Contribution of de novo fatty acid synthesis to hepatic steatosis and insulin resistance: lessons from genetically engineered mice.

By C. Postic, J. Girard. Journal of Clinical Investigation, 2008

1,222 citations recorded by the source corpus.

Subfields: Biochemistry, Endocrinology, Diabetes and Metabolism, Epidemiology

View Paper: https://www.semanticscholar.org/paper/4603d9c4dd067b925108fd9273dcea3bb8d9572a

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Biochemistry

1. M. Pinzani
2. G. Hotamışlıgil

In Endocrinology, Diabetes and Metabolism

1. Herbert Tilg
2. B. Thorens
3. M. Pinzani
4. A. Moschen
5. E. Tsochatzis
6. E. Buzzetti
7. G. Hotamışlıgil
8. Haiming Cao

In Epidemiology

1. Herbert Tilg
2. A. Moschen
3. M. Pinzani
4. Ali Canbay
5. M. Trauner
6. G. Gerken
7. Rebekka A. Hannivoort
8. L. Bechmann

Citations in the corpus

• Evolution of inflammation in nonalcoholic fatty liver disease: The multiple parallel hits hypothesis (2010, background): “A fatty liver is the result of the accumulation of various lipids.(10) Several mechanisms may lead to a fatty liver: (1) increased free fatty acids supply due to increased lipolysis from both visceral/subcutaneous adipose tissue and/or increased intake of dietary fat; (2) decreased free fatty oxidat”
• Pathogenesis of non-alcoholic fatty liver disease (2009, background): “FFAs arise in the liver from three distinct sources; lipolysis (the hydrolysis of FFA and glycerol from triglyceride) within adipose tissue, dietary sources, and de novo lipogenesis (DNL).(30) In contrast, FFA may be utilized either through b-oxidation, re-esterification to triglycerides and storage”
• Impact of Dietary Polyphenols on Carbohydrate Metabolism (2010, background): “causal role in the development of hepatic or systemic insulin resistance [130].”
• The interaction of hepatic lipid and glucose metabolism in liver diseases. (2012, background): “De novo lipogenesis (DNL) further contributes to hepatic steatosis [4].”
• The multiple-hit pathogenesis of non-alcoholic fatty liver disease (NAFLD). (2016, background): “Also, β-oxidation of FFAs is inhibited in insulin resistance states, thus further promoting hepatic lipids accumulation [28].”
• Glucose transporters in the 21st Century. (2010, background): “The transcription factor carbohydrate response elementbinding protein (ChREBP) mediates the effect of glucose on glycolytic and lipogenic gene expression (32).”
• Role of Dietary Fructose and Hepatic de novo Lipogenesis in Fatty Liver Disease (2016, background): “The importance of endogenous DNL to NAFLD development may also be inferred from studies utilizing genetically engineered mice with single-enzyme perturbation in this pathway (reviewed in [50, 51].”