown. Therefore, the purpose of this study is to explore the association between the TyG index and NAFLD in AF.MethodsThis retrospective study was performed at Nanchang University’s Second Affiliated Hospital. The AF patients who were hospitalized from January 2021 to December 2022 were enrolled. The association between the TyG index and NAFLD in AF patients was assessed by logistic regression and restricted cubic spline analysis. The ability of TyG index for identifying NAFLD was estimated by the area under the receiver operating characteristic (ROC).ResultsIn this study, 632 people participated in the final analysis, with 176 (27.84%) having NAFLD. In the full adjustment model, there is an association between the TyG index and NAFLD [per 1 unit increment; odds ratios (ORs): 3.28; 95% confidence interval (CI) 2.14, 5.03]. Compared to the lowest tertile (TyG index < 8.29), the ORs for the highest tertile (TyG index ≥ 8.82) were 4.15 (95%CI: 2.28, 7.53). Dose–response analysis showed that the TyG index and NAFLD have a nearly linear relationship (P non-linear = 0.71). The area under the curve (AUC) of the TyG index is 0.735.ConclusionsOur findings showed a significant association between the TyG index and NAFLD. The TyG index may be a good marker for predicting NAFLD in AF patients.

Level of IL-6 and IL-8 and their associations with non-alcoholic fatty liver disease in patients with type 2 diabetes

non-alcoholic fatty liver disease (NAFLD) is indicated by the accumulation of lipids within the hepatocytes exceeding 5% of liver weight without excessive alcohol intake and secondary liver diseases. The efforts of many scientists worldwide are focused on improving the understanding of pathogenic processes and triggers of NAFLD progression, with an emphasis on the simultaneous study of several pathophysiological pathways to identify disorders throughout the disease spectrum. The aim was to examine the serum levels of IL-6 and IL-8 and its associative relationships with anthropometric parameters and metabolic profiles in patients with T2D, depending on the presence of NAFLD. This cross-sectional study involved 375 patients aged 40–80 with type 2 diabetes. They were divided into 3 groups. The control group included 98 T2D patients without NAFLD. The main group included T2D patients with NAFLD, which was separated into two subgroups depending on the level of transaminases: normal (group 2A, n=150) and increased (group 2B, n=127) transaminases group. In order to identify predictors of rapid progression of liver fibrosis in patients with T2D, a sub-analysis was conducted, which included 82 patients from group 2. We found significant relationships between the level of studied interleukins and the components of the metabolic syndrome. Both IL-6 and Il-8 levels are significantly associated with gender, duration and severity of T2D, BMI, ALT, AST and total bilirubin level in a simple logistic regression analysis. However, step-by-step multiple logistic regression analysis revealed no reliable link between both cytokines and NAFLD development. From the other hand elevated IL-8 and decreased IL-6 had a significant effect on the fibrosis progression in patients with NAFLD associated with T2D. Our study has demonstrated significant links between the level of IL-6 and IL-8 and the components of the metabolic syndrome such as obesity or transaminase activity, but not with NAFLD itself.

Frequency of Non-Alcoholic Fatty Liver Disease in Adults with Diabetes Mellitus

Objective: To compare the frequency of non-alcoholic fatty liver disease in patients with diabetes of different age groups, body mass indexes and duration of diabetes.&#x0D; Study Design: Comparative cross-sectional study.&#x0D; Place and Duration of Study: Department of General Medicine, Combined Military Hospital, Quetta Pakistan, from Jun to Nov 2019.&#x0D; Methodology: One hundred thirty-two patients of either gender with diabetes for more than one year were included. All patients underwent ultrasound to scan for fatty liver, and a consultant radiologist confirmed the findings. Non-alcoholic fatty liver disease was diagnosed as per operational definition.&#x0D; Results: Of the total 132, 89(67.5%) were males, and 43(32.5%) were females. The mean age of the patients was 49.34±5.76 years. The mean weight of the patients was 72.91±13.40 Kg, the mean height was 1.56±0.09 meters, and 6.35±2.99 years was the mean duration of diabetes. Most patients were 46-60 years (78.8%). NAFLD was seen in 58.5% of patients with diabetes with female preponderance.&#x0D; Conclusion: Non-alcoholic fatty liver disease was found to be more frequent in patients of the age group 46-60 years, and also it has a strong correlation with body mass index of &gt;25 kg/m2 and longer duration of diabetes. A significant proportion of patients with diabetes were also found to have ‘lean non-alcoholic fatty liver disease.

