Recent advances in the pathogenesis of hereditary fructose intolerance: implications for its treatment and the understanding of fructose-induced non-alcoholic fatty liver disease.
Recent advances in the pathogenesis of hereditary fructose intolerance: implications for its treatment and the understanding of fructose-induced non-alcoholic fatty liver disease. Cell Mol Life Sci. 2019 Nov 12;: Authors: Buziau AM, Schalkwijk CG, Stehouwer CDA, Tolan DR, Brouwers MCGJ Abstract Hereditary fructose intolerance (HFI) is a rare inborn disease characterized by a deficiency in aldolase B, which catalyzes the cleavage of fructose 1,6-bisphosphate and fructose 1-phosphate (Fru 1P) to triose molecules. In patients with HFI, ingestion of fructose results in accumulation of Fru 1P and depletion of ATP, which are believed to cause symptoms, such as nausea, vomiting, hypoglycemia, and liver and kidney failure. These sequelae can be prevented by a fructose-restricted diet. Recent studies in aldolase B-deficient mice and HFI patients have provided more insight into the pathogenesis of HFI, in particular the liver phenotype. Both aldolase B-deficient mice (fed a very low fructose diet) and HFI patients (treated with a fructose-restricted diet) displayed greater intrahepatic fat content when compared to controls. The liver phenotype in aldolase B-deficient mice was prevented by reduction in intrahepatic Fru 1P concentrations by crossing these mice with mice deficient for ketohexokinase, the enzyme that catalyzes the synthesis of Fru 1P. These new findings not only provide a potential novel treatment for HFI, but lend insight into the pathogenesis of fru...
DiscussionThis overview will assess current evidence from systematic reviews for the association between cadmium exposure and risk of T2DM and other metabolic morbidities. This overview may be helpful for policy-makers and healthcare teams aiming to mitigate T2DM risk in populations at risk of cadmium exposure.Systematic review registrationPROSPERO CRD42019125956
This article reviews the most updated information about NAFLD-related HCC and provides some insight into strategies that must be considered to reduce its potential disease burden.
ConclusionThis is the first study demonstrating an improvement in disease activity in mice with advanced NASH with fibrosis by a diet containing Mastiha.
Obesity is a worldwide epidemic leading to non-alcoholic fatty liver disease. Alterations of liver fat by magnetic resonance imaging (MRI) following bariatric surgery is a promising feature, but few studies have been fully elucidated. Purpose. MRI was used to determine alterations of liver fat fraction (LFF) features following surgery. These were compared with the clinical non-alcoholic steatohepatitis score (C-NASH score) and evaluated for predictive factors for score changes postoperatively. Methods.
EchoSens creates non-invasive liver diagnosis medical devices. The company’s line of products, called FibroScan, work by measuring the speed of ultrasound waves as they move through liver tissue. This measurement can tell us about the state of ...
CONCLUSION: Overall, these data suggest that chronic HFD consumption in mice can mimic pathophysiological and some microbial events observed in NAFLD patients. PMID: 31528245 [PubMed]
nia Non-alcoholic fatty liver disease (NAFLD) is one of the most prevalent forms of chronic liver disorders among adults, children, and adolescents, and a growing epidemic, worldwide. Notwithstanding the known susceptibility factors for NAFLD, i.e., obesity and metabolic syndrome, the exact cause(s) of this disease and the underlying mechanisms of its initiation and progression are not fully elucidated. NAFLD is a multi-faceted disease with metabolic, genetic, epigenetic, and environmental determinants. Accumulating evidence shows that exposure to environmental toxicants contributes to the development of NAFLD by promo...
Conclusion: The presence of the PNPLA3 G allele is associated with a risk of NAFLD. Our study shows that subjects with variant PNPLA3 are not only at increased risk for the development and progression of NAFLD, but also have increased insulin resistance. PMID: 31304703 [PubMed - in process]
The recent epidemic of chronic liver disease is related to the burden of non-alcoholic fatty liver disease (NAFLD), paralleling the worldwide increase of obesity.1 NAFLD is a complex condition related to metabolic derangements in insulin resistance (IR), but in a subset of patients the liver becomes the target of multiple hits leading to non-alcoholic steatohepatitis (NASH), the histological phenotype that may progressively lead to the development of liver fibrosis, cirrhosis and possibly hepatocellular carcinoma.
The recent epidemic in chronic liver disease is related to the burden of Non-Alcoholic Fatty Liver Disease (NAFLD), paralleling the worldwide increase of obesity.  NAFLD is a complex condition related to metabolic derangements in insulin resistance (IR), but in a subset of patients the liver becomes the target of multiple hits leading to Non-Alcoholic SteatoHepatitis (NASH), the histological phenotype that may progressively develop liver fibrosis, cirrhosis and possibly hepatocellular carcinoma.