Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity
By E. Fabbrini, F. Magkos, B. S. Mohammed, T. Pietka, N. Abumrad, B. Patterson, A. Okunade, S. Klein. Proceedings of the National Academy of Sciences of the United States of America, 2009
998 citations recorded by the source corpus.
Subfields: Endocrinology, Diabetes and Metabolism, Epidemiology, Physiology
View Paper: https://www.semanticscholar.org/paper/429377a051f8aa5819de277b1869e8f8153ad424
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Endocrinology, Diabetes and Metabolism
- Gerald I. Shulman
- V. Samuel
- André Tchernof
- J. Despres
- A. Okunade
- B. Patterson
- S. Klein
- Andreas L. Birkenfeld
In Epidemiology
- Gerald I. Shulman
- V. Samuel
- André Tchernof
- P. Tveden‐Nyborg
- D. H. Ipsen
- J. Lykkesfeldt
- A. Okunade
- B. Patterson
In Physiology
- V. Samuel
- Gerald I. Shulman
- J. Despres
- C. Choi
- Shin-Hae Lee
- Shi-Young Park
- A. Chait
- Laura J. den Hartigh
Citations in the corpus
- Insulin Resistance: From Mechanisms to Therapeutic Strategies (2021, background): “Furthermore, intrahepatic and intramyocellular lipid contents are considered to be much better predictors of insulin resistance than visceral adipose tissue volume, which strongly indicates that increased lipid accumulation in liver and skeletal muscle could impair insulin signaling and induce insul”
- Adipose Tissue Distribution, Inflammation and Its Metabolic Consequences, Including Diabetes and Cardiovascular Disease (2020, background): “In one such study, significant differences in insulin sensitivity in the liver, skeletal muscle, and adipose tissue were reported in obese human subjects who differed in hepatic lipid content, with no such differences observed in obese subjects who differed in visceral adiposity (291).”
- Insulin resistance drives hepatic de novo lipogenesis in nonalcoholic fatty liver disease. (2019, methodology): “The contribution of palmitate made de novo in adipose tissue that were incorporated into circulating TRL-TG was estimated by: i) directly measuring the contribution of palmitate made by DNL in adipose tissue TGs; and ii) estimating the relative incorporation of the release of these fatty acids into ”
- Non-Alcoholic Fatty Liver Disease as a Nexus of Metabolic and Hepatic Diseases (2017, positive): “And intrahepatic lipid content, not VATmass, better relates tomeasures of hepatic insulin sensitivity (Fabbrini et al., 2009), even in patients with marked obesity (Magkos et al., 2010).”
- The role of fructose in the pathogenesis of NAFLD and the metabolic syndrome (2010, background): “Furthermore, the degree of intrahepatic lipid predicts metabolic dysfunction even better than does the degree of visceral adipose tissue”
- Molecular mechanisms of hepatic lipid accumulation in non-alcoholic fatty liver disease (2018, background): “VLDL secretion was increased in patients with NAFLD [65, 110, 119] and liver triglyceride content was directly associated with VLDL-TG secretion rates [65, 66, 110, 119].”
- Non Alcoholic Fatty Liver Disease, Hepatic Insulin Resistance and Type 2 Diabetes (2014, background): “FATPs and FAT/CD36 have been shown to be increased in liver, but decreased in adipose tissue of obese patients with NAFLD, compared to obese subjects with normal intrahepatic lipid content.(48,49) Hepatic overexpression of LpL(50,51) or viral gene delivery of hepatic CD36 causes specific accumulatio”