scholarly journals MAFLD/NAFLD Biopsy-Free Scoring Systems for Hepatic Steatosis, NASH, and Fibrosis Diagnosis

2022 ◽  
Vol 8 ◽  
Author(s):  
Nancy de los Ángeles Segura-Azuara ◽  
Carlos Daniel Varela-Chinchilla ◽  
Plinio A. Trinidad-Calderón
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Hepatic Steatosis ◽  
Fatty Liver Disease ◽  
Performance Metrics ◽  
Scoring Systems ◽  
Liver Disorder ◽  
Variable Degree ◽  
Nonalcoholic Fatty Liver ◽  
Non Invasive

Metabolic dysfunction-associated fatty liver disease (MAFLD), formerly known as nonalcoholic fatty liver disease, is the most prevalent liver disorder worldwide. Historically, its diagnosis required biopsy, even though the procedure has a variable degree of error. Therefore, new non-invasive strategies are needed. Consequently, this article presents a thorough review of biopsy-free scoring systems proposed for the diagnosis of MAFLD. Similarly, it compares the severity of the disease, ranging from hepatic steatosis (HS) and nonalcoholic steatohepatitis (NASH) to fibrosis, by contrasting the corresponding serum markers, clinical associations, and performance metrics of these biopsy-free scoring systems. In this regard, defining MAFLD in conjunction with non-invasive tests can accurately identify patients with fatty liver at risk of fibrosis and its complications. Nonetheless, several biopsy-free scoring systems have been assessed only in certain cohorts; thus, further validation studies in different populations are required, with adjustment for variables, such as body mass index (BMI), clinical settings, concomitant diseases, and ethnic backgrounds. Hence, comprehensive studies on the effects of age, morbid obesity, and prevalence of MAFLD and advanced fibrosis in the target population are required. Nevertheless, the current clinical practice is urged to incorporate biopsy-free scoring systems that demonstrate adequate performance metrics for the accurate detection of patients with MAFLD and underlying conditions or those with contraindications of biopsy.

scholarly journals Dissociation of hepatic insulin resistance from susceptibility of nonalcoholic fatty liver disease induced by a high-fat and high-carbohydrate diet in mice

2014 ◽  
Vol 306 (6) ◽  
pp. G496-G504 ◽  
Author(s):  
Akihiro Asai ◽  
Pauline M. Chou ◽  
Heng-Fu Bu ◽  
Xiao Wang ◽  
M. Sambasiva Rao ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Hepatic Steatosis ◽  
Fatty Liver Disease ◽  
Diet Group ◽  
High Fat ◽  
Nonalcoholic Fatty Liver ◽  
Akt Phosphorylation ◽  
High Carbohydrate

Liver steatosis in nonalcoholic fatty liver disease is affected by genetics and diet. It is associated with insulin resistance (IR) in hepatic and peripheral tissues. Here, we aimed to characterize the severity of diet-induced steatosis, obesity, and IR in two phylogenetically distant mouse strains, C57BL/6J and DBA/2J. To this end, mice (male, 8 wk old) were fed a high-fat and high-carbohydrate (HFHC) or control diet for 16 wk followed by the application of a combination of classic physiological, biochemical, and pathological studies to determine obesity and hepatic steatosis. Peripheral IR was characterized by measuring blood glucose level, serum insulin level, homeostasis model assessment of IR, glucose intolerance, insulin intolerance, and AKT phosphorylation in adipose tissues, whereas the level of hepatic IR was determined by measuring insulin-triggered hepatic AKT phosphorylation. We discovered that both C57BL/6J and DBA/2J mice developed obesity to a similar degree without the feature of liver inflammation after being fed an HFHC diet for 16 wk. C57BL/6J mice in the HFHC diet group exhibited severe pan-lobular steatosis, a marked increase in hepatic triglyceride levels, and profound peripheral IR. In contrast, DBA/2J mice in the HFHC diet group developed only a mild degree of pericentrilobular hepatic steatosis that was associated with moderate changes in peripheral IR. Interestingly, both C57BL/6J and DBA/2J developed severe hepatic IR after HFHC diet treatment. Collectively, these data suggest that the severity of diet-induced hepatic steatosis is correlated to the level of peripheral IR, not with the severity of obesity and hepatic IR. Peripheral rather than hepatic IR is a dominant factor of pathophysiology in nonalcoholic fatty liver disease.

