scholarly journals Metabolic Syndrome (MetS) as a Predictor of Fatty Liver in HIV Infected Adults from the Miami Adult Studies on HIV (MASH) Cohort (FS12-06-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Colby Teeman ◽  
Yongjun Huang ◽  
Qingyun Liu ◽  
Jacqueline Hernandez ◽  
Javier Tamargo ◽  
...  

Abstract Objectives One of the major comorbidities among people living with HIV (PLWH) is liver disease. MetS is common in this population and may also play a role in the development of liver disease. In order to better understand the mechanisms of liver disease in PLWH, it is important to investigate the relationship between components of MetS and the risk of fatty liver, an early precursor to liver disease. The objective of this study was to determine if the 5 criteria used to diagnose MetS contribute to liver steatosis. Methods Crossectional analyses of data from the MASH cohort were analyzed. Waist circumference (WC) and blood pressure (BP) were measured by a research nurse. Serum triglycerides (TRG), glucose (GLU), and HDL were determined in fasting by LabCorp. Liver fat % was estimated with proton density fat fraction using Magnetic Resonance Elastography conducted on a 3T Siemens MAGNETOM Prisma MRI. Liver fat >5% was defined as stage 1 steatosis. Components of MetS were taken from the NCEP ATP III definition of MetS. Spearman correlations and logistic regression were used for analyses. Results A total of 324 PLWH aged 53.5 ± 7.5 years were included. Liver fat% was correlated with WC (r = 0.394, P < 0.001), TRG (r = 0.332, P < 0.001), GLU (r = 0.358, P < 0.001), and systolic BP (r = 0.183, P = 0.011), inversely correlated with HDL (r = −0.236, P = 0.001), and trended toward significance with diastolic BP (r = 0.133, P = 0.065). Participants with stage 1 steatosis had a larger WC (41.02in ± 5.3 vs 36.95 ± 5.5, P = 0.001), higher TRG (210.3 mg/dL ± 173.9 vs 121.3 ± 67.9, P = 0.002), and higher GLU (126.1 mg/dL ± 77.7 vs 93.92 ± 50.8, P = 0.001) than those without steatosis. No significant difference was found for HDL cholesterol, SBP, or DBP. A logistic regression model that included all 5 MetS criteria and was controlled for age, gender, and alcohol AUDIT score >8 found that WC (OR 1.11, 95% CI 1.01–1.23, P = 0.030), TRG (OR 1.01, 95% CI 1.00–1.01, P = 0.040), and GLU (OR 1.01, 95% CI 1.00–1.03, P = 0.033) are significant predictors of stage 1 steatosis. Conclusions WC, TRG, and GLU, three of the 5 criteria for diagnosing MetS were significant predictors of stage 1 steatosis in PLWH. Future studies investigating the risk of liver disease progression in PLWH need to account for these confounding factors as they explore HIV specific mechanisms for liver disease. Funding Sources National Institutes on Drug Abuse #5UO1DA040381.

Author(s):  
N. A. Nosko ◽  
O. M. Rud

Objective — to systematize literature data on the presence of 677C > T and 1298A > C polymorphisms in the MTHFR gene and homocysteine levels in patients with non‑alcoholic fatty liver disease (NAFLD); to calculate the frequencies 677C > T and 1298A > C polymorphisms combinations in the MTHFR gene and their impact on NAFLD development; to compare homocysteine levels in patients with and without NAFLD. Materials and methods. The analysis has been performed for the results of investigation of 49 patients, from them 17 subjects with NAFLD and 32 without it. Clinical, laboratory, statistical and ontological methods were used in the study. The MTHFR 677C > T and MTHFR 1298A > C polymorphisms in the MTHFR gene were investigated with the use of real time polymerase chain reaction (RT‑PCR) technique. Homocysteine levels were determined with chemiluminescent immunoassay with reference values 3.7 — 13.9 µmol/L. Multiple logistic regression method was used to evaluate the effects 677C > T and 1298A > C polymorphisms in the MTHFR gene on NAFLD development. Results. The variant of combination of 667С/С/1298А/А polymorphisms in the MTHFR gene (absence of mutation) was reveled in 6 (12 %) persons, that showed a widespread prevalence of variants with the presence of mutations. The correlation between variants of 677C > T and 1298A > C polymorphism in the MTHFR gene has been established (r = 0.429; p < 0.05). The results of multiple logistic regression demonstrated absence of the significant effects of 677C > T and 1298A > C polymorphisms in the MTHFR gen on NAFLD development (p > 0.05). Comparison of the homocysteine levels in patients with and without NAFLD didn’t reveal significant difference (р > 0.05), as well as comparison in the groups with combinations of 677C > T and 1298А > С polymorphisms in the MTHFR gen (р > 0.05). This can be explained by the fact that NAFLD group consisted of manly young patients without hypertension, type 2 diabetes mellitus and severe liver fibrosis. Conclusions. Ontological systematization of the scientific data on NAFLD revealed that 677C > T and 1298A > C polymorphisms in the MTHFR gen are pathogenetically associated with the significant increase in homocysteine levels as a marker of cardiovascular pathology. Giving the multifactorial nature of hyperhomocysteinemia and wide spread of 677C > T and 1298A > C polymorphisms in the MTHFR gen in population, it seems to be impractical to use genetic investigations for MTHFR gen polymorphism in NAFLD patients routinely, but only for the purpose of differential diagnosis of hyperhomocysteinemia.  


