scholarly journals Association of Hepatic Steatosis Index with Nonalcoholic Fatty Liver Disease Diagnosed by Non-Enhanced CT in a Screening Population

Diagnostics ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 2168
Author(s):  
Jieun Chung ◽  
Hee-Sun Park ◽  
Young-Jun Kim ◽  
Mi-Hye Yu ◽  
Sungeun Park ◽  
...  
Keyword(s):  
Logistic Regression ◽  
Hepatic Steatosis ◽  
Fasting Glucose ◽  
Clinical Parameters ◽  
Laboratory Findings ◽  
Nonalcoholic Fatty Liver ◽  
Asymptomatic Patients ◽  
Enhanced Ct ◽  
Screening Population ◽  
Hepatic Steatosis Index

The noninvasive diagnosis of hepatic steatosis is of increasing concern. This study investigated the association of hepatic steatosis determined by non-enhanced CT criteria with clinical parameters in a screening population. Asymptomatic patients who underwent abdominal CT at our healthcare center were retrospectively analyzed (n = 339). Two radiologists measured the attenuation values of the liver parenchyma and spleen using non-enhanced CT images. CT criteria for hepatic steatosis were (a) absolute liver attenuation value <48 Hounsfield units (HU), (b) liver-to-spleen attenuation ratio <0.8, and (c) attenuation difference between the liver and spleen <−10. Body mass index (BMI) and hepatic steatosis index (HSI) were calculated, and laboratory findings were recorded. The association of hepatic steatosis with clinical parameters was assessed using univariate and logistic regression analyses. The presence of hepatic steatosis was significantly associated with the levels of serum fasting glucose and triglycerides, the alanine aminotransferase to aspartate aminotransferase (ALT/AST) ratio, BMI, and HSI values using any of the CT criteria. Logistic regression analysis revealed that the serum fasting glucose level and HSI were significantly associated with hepatic steatosis using criterion (a), while the ALT/AST ratio and HSI were associated with hepatic steatosis using criteria (b) and (c). The presence of hepatic steatosis on non-enhanced CT should be considered to indicate possible clinical profile abnormalities regarding metabolic syndrome.

Hepatic steatosis index: A simple screening tool reflecting nonalcoholic fatty liver disease

2010 ◽  
Vol 42 (7) ◽  
pp. 503-508 ◽  
Author(s):  
Jeong-Hoon Lee ◽  
Donghee Kim ◽  
Hwa Jung Kim ◽  
Chang-Hoon Lee ◽  
Jong In Yang ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Hepatic Steatosis ◽  
Fatty Liver Disease ◽  
Screening Tool ◽  
Nonalcoholic Fatty Liver ◽  
Hepatic Steatosis Index ◽  
Simple Screening

scholarly journals E3 ubiquitin ligase Grail promotes hepatic steatosis through Sirt1 inhibition

2021 ◽  
Vol 12 (4) ◽  
Author(s):  
Pei-Yao Liu ◽  
Cheng-Cheung Chen ◽  
Chia-Ying Chin ◽  
Te-Jung Liu ◽  
Wen-Chiuan Tsai ◽  
...  
Keyword(s):  
Hepatic Steatosis ◽  
Lipid Accumulation ◽  
Acid Synthesis ◽  
Sirtuin 1 ◽  
Nonalcoholic Fatty Liver ◽  
Expression Of Genes ◽  
Hepatic Fat ◽  
Underlying Mechanisms

AbstractIn obese adults, nonalcoholic fatty liver disease (NAFLD) is accompanied by multiple metabolic dysfunctions. Although upregulated hepatic fatty acid synthesis has been identified as a crucial mediator of NAFLD development, the underlying mechanisms are yet to be elucidated. In this study, we reported upregulated expression of gene related to anergy in lymphocytes (GRAIL) in the livers of humans and mice with hepatic steatosis. Grail ablation markedly alleviated the high-fat diet-induced hepatic fat accumulation and expression of genes related to the lipid metabolism, in vitro and in vivo. Conversely, overexpression of GRAIL exacerbated lipid accumulation and enhanced the expression of lipid metabolic genes in mice and liver cells. Our results demonstrated that Grail regulated the lipid accumulation in hepatic steatosis via interaction with sirtuin 1. Thus, Grail poses as a significant molecular regulator in the development of NAFLD.

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.

scholarly journals Treatment with Lobeglitazone Attenuates Hepatic Steatosis in Diet-Induced Obese Mice

PPAR Research ◽  
2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Sorim Choung ◽  
Kyong Hye Joung ◽  
Bo Ram You ◽  
Sang Ki Park ◽  
Hyun Jin Kim ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Hepatic Steatosis ◽  
Plasma Cholesterol ◽  
Cholesterol Biosynthesis ◽  
Peroxisome Proliferator ◽  
Obese Mice ◽  
Nonalcoholic Fatty Liver ◽  
Hepatic Lipid ◽  
Hepatic Expression ◽  
Expression Of Genes

Nonalcoholic fatty liver disease (NAFLD) is strongly associated with insulin resistance. The peroxisome proliferator-activated receptor (PPAR) activators, thiazolidinediones, (TZDs), are insulin sensitizers used as a treatment for NAFLD. However, TZDs are a controversial treatment for NAFLD because of conflicting results regarding hepatic steatosis and fibrosis. To evaluate a possible effective drug for treatment of NAFLD, we investigated the effects of a newly developed TZD, lobeglitazone, with an emphasis on hepatic lipid metabolism. Lobeglitazone treatment for 4 weeks in high fat diet- (HFD-) induced obese mice (HL group) improved insulin resistance and glucose intolerance compared to HFD-induced obese mice (HU group). The gene levels related to hepatic gluconeogenesis also decreased after treatment by lobeglitazone. The livers of mice in the HL group showed histologically reduced lipid accumulation, with lowered total plasma cholesterol and triglyceride levels. In addition, the HL group significantly decreased the hepatic expression of genes associated with lipid synthesis, cholesterol biosynthesis, and lipid droplet development and increased the hepatic expression of genes associated with fatty acid β-oxidation, thus suggesting that lobeglitazone decreased hepatic steatosis and reversed hepatic lipid dysregulation. Livers with steatohepatitis contained increased levels of PPARγ and phosphorylated PPARγ at serine 273, leading to downregulation of expression of genes associated with insulin sensitivity. Notably, the treatment of lobeglitazone increased the protein levels of PPARα and diminished levels of PPARγ phosphorylated at serine 273, which were increased by a HFD, suggesting that induction of PPARα and posttranslational modification of PPARγ in livers by lobeglitazone might be an underlying mechanism of the improvement seen in NAFLD. Taken together, our data showed that lobeglitazone might be an effective treatment for NAFLD.

Sign in / Sign up

Export Citation Format

Share Document