Analysis of genetic factors associated with fatty liver disease-related hepatocellular carcinoma.

Single-nucleotide polymorphisms (SNPs) in PNPLA3 and hydroxysteroid 17-beta dehydrogenase 13 (HSD17B13) genes are associated with fatty liver disease (FLD) progression and carcinogenesis. In the present study, we evaluated the characteristics of Japanese FLD patients according to HSD17B13 polymorphisms. We enrolled 402 patients who were clinically and pathologically diagnosed with FLD (alcoholic: 63 cases, nonalcoholic: 339 cases) at our hospital in 1990-2018 (228 males; median age: 54.9 [14.6-83.6] years). FLD patients with HSD17B13 A/A (212 cases) and others (A/AA or AA/AA; 190 cases) were compared. Compared to patients with HSD17B13 A/A and others, those with the A/A genotype showed increased incidence of hepatocellular carcinoma (HCC) (A/A vs. others; 18.4% vs. 9.5%, p = 0.01), cardiovascular diseases (14.2% vs. 4.2%, p < 0.01), and hypertension (56.6% vs. 47.4%, p = 0.06). In patients without A/A, the HCC incidence was significantly reduced in those with alcohol-related FLD, fibrosis-4 index <2.67, and the PNPLA3 CC genotype; however, there was no significant difference in nonalcoholic-FLD. Patients without HSD17B13 A/A showed severe steatosis (77% vs. 88.6%, p < 0.01). New HCC developed in 11 cases and the 5-year incidence rate of HCC was 3.3% in patients with both PNPLA3 GG/GC and HSD17B13 A/A, which was significantly higher than the rate for those with other SNP profiles (0.6%, p = 0.03). Inhibiting HSD17B13 activity may prevent HCC development, particularly in alcohol-related FLD and low-risk patients. Therefore, combinations of SNPs and other risk factors can be used for screening FLD-HCC.

Nonalcoholic Fatty Liver Disease in Patients with Type 2 Diabetes: Screening, Diagnosis, and Treatment.

Nonalcoholic fatty liver disease (NAFLD), recently renamed metabolic dysfunction-associated steatotic liver disease (MASLD) affects ~70% of patients with type 2 diabetes (T2D), with ~20% showing signs of advanced liver fibrosis. Patients with T2D are at an increased risk of developing cirrhosis, liver failure, and hepatocellular carcinoma and their liver-related mortality is doubled compared with non-diabetic individuals. Nonetheless, the condition is frequently overlooked and disease awareness is limited both among patients and among physicians. Given recent epidemiological evidence, clinical practice guidelines recommend screening for NAFLD/MASLD and advanced liver fibrosis in patients with T2D. While many drugs are currently being tested for the treatment of NAFLD/MASLD, none of them have yet received formal approval from regulatory agencies. However, several classes of antidiabetic drugs (namely pioglitazone, sodium-glucose transporter 2 inhibitors, glucagon-like peptide 1 receptor agonists, and multi-agonists) have shown favorable effects in terms of liver enzymes, liver fat content and, in some occasions, on histologic features such as inflammation and fibrosis. Therefore, diabetologists have the opportunity to actively treat NAFLD/MASLD, with a concrete possibility of changing the natural history of the disease. In the present narrative review, we summarize evidence and clinical recommendations for NAFLD/MAFLD screening in the setting of T2D, as well as on the effect of currently available glucose-lowering drugs on hepatic endpoints.

Association between dietary glycemic index and non-alcoholic fatty liver disease in patients with type 2 diabetes mellitus.