2017 ◽  
Vol 2017 ◽  
pp. 1-5 ◽  
Author(s):  
Tamara Milovanovic Alempijevic ◽  
Milica Stojkovic Lalosevic ◽  
Igor Dumic ◽  
Nevena Jocic ◽  
Aleksandra Pavlovic Markovic ◽  
...  

Objective. Keeping in mind the rising prevalence of nonalcoholic fatty liver disease (NAFLD) and the need to establish noninvasive tests for its detection, the aim of our study was to investigate whether platelet count (PC), mean platelet volume (MPV), and platelet distribution width (PDW) can predict the presence of liver fibrosis in this group of patients. Methods. In 98 patients with NAFLD and 60 healthy volunteers, complete blood counts with automated differential counts were performed and values of PC, PDW, MPV, and PCT were analyzed. Results. Patients with NAFLD had lower PC and higher MPV, PCT, and PDW compared to the controls (P < 0.05). When NAFLD group was stratified according to severity of liver fibrosis, there was a statistically significant difference in the average values of PDW and PC between the groups (P < 0.05). Conclusion. Patients with NAFLD have significantly higher values of PCT, PDW, and MPV when compared to the healthy controls. Further studies are needed to establish their potential use for prediction of the degree of liver steatosis and fibrosis in NAFLD patients.


2018 ◽  
Vol 12 (3) ◽  
pp. 639-648 ◽  
Author(s):  
Uriel A. López-Lemus ◽  
Raquel Garza-Guajardo ◽  
Oralia Barboza-Quintana ◽  
Alejandrina Rodríguez-Hernandez ◽  
Alejandro García-Rivera ◽  
...  

Metabolic syndrome (MS) has been associated with testicular damage. Nonalcoholic fatty liver disease (NAFLD) is a multisystemic disease that affects different organs, but its effect on the testes is unknown. A study analyzing germ cell involvement on BALB/c mice was carried out. A parallel comparative study was conducted that investigated alterations in the germinal epithelium of male humans that died from an unrelated acute event. The complete medical histories and histologic samples of the thoracic aorta, liver tissue, and testicular tissue from the deceased subjects were collected. The degree of germinal epithelial loss (DGEL) was evaluated and the clinical and histologic data were compared between individuals with and without NAFLD. The only metabolic or morphologic variable that caused a significant difference in the DGEL, in both the animal model and humans, was the presence of liver steatosis. The percentage of steatosis was also correlated with the percentage of the DGEL. In humans, steatosis (greater than 20%) increased the risk 12-fold for presenting with a severe DGEL (OR: 12.5; 95% CI [1.2, 128.9]; p = .03). There was no association with age above 50 years or MS components. Steatosis grade was also correlated with atherosclerosis grade. NAFLD was a strongly associated factor implicated in severe DGEL, as well as the testis was identified as a probable target organ for damage caused by the disease. This finding could result in the search for new approach strategies in the management of men with fertility problems. Further studies are required to confirm these results.


