Nonalcoholic Fatty Liver Disease Liver Fat Score and Fat Equation to Predict and Quantitate Hepatic Steatosis: Promising But Not Prime Time!

2009 ◽  
Vol 137 (3) ◽  
pp. 772-775 ◽  
Author(s):  
Naga Chalasani
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Hepatic Steatosis ◽  
Fatty Liver Disease ◽  
Liver Fat ◽  
Prime Time ◽  
Nonalcoholic Fatty Liver ◽  
Fat Score

Therapeutic role of niacin in the prevention and regression of hepatic steatosis in rat model of nonalcoholic fatty liver disease

2014 ◽  
Vol 306 (4) ◽  
pp. G320-G327 ◽  
Author(s):  
Shobha H. Ganji ◽  
Gary D. Kukes ◽  
Nils Lambrecht ◽  
Moti L. Kashyap ◽  
Vaijinath S. Kamanna
Keyword(s):  
Fatty Acid ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Hepatic Steatosis ◽  
Fatty Liver Disease ◽  
Fatty Acid Synthase ◽  
Liver Fat ◽  
Mrna Levels ◽  
Nonalcoholic Fatty Liver

Nonalcoholic fatty liver disease (NAFLD), a leading cause of liver damage, comprises a spectrum of liver abnormalities including the early fat deposition in the liver (hepatic steatosis) and advanced nonalcoholic steatohepatitis. Niacin decreases plasma triglycerides, but its effect on hepatic steatosis is elusive. To examine the effect of niacin on steatosis, rats were fed either a rodent normal chow, chow containing high fat (HF), or HF containing 0.5% or 1.0% niacin in the diet for 4 wk. For regression studies, rats were first fed the HF diet for 6 wk to induce hepatic steatosis and were then treated with niacin (0.5% in the diet) while on the HF diet for 6 wk. The findings indicated that inclusion of niacin at 0.5% and 1.0% doses in the HF diet significantly decreased liver fat content, liver weight, hepatic oxidative products, and prevented hepatic steatosis. Niacin treatment to rats with preexisting hepatic steatosis induced by the HF diet significantly regressed steatosis. Niacin had no effect on the mRNA expression of fatty acid synthesis or oxidation genes (including sterol-regulatory element-binding protein 1, acetyl-CoA carboxylase 1, fatty acid synthase, and carnitine palmitoyltransferase 1) but significantly inhibited mRNA levels, protein expression, and activity of diacylglycerol acyltrasferase 2, a key enzyme in triglyceride synthesis. These novel findings suggest that niacin effectively prevents and causes the regression of experimental hepatic steatosis. Approved niacin formulation(s) for other indications or niacin analogs may offer a very cost-effective opportunity for the clinical development of niacin for treating NAFLD and fatty liver disease.

Nonalcoholic fatty liver disease liver fat score (NAFLD-LFS) could be used for the assessment of NAFLD in women with PCOS

2017 ◽  
Author(s):  
Jelica Bjekic-Macut ◽  
Ivana Bozic-Antic ◽  
Konstantinos Tziomalos ◽  
Dusan Ilic ◽  
Danijela Vojnovic-Milutinovic ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Liver Fat ◽  
Nonalcoholic Fatty Liver ◽  
Fat Score

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.

Abstract 05: Association of 25-Year Body Mass Index Trajectories Throughout Early Adulthood With Nonalcoholic Fatty Liver Disease in Middle Age: The Coronary Artery Risk Development in Young Adults (CARDIA) Study

Circulation ◽  
2017 ◽  
Vol 135 (suppl_1) ◽  
Author(s):  
Lisa B VanWagner ◽  
Sadiya Khan ◽  
Hongyan NIng ◽  
Juned Siddique ◽  
Cora E Lewis ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Body Mass ◽  
Fatty Liver Disease ◽  
Early Adulthood ◽  
Liver Fat ◽  
Nonalcoholic Fatty Liver ◽  
Bmi Trajectory