Managing dietary glycemic index (GI) deserves further attention in the interplay between non-alcoholic fatty liver disease (NAFLD) and type 2 diabetes mellitus (T2DM). This study aimed to evaluate the relationship between dietary GI and the odds of NAFLD in patients with T2DM. A cross-sectional study was carried out between April 2021 and February 2022, including 200 participants with T2DM aged 18-70 years, of which 133 had NAFLD and 67 were in the non-NAFLD group. Cardiometabolic parameters were analyzed using standard biochemical kits and dietary intake was assessed using a validated food frequency questionnaire. Binary logistic regression was applied to explore odds ratios (ORs) and 95% confidence intervals (CIs) for NAFLD according to tertiles of dietary GI. Highest vs. lowest tertile (< 57 vs. > 60.89) of energy-adjusted GI was not associated with the odds of having NAFLD (OR 1.25, 95% CI = 0.6-2.57; P-trend = 0.54) in the crude model. However, there was an OR of 3.24 (95% CI = 1.03-10.15) accompanied by a significant trend (P-trend = 0.04) after full control for potential confounders (age, gender, smoking status, duration of diabetes, physical activity, waist circumference, HbA1c, triglycerides, total cholesterol, dietary intake of total carbohydrates, simple carbohydrates, fat, and protein). High dietary GI is associated with increased odds of NAFLD in subjects with T2DM. However, interventional and longitudinal cohort studies are required to confirm these findings.

Plasma Heparin Cofactor II Activity Is Inversely Associated with Hepatic Fibrosis of Non-Alcoholic Fatty Liver Disease in Patients with Type 2 Diabetes Mellitus.

Thrombin exerts various pathophysiological functions by activating protease-activated receptors (PARs), and thrombin-induced activation of PARs promotes the development of non-alcoholic fatty liver disease (NAFLD). Since heparin cofactor II (HCII) specifically inactivates thrombin action, we hypothesized that plasma HCII activity correlates with the severity of NAFLD. A cross-sectional study was conducted. Plasma HCII activity and noninvasive clinical markers of hepatic fibrosis including fibrosis-4 (FIB-4) index, NAFLD fibrosis score (NFS) and aspartate aminotransferase-to-platelet ratio index (APRI) were determined in 305 Japanese patients with type 2 diabetes mellitus (T2DM). The relationships between plasma HCII activity and the clinical markers were statistically evaluated. Multiple regression analysis including confounding factors showed that plasma HCII activity independently contributed to decreases in FIB-4 index (p＜0.001), NFS (p＜0.001) and APRI (p=0.004). In addition, logistic regression analysis for the prevalence of advanced hepatic fibrosis defined by the cutoff points of the clinical scores showed that plasma HCII activity was the sole and common negative factor for prevalence of advanced hepatic fibrosis (FIB-4 index: p=0.002, NFS: p=0.026 and APRI: p=0.012). Plasma HCII activity was inversely associated with clinical hepatic fibrosis indices including FIB-4 index, NFS and APRI and with the prevalence of advanced hepatic fibrosis in patients with T2DM. The results suggest that HCII can serve as a novel biomarker for assessment of hepatic fibrosis of NAFLD in patients with T2DM.

LINC01705 derived from adipocyte exosomes regulates hepatocyte lipid accumulation via an miR-552-3p/LXR axis.

High glucose increases the accumulation of lipid droplets in hepatocytes, which eventually results in nonalcoholic fatty liver disease in patients with diabetes. However, the specific mechanism or communication between adipocyte and hepatocyte lipid metabolism is still ambiguous. In this study, exosomes released from human adipocytes were isolated and identified by their morphology, size, and marker proteins by using transmission electron microscopy (TEM), nanoparticle tracking analysis (NTA), and western blotting (WB). Gene expression was detected by qRT-PCR and WB. Lipid accumulation was determined by oil red O staining and analyses of total cholesterol (TC) and triglyceride (TG) content. Our results showed that co-culture of HepG2 cells with adipocytes under high glucose conditions stimulated lipid deposition and LINC01705 expression in the HepG2 cells. Exosomes extracted from adipocytes cultured under high glucose conditions had higher levels of LINC01705 than exosomes extracted from adipocytes cultured under normal glucose conditions. Moreover, LINC01705 expression was also elevated in exosomes extracted from diabetes patients when compared with exosomes isolated from normal volunteers, and exosomes from patients who had diabetes complicated with fatty liver (DCFL) had the highest levels of LINC01705 expression. Treatment of HepG2 cells with exosomes extracted from high glucose-stimulated adipocytes promoted lipid deposition and LINC01705 expression in HepG2 cells. Further experiments showed that overexpression of LINC01705 promoted HepG2 lipid metabolism, while inhibition of LINC01705 had the opposite effect. Mechanistically, LINC01705 competitively bound to miR-552-3p, and treatment with miR-552-3p inhibitor reversed the effects induced by LINC01705 knockdown. Moreover, miR-552-3p was found to regulate the transcription activity of LXRα and thereby modulate lipid metabolism-related gene expression. When taken together, our findings showed that high glucose increased the LINC01705 levels in adipocyte exosomes, and thereby improved HepG2 lipid accumulation via an miR-552-3p/LXR axis.