2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Paola Dongiovanni ◽  
Stefano Romeo ◽  
Luca Valenti

Liver fat accumulation generally related to systemic insulin resistance characterizes nonalcoholic fatty liver disease (NAFLD), which in the presence of nonalcoholic steatohepatitis (NASH) can progress towards cirrhosis and hepatocellular carcinoma. Due to the epidemic of obesity, NAFLD is now the most frequent liver disease in Western countries. Epidemiological, familial, and twin studies provide evidence for a strong genetic component of NAFLD susceptibility. Recently, genome-wide association studies led to the identification of the major inherited determinants of hepatic fat accumulation:patatin-like phospholipase domain-containing 3 (PNPLA3)I148M gene andtransmembrane 6 superfamily member 2 (TM6SF2)E167K gene variants, involved in lipid droplets remodelling and very low-density lipoproteins secretion, are the major determinants of interindividual differences in liver steatosis, and susceptibility to progressive NASH. In this review, we aimed to provide an overview of recent insights into the genetics of hepatic fat accumulation and steatohepatitis.


2020 ◽  
Vol 47 (2) ◽  
pp. 66-71
Author(s):  
V. A. Akhmedov ◽  
N. F. Mamedova ◽  
A. V. Verbanov ◽  
O. V. Gaus ◽  
O. V. Gaus

This article reflects the course of non-alcoholic fatty liver disease (NAFLD) in HIV-infected individuals. It is noted that long-term antiretroviral therapy and the use of D-drugs can explain the high prevalence of steatosis in this category of patients. The results of experimental studies that demonstrate the direct effect of HIV on liver steatosis by infection of stellate liver cells, stimulation of abnormal expression of SREBP-1 and PPARγ are considered. The role of HIV-mediated microbial translocation as one of the triggers for the development of non-alcoholic steatohepatitis (NASH), which contributes to chronic inflammation due to an increase in the permeability of the intestinal barrier to bacterial products and endotoxins, is noted. Data are presented confirming the high prevalence of the abnormal distribution of fat and visceral obesity (components of lipodystrophy syndrome) in a cohort of HIV-infected individuals. There was a high prevalence of steatosis and steatohepatitis in HIV-infected patients with lipodystrophy as compared with HIV-infected patients without lipodystrophy. Data showing the high prevalence of NASH in HIV-infected individuals are presented. A high rate of progression of NAFLD in a cohort of HIV-infected individuals was observed, regardless of the presence/absence of a combined viral infection (chronic hepatitis C). It has been established that the classic risk factors for NAFLD (high body mass index, dyslipidemia, metabolic syndrome) can contribute to the rapid progression of the disease in people living with HIV, compared with representatives of the general population.


2021 ◽  
Vol 8 ◽  
Author(s):  
Ying Liu ◽  
Dongyu Li ◽  
Yuping Liu ◽  
Ping Shuai

Background: Both nonalcoholic fatty liver disease (NAFLD) and Helicobacter pylori (H. pylori) infection have high prevalence worldwide, and the relationship between both remains controversial. We try to investigate whether H. pylori infection is associated with NAFLD and increased liver fat deposition and stiffness in this cross-sectional study.Methods: The physical examination data of 5,665 subjects were obtained from February 2018 to June 2019 in this study. Clinical and biochemical data were collected. NAFLD was diagnosed using abdominal color Doppler ultrasonography. Liver steatosis and stiffness were understood by two parameters of transient elastography (TE): fat attenuation parameter (FAP) and liver stiffness measurement (LSM). H. pylori infection was determined using the 13C urea breath tests.Results: The total prevalence of NAFLD and H. pylori infection was 30.2 and 37.0%, respectively. In men, the prevalence of NAFLD and the levels of FAP and LSM in H. pylori-positive group were significantly higher than H. pylori-negative group (all p &lt; 0.01), but no significant difference was found in women. In men, the infection rate of H. pylori in NAFLD group and LSM ≥ 7.4 kPa group was significantly higher than control group. Multivariate logistic regression analysis revealed that H. pylori infection was not independently associated with NAFLD and FAP ≥ 240 dB/m. However, H. pylori infection was associated with LSM ≥ 7.4 kPa in men.Conclusions: Our study suggests that H. pylori infection is not significantly associated with NAFLD and elevated liver steatosis, whereas it may be the risk factor of elevated liver stiffness in men.


Author(s):  
Hijrawati Ayu Wardani ◽  
Mahardian Rahmadi ◽  
Chrismawan Ardianto ◽  
Santhra Segaran Balan ◽  
Norshafarina Shari Kamaruddin ◽  
...  