Background: Nonalcoholic Fatty Liver Disease (NAFLD) has increased in parallel with obesity, is a risk factor for cirrhosis and liver cancer, and has few effective treatments. Identifying modifiable risk factors for NAFLD development is essential to effectively design prevention programs. We tested whether trajectories of body mass index (BMI) change throughout early adulthood were associated with risk of prevalent NAFLD in midlife independent of current BMI. Methods: Participants from the CARDIA study, a prospective multicenter population-based biracial cohort of adults (baseline age 18-30 years), underwent BMI measurement at exam years 0, 2, 5, 7, 10, 15, 20, and 25. At Year 25 (Y25, 2010-2011), liver fat was assessed by computed tomography. NAFLD was identified after exclusion of other causes of liver fat (alcohol/hepatitis). Latent mixture modeling was used to identify 25-year trajectories in BMI percent (%) change relative to baseline BMI over time. Multivariable logistic regression models were used to assess associations between BMI trajectory group and prevalent NAFLD with adjustment for baseline or current Y25 BMI. Results: Among 4,423 participants, we identified 4 distinct trajectories of BMI %change: stable BMI (26.2% of the cohort, 25-year mean BMI Δ=0.7 kg/m 2 ), mild increase (46.0%, BMI Δ=5.2 kg/m 2 ), moderate increase (20.9%, BMI Δ=10.0 kg/m 2 ), and extreme increase (6.9%, BMI Δ=15.1 kg/m 2 ) (Figure). NAFLD prevalence at Y25 was higher with increasing BMI trajectory: 4.1%, 9.3%, 13.0%, and 17.6% (p-trend <0.0001). At baseline, 34.6% of participants had overweight or obesity. After adjustment for confounders, trajectories of greater BMI increase were associated with greater NAFLD prevalence independent of baseline or current Y25 BMI (Figure). Conclusion: Weight gain throughout adulthood is associated with greater prevalence of NAFLD in midlife independent of baseline or current BMI. These findings highlight weight maintenance throughout adulthood as a potential target for primary prevention of NAFLD.

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.

Abstract 52: Associations of Nonalcoholic Fatty Liver Disease with Subclinical Myocardial Dysfunction: The CARDIA Study

Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Lisa B VanWagner ◽  
Jane E Wilcox ◽  
Laura A Colangelo ◽  
Donald M Lloyd-Jones ◽  
J J Carr ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Myocardial Dysfunction ◽  
Large Population ◽  
Left Ventricular ◽  
Liver Fat ◽  
Nonalcoholic Fatty Liver ◽  
Lv Mass

Background: Nonalcoholic fatty liver disease (NAFLD) is an obesity-related condition with high cardiovascular morbidity. NAFLD patients often have echocardiographic features of left ventricular (LV) diastolic dysfunction. In a large population-based cross-sectional sample of black and white adults free from prevalent liver or heart disease, we tested the hypothesis that NAFLD is associated with subclinical myocardial dysfunction independent of BMI or visceral adipose tissue (VAT). Methods: Participants from the Coronary Artery Risk Development in Young Adults study (Y25 exam; age 43-55 years) with concurrent CT quantification of liver fat and tissue Doppler echocardiography with myocardial strain measured by speckle tracking were included (n=2,572). NAFLD was defined as liver attenuation ≤ 40 Hounsfield units after exclusion of other causes of liver fat (medication/alcohol use). Linear regression models were used to test associations. Results: NAFLD prevalence was 9.9%. NAFLD participants were more likely to be male (57.1% vs. 41.5%), white (57.5% vs. 50.6%), and had higher BMI (36.3 vs. 29.8 kg/m2) and VAT (222.4 vs. 120.5 cm3) than non-NAFLD. Those with NAFLD also had lower e’ tissue velocity (10.8 vs. 11.9 cm/s), lower E/A ratio (1.2 vs. 1.3), and higher E/e’ ratio (8.4 vs. 7.7). Increased LV mass, left atrial area, LV relative wall thickness, and cardiac output (CO) were present in NAFLD. Global longitudinal strain was also worse in NAFLD (-14.2% vs. -15.2%, all p<0.05). In multivariable analyses adjusted for demographics, health behaviors and BMI, the associations of NAFLD with markers of subclinical myocardial dysfunction were attenuated but remained significant (Table 1). Only e’ velocity, LV mass and CO remained significant after adjustment for VAT. Effect modification by race and sex was not statistically significant. Conclusion: NAFLD is associated with subclinical myocardial dysfunction independent of BMI. Attenuation of the relationship by VAT supports the hypothesis that VAT may be a marker of NAFLD.

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.

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