Plasma Osteopontin Level and Nonalcoholic Fatty Liver Disease in Patients with Type 2 Diabetes Mellitus

Plasma Osteopontin Level and Nonalcoholic Fatty Liver Disease in Patients with Type 2 Diabetes Mellitus

Steroid Use and Risk of Nonalcoholic Fatty Liver Disease in Patients With Inflammatory Bowel Disease: Systematic Review and Meta-analysis.

We sought to evaluate the association of steroids with nonalcoholic fatty liver disease (NAFLD) among patients with inflammatory bowel disease (IBD). Patients with IBD are at increased risk of NAFLD. Steroids may have a role in the pathogenesis of NAFLD. We searched MEDLINE (through PubMed) and Embase for studies from inception to July 2021. We included published interventional and observational studies of adults 18 years or older with ulcerative colitis or Crohn's disease. We reported odds ratios, 95% confidence intervals, and generated forest plots. A random effects model generated a summary effect estimate. Publication bias was assessed by funnel plot and Egger's test. Study quality was examined using modified Newcastle-Ottawa scale (NOS) and Agency for Healthcare Research and Quality (AHRQ). A total of 12 observational studies with 3497 participants were included. NAFLD was identified in 1017 (29.1%) patients. The pooled odds ratio for the development of NAFLD in steroid users versus non-users was 0.87 (95% confidence interval: 0.72-1.04). There was no significant heterogeneity between studies (I²=0.00%, P=0.13). No publication bias was detected by funnel plot or Egger's test (P=0.24). Findings were consistent among subgroup analyses stratified by study quality. In this meta-analysis, steroids were not associated with NAFLD in patients with IBD. Steroids may not need to be withheld from patients with IBD for the purposes of preventing NAFLD. Additional prospective studies that systematically document steroid exposure and important confounders among patients with IBD are warranted.

On dual-energy X-ray absorbtiometry use in patients with metabolic syndrome and associated fatty liver disease

Objective. To demonstrate the possibilities of using dual-energy X-ray absorptiometry in the ‘Whole-Body’ mode in the algorithm for diagnosing and monitoring metabolically associated fatty liver disease in patients with metabolic syndrome.Material and methods. All patients were examined according to a single diagnostic algorithm, consisting of a physical examination with anthropometry, dual-energy X-ray absorptiometry in the ‘Whole-Body’ mode and quantitative ultrasound steatometry. In addition to the main study group (n = 118), two control groups were recruited: the first with an increased body mass index, but without signs of metabolically associated fatty liver disease (n = 101), the second with a normal body mass index, without signs of liver damage (n = 84).Results. In a larger number of patients with confirmed metabolically associated fatty liver disease, according to clinical, laboratory and instrumental data, a predominance of visceral adipose tissue over subcutaneous adipose tissue was observed (compared to patients without confirmed metabolically associated fatty liver disease). At the same time, the percentage of fat in patients of the main study group and control group No. 1 is within the normal range of age intervals. Quantitative ultrasound steatometry data have a high correlation with data describing the components of the metabolic syndrome according to dual-energy X-ray absorptiometry in the ‘Whole-Body’ mode with a direct relationship.Conclusion. Dual-energy X-ray absorptiometry in the ‘Whole-Body’ mode can be used both for screening and for diagnosing the components of the metabolic syndrome due to high information content and minimal radiation exposure. Patients in whom visceral subcutaneous tissue predominates over subcutaneous adipose tissue are at greater risk of developing metabolically associated fatty liver disease. Quantitative ultrasound steatometry complements the picture of diffuse liver changes in patients with metabolic syndrome.