Focal fatty sparing as an indicator of higher-grade fatty liver assessed by attenuation imaging: a prospective clinical study in NAFLD population

2021 ◽  
Author(s):  
Elisabeth Miller ◽  
Julian Schmidberger ◽  
Wolfgang Kratzer
Keyword(s):  
Liver Disease ◽  
Clinical Study ◽  
Fatty Liver ◽  
Hepatic Steatosis ◽  
Patient Population ◽  
Fatty Liver Disease ◽  
Fatty Degeneration ◽  
Prospective Clinical Study ◽  
Nonalcoholic Fatty Liver ◽  
Attenuation Imaging

Abstract Background As part of a prospective clinical study, the degree of hepatic fatty degeneration was quantified in a patient population with nonalcoholic fatty liver disease and sonographically diagnosed with hepatic steatosis using attenuation imaging. Methods A total of 113 patients with hepatic steatosis were examined, of whom 35 showed focal fatty sparing. Patients with the condition after right nephrectomy, other known liver diseases, and relevant alcohol consumption were excluded from the evaluation. B-scan sonography and sonographic quantification of steatosis content using attenuation imaging (Aplio i800 Canon Medical Systems) were performed. Attenuation imaging is a new ultrasound-based measurement technique that allows objective detection and quantification of hepatic steatosis. Results The prevalence of focal fatty sparing was 31.0% in the patient population examined. Patients with focal fatty sparing showed a statistically significantly higher attenuation coefficient in contrast to patients without focal fatty sparing (0.79 ± 0.10 vs. 0.66 ± 0.09 dB/cm/MHz, p < 0.0001). Conclusion Detection of focal fatty sparing is associated with an increased attenuation coefficient and is thus an expression of higher-grade hepatic fatty degeneration. Patients with focal fatty sparing are more often male and have a higher BMI and a larger liver than patients with nonalcoholic fatty liver disease without focal fatty sparing.

scholarly journals Reproductive Endocrinology of Nonalcoholic Fatty Liver Disease

2018 ◽  
Vol 40 (2) ◽  
pp. 417-446 ◽  
Author(s):  
Mathis Grossmann ◽  
Margaret E Wierman ◽  
Peter Angus ◽  
David J Handelsman
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Hepatic Steatosis ◽  
Fatty Liver Disease ◽  
Energy Homeostasis ◽  
Sex Hormone Binding Globulin ◽  
Sex Steroid ◽  
Receptor Signaling ◽  
Nonalcoholic Fatty Liver

Abstract The liver and the reproductive system interact in a multifaceted bidirectional fashion. Sex steroid signaling influences hepatic endobiotic and xenobiotic metabolism and contributes to the pathogenesis of functional and structural disorders of the liver. In turn, liver function affects the reproductive axis via modulating sex steroid metabolism and transport to tissues via sex hormone–binding globulin (SHBG). The liver senses the body’s metabolic status and adapts its energy homeostasis in a sex-dependent fashion, a dimorphism signaled by the sex steroid milieu and possibly related to the metabolic costs of reproduction. Sex steroids impact the pathogenesis of nonalcoholic fatty liver disease, including development of hepatic steatosis, fibrosis, and carcinogenesis. Preclinical studies in male rodents demonstrate that androgens protect against hepatic steatosis and insulin resistance both via androgen receptor signaling and, following aromatization to estradiol, estrogen receptor signaling, through regulating genes involved in hepatic lipogenesis and glucose metabolism. In female rodents in contrast to males, androgens promote hepatic steatosis and dysglycemia, whereas estradiol is similarly protective against liver disease. In men, hepatic steatosis is associated with modest reductions in circulating testosterone, in part consequent to a reduction in circulating SHBG. Testosterone treatment has not been demonstrated to improve hepatic steatosis in randomized controlled clinical trials. Consistent with sex-dimorphic preclinical findings, androgens promote hepatic steatosis and dysglycemia in women, whereas endogenous estradiol appears protective in both men and women. In both sexes, androgens promote hepatic fibrosis and the development of hepatocellular carcinoma, whereas estradiol is protective.

A Correlational Study of Hepatic Steatosis (Fatty Liver Disease) and Liver Enzymes (ALT, AST, GGT) In The Scenario of Insulin Resistance Among Young Medicos.

2021 ◽  
Vol 17 (4) ◽  
pp. 717-725
Author(s):  
Samarpita Mukherjee ◽  
Shubhrajit Saha ◽  
Ushasi Banerjee ◽  
Arup Kumar Banerjee ◽  
Ritam Banerjee
Keyword(s):  
Insulin Resistance ◽  
Liver Disease ◽  
Fatty Liver ◽  
Hepatic Steatosis ◽  
Fatty Liver Disease ◽  
Lifestyle Modifications ◽  
Cross Sectional ◽  
Mean Values ◽  
Nonalcoholic Fatty Liver ◽  
Study Population