Abstract Background Nonalcoholic fatty liver disease (NAFLD) is indicated by liver steatosis without excessive alcohol use or other liver disease. Several studies have reported that metabolic syndromes such as obesity, type 2 diabetes mellitus, and dyslipidemia have a linear correlation associated with NAFLD pathophysiology. One of the characteristics of dyslipidemia in NAFLD is increase in serum triglycerides. This study aimed to develop a model of NAFLD characterized by an increase in serum triglyceride levels and histological profile of liver steatosis by high-fat diet in rats. Methods Twelve Wistar rats were fed with pellets enriched with 60% fat. They were housed individually, and the remaining pellets were weighted every day for intake evaluation. Blood samples were collected at day 0 and at the end of each trial period at days 7, 14, 21, and 28 for the measurement of triglyceride levels. Every animal from each group was also sacrificed for liver histopathological examination. Results This study has established developing the NAFLD animal model by induction of a high-fat diet. The levels of serum triglycerides were increased from baseline 80.41 ± 12.82 to 1152.00 ± 73.62, 493.66 ± 159.98, 556.00 ± 120.79, and 489.00 ± 156.75 mg/dL at days 7, 14, 21, and 28, respectively. Liver histology also showed liver steatosis development, inflammation, and hepatocellular ballooning, which were associated with the NAFLD state. Conclusions High-fat diet in rats induced hypertriglyceridemia along with NAFLD-like liver histopathology.


AIDS ◽  
2020 ◽  
Vol 34 (13) ◽  
pp. 1915-1921
Author(s):  
Jovana Milic ◽  
Valentina Menozzi ◽  
Filippo Schepis ◽  
Andrea Malagoli ◽  
Giulia Besutti ◽  
...  

2021 ◽  
Vol 22 (18) ◽  
pp. 9931
Author(s):  
Koichi Fujisawa ◽  
Taro Takami ◽  
Shoki Okubo ◽  
Yuto Nishimura ◽  
Yusaku Yamada ◽  
...  

Among lifestyle-related diseases, fatty liver is the most common liver disease. To date, mammalian models have been used to develop methods for inhibiting fatty liver progression; however, new, more efficient models are expected. This study investigated the creation of a new model to produce fatty liver more efficiently than the high-fat diet medaka model that has been used to date. We compared the GAN (Gubra-Amylin nonalcoholic steatohepatitis) diet, which has been used in recent years to induce fatty liver in mice, and the high-fat diet (HFD). Following administration of the diets for three months, enlarged livers and pronounced fat accumulation was noted. The GAN group had large fat vacuoles and lesions, including ballooning, compared to the HFD group. The GAN group had a higher incidence of lesions. When fenofibrate was administered to the fatty liver model created via GAN administration and liver steatosis was assessed, a reduction in liver fat deposition was observed, and this model was shown to be useful in drug evaluations involving fatty liver. The medaka fatty liver model administered with GAN will be useful in future fatty liver research.


2021 ◽  
Vol 12 (3) ◽  
Author(s):  
Zhe Zheng ◽  
Yue Li ◽  
Siyuan Fan ◽  
Jie An ◽  
Xi Luo ◽  
...  

AbstractNonalcoholic fatty liver disease (NAFLD) is prevalent clinically and can lead to more serious chronic liver disease. However, the pathological mechanism is still unclear, and thus, there are no approved drugs on the market. Transcriptional coactivator WW domain-binding protein 2 (WBP2) is a newly discovered oncogene that has an important relationship with the occurrence and development of breast cancer and mediates the interaction between Wnt and various other signaling pathways. The expression level of WBP2 was decreased in NAFLD. Overexpression of WBP2 with AAV in vivo alleviated liver fat deposition and insulin resistance induced by a high-fat diet (HFD). Knockdown of WBP2 with AAV aggravated HFD-induced fatty liver and insulin resistance. In vitro experiments showed that in the human normal hepatocyte cell line LO2 and primary hepatocytes isolated from mice, overexpression of WBP2 reduced fat deposition, and knocking out or knocking down WBP2 aggravated PA-induced fat deposition. Through mass spectrometry, we found that WBP2 can bind to AMPKβ1, and by mutating AMPKβ1, we found that WBP2 can induce phosphorylation of AMPKβ1 at S108 and then activate the AMPK pathway to affect lipid metabolism. The effect of WBP2 on NAFLD provides a possible new direction for future research on NAFLD.


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