1565-P: Relationship between Glycemic Control, Body Weight, and Nonalcoholic Fatty Liver Disease in Patients with Type 1 Diabetes

Increased body weight is a common risk factor for nonalcoholic fatty liver disease (NAFLD). Although the prevalence of overweight and obesity among patients with type 1 diabetes (T1D) is rising, most patients are still lean. Currently, little is known about the relationship between glycemic parameters, body weight and NAFLD in patients with T1D. In this study, we evaluated glycemic parameters in 200 participants with T1D (mean age 46.9±16.5 years, 55.5% females, mean diabetes duration 27.4±15.7 years, mean BMI 26.9±5.0 kg/m2) who underwent screening for NAFLD. We used transient elastography to measure controlled attenuation parameter (CAP) as an indicator of hepatic steatosis, and liver stiffness measurement (LSM) as an indicator of hepatic fibrosis. We assessed glycemic parameters by measuring A1C and collecting 3 months of continuous glucose monitoring (CGM) data. CAP score was found to be positively correlated with A1C (p=0.009) and BMI (p&amp;lt;0.001). Participants with NAFLD (CAP≥274 dB/m) had significantly higher A1C (p=0.025). Using CGM parameters, CAP positively correlated with average blood glucose (p=0.029) and Glucose Management Indicator (GMI) (p=0.008). CAP positively correlated with coefficient of glucose variability (CV) only in lean individuals (BMI≤25 kg/m2) (p=0.031), suggesting a link between blood glucose variability and hepatic steatosis in the absence of overweight or obesity. LSM score positively correlated with BMI (p&amp;lt;0.001), but not with A1C or CGM parameters. We conclude that poor glycemic control is associated with hepatic steatosis while high BMI is associated with increased risk of hepatic fibrosis in patients with T1D. Blood glucose variability is particularly associated with hepatic steatosis in lean patients with T1D. These results may suggest the need of evaluating uncontrolled patients with T1D for NAFLD, specifically those with high BMI and those with high glucose variability. Disclosure S.E.Dhaver: None. T.Salah: None. M.Al-badri: None. K.Kibaa: None. A.Khater: None. R.Mccarragher: None. F.Al-roomi: None. L.Demattos: None. O.Hamdy: Advisory Panel; Abbott Nutrition, Nemaura Medical, L-Nutra Inc., Twin Health, Consultant; Sanofi, Research Support; Novo Nordisk, Eli Lilly and Company, Gilead Sciences, Inc., Stock/Shareholder; Healthimation.

The Effect of Laparoscopic Sleeve Gastrectomy on the Course of Non-Alcoholic Fatty Liver Disease in Morbidly Obese Patients during One Year of Follow Up.

Morbid obesity co-exists with non-alcoholic fatty liver disease in up to 90% of cases. Laparoscopic sleeve gastrectomy leads to a reduction in body mass and thus may improve the course of non-alcoholic fatty liver disease. The aim of this study was to evaluate the effect of laparoscopic sleeve gastrectomy on the resolution of non-alcoholic fatty liver disease. The study included 55 patients with non-alcoholic fatty liver disease who underwent laparoscopic sleeve gastrectomy at a tertiary institution. The analysis consisted of preoperative liver biopsy, abdominal ultrasound, weight loss parameters, Non-Alcoholic Fatty Liver Fibrosis Score and selected laboratory parameters. Before the surgery, 6 patients were diagnosed with grade 1 liver steatosis, 33 patients with grade 2 and 16 patients with grade 3. One year after the surgery, only 21 patients had features of liver steatosis at ultrasound. All weight loss parameters showed statistically significant changes during the observation; the median percentage of total weight loss was 31.0% (IQR: 27.5; 34.5) with p = 0.0003, the median percentage of excess weight loss was 61.8% (IQR: 52.4; 72.3) with p = 0.0013 and the median percentage of excess body mass index loss was 71.0% (IQR: 61.3; 86.9) with p = 0.0036 12 months after laparoscopic sleeve gastrectomy. The median Non-Alcoholic Fatty Liver Fibrosis Score at baseline was 0.2 (IQR: -0.8; 1.0) and decreased to -1.6 (IQR: -2.4; -0.4) (p < 0.0001). Moderate negative correlations between Non-Alcoholic Fatty Liver Fibrosis Score and percentage of total weight loss (r = -0.434, p < 0.0001), percentage of excess weight loss (r = -0.456, p < 0.0001) and percentage of excess body mass index loss (r = -0.512, p < 0.0001) were found. The study supports the thesis that laparoscopic sleeve gastrectomy is an effective method for treatment of non-alcoholic fatty liver disease in patients with morbid obesity.