Background and Objectives In the last few decades,Nonalcoholic Fatty Liver Disease (NAFLD) has become a common health issue that leads to serious complications like cirrhosis, cardiovascular disease, etc. Insulin resistance (IR) is the key pathogenic factor for NAFLD. The young medicos being habituated in stressful and sedentary lifestyle and representative of the youth as well can fully justify their selection as study population and help to build social awareness by emphasizing the importance of early lifestyle modifications in preventing or delaying the severe complications of NAFLD. This study is aiming to find out if there is any correlation of hepatic steatosis with IR, Alanine Transaminases (ALT), Aspartate Transaminases (AST) or Gama Glutamyl Transferases (GGT) and also to identify if one enzyme is better correlating with hepatic steatosis than others in the scenario of Insulin Resistance among young medicos. METHODS: 132 medical students of North Bengal Medical College, aged between 18-25 years were included in this institution based observational cross-sectional study. Their Fasting Insulin, glucose, ALT, AST, GGT were measured, and IR was calculated by the Homeostatic Assessment of Insulin Resistance (HOMA-IR) calculator. Sonography was done to assess Hepatic steatosis. RESULTS: Among 132 subjects normal, grade 1 and grade 2 fatty changes have been found in 67.4%, 25%, and 7.6% of the study population respectively. The Grouping was done using the cut-off value of IR (i.e. subjects with IR<1.525 vs. IR≥1.525). Significant differences were found in the mean values of ALT, AST, GGT between groups. Significant positive concordances were found between enzymes ALT, GGT, and hepatic steatosis in subjects having IR ≥ 1.525.Regression analysis showed that higher GGT values have a stronger positive correlation with hepatic steatosis than ALT among the same. Interpretation and Conclusion From this study, we can interpret that subjects having higher GGT values are better associated with steatosis than those having higher ALT values and can lead us to the conclusion that GGT might be an important independent marker for NAFLD associated with IR. Furthermore, such observations may suggest considering GGT as a marker for assessing the severity of fatty liver irrespective of etiopathogenesis, though the population-based vivid evaluation is highly recommended.

scholarly journals Protective Effect of a Mixture of Astragalus membranaceus and Lithospermum erythrorhizon Extract against Hepatic Steatosis in High Fat Diet-Induced Nonalcoholic Fatty Liver Disease Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Doo Jin Choi ◽  
Seong Cheol Kim ◽  
Gi Eun Park ◽  
Bo-Ram Choi ◽  
Dae Young Lee ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Hepatic Steatosis ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Density Lipoprotein ◽  
Lithospermum Erythrorhizon ◽  
High Fat ◽  
Nonalcoholic Fatty Liver

The present study aimed to evaluate the potential synergistic and protective effects of ALM16, a mixture of Astragalus membranaceus (AM) and Lithospermum erythrorhizon (LE) extract in a ratio of 7 : 3, against hepatic steatosis in high fat diet (HFD)-induced nonalcoholic fatty liver disease (NAFLD) mice. Forty-eight mice were randomly divided into eight groups and orally administered daily for 6 weeks with a normal diet (ND) or high fat diet alone (HFD), HFD with AM (HFD + 100 mg/kg AM extract), HFD with LE (HFD + 100 mg/kg LE extract), HFD with ALM16 (HFD + 50, 100, and 200 mg/kg ALM16), or HFD with MT (HFD + 100 mg/kg Milk thistle extract) as a positive control. ALM16 significantly decreased the body and liver weight, serum and hepatic lipid profiles, including triglyceride (TG), total cholesterol (TC), high-density lipoprotein-cholesterol (HDL), and low-density lipoprotein-cholesterol (LDL), and serum glucose levels, compared to the HFD group. Moreover, ALM16 significantly ameliorated the HFD-induced increased hepatic injury markers, including aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), and gamma-glutamyltransferase (GGT)-1. Furthermore, as compared to the mice fed HFD alone, ALM16 increased the levels of phosphorylated AMP-activated protein kinase (p-AMPK) and acetyl-CoA carboxylase (p-ACC), thereby upregulating the expression of carnitine palmitoyltransferase (CPT)-1 and downregulating the expression of sterol regulatory element-binding protein (SREBP)-1c and fatty acid synthase (FAS). These results demonstrated that ALM16 markedly inhibited HFD-induced hepatic steatosis in NAFLD mice by modulating AMPK and ACC signaling pathways, and may be more effective than the single extracts of AM or LE.

scholarly journals Assessment of Hepatic Steatosis in Nonalcoholic Fatty Liver Disease by Using Quantitative US

Radiology ◽  
2020 ◽  
Vol 295 (1) ◽  
pp. 106-113 ◽  
Author(s):  
Aiguo Han ◽  
Yingzhen N. Zhang ◽  
Andrew S. Boehringer ◽  
Vivian Montes ◽  
Michael P. Andre ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Hepatic Steatosis ◽  
Fatty Liver Disease ◽  
Nonalcoholic Fatty Liver ◽  
Quantitative Us
Sign in / Sign up

Export Citation Format

Share Document