Disordered fat storage and mobilization in the pathogenesis of insulin resistance and type 2 diabetes.

By G. Lewis, A. Carpentier, K. Adeli, A. Giacca. Endocrine reviews, 2002

1,425 citations recorded by the source corpus.

Subfields: Endocrine and Autonomic Systems, Epidemiology, Physiology

View Paper: https://www.semanticscholar.org/paper/a434d08de51cd20bd27628dbaaa397bff0069383

How researchers see this paper

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

In Epidemiology

1. P. Newsome
2. J. Tomlinson
3. J. Dowman
4. Hannele Yki-Järvinen
5. M. Pinzani
6. E. Tsochatzis
7. P. Ferré
8. F. Foufelle

In Physiology

1. Hannele Yki-Järvinen
2. Marja-Riitta Taskinen
3. H. Fang
4. R. L. Judd

Citations in the corpus

• The Product of Fasting Glucose and Triglycerides As Surrogate for Identifying Insulin Resistance in Apparently Healthy Subjects (2008, neutral): “6 10–13 These findings support the important role that triglycerides play in insulin resistance.”
• Sugar consumption, metabolic disease and obesity: The state of the controversy (2015, neutral): “Due to selective insulin resistance, DNL is even more strongly activated in the insulin resistant liver (41).”
• BRAIN FUEL METABOLISM, AGING AND ALZHEIMER’S DISEASE (2010, background): “, to decrease free fatty acid release from adipose tissue triglycerides [94].”
• Hepatic steatosis: a role for de novo lipogenesis and the transcription factor SREBP‐1c (2010, background): “Studies in rodents and humans have revealed that the excessive accumulation of TG observed in hepatic steatosis is mainly because of an overflow of fatty acids coming from the lipolysis of hypertrophied (and insulin resistant) adipose tissue and from the lipogenic pathway while lipid disposal throug”
• MCP-1 contributes to macrophage infiltration into adipose tissue, insulin resistance, and hepatic steatosis in obesity. (2006, background): “These changes in serum FFA level might also contribute to the associated changes in hepatic triglyceride content and insulin resistance (36).”
• Overproduction of large VLDL particles is driven by increased liver fat content in man (2006, background): “Increased NEFA flux is a major contributor to the availability of TG for VLDL assembly [27, 28].”
• Population-Level Prediction of Type 2 Diabetes From Claims Data and Analysis of Risk Factors (2015, neutral): “Elevated liver function tests are early manifestations of insulin resistance 63 and are detectable earlier than fasting glycemia.”
• Diabetic dyslipidaemia: from basic research to clinical practice* (2003, background): “High rates of DNL are invariably associated with a shift of cellular metabolism from lipid oxidation to lipid storage in the liver increasing the availability of triglycerides for VLDL assembly [53].”
• The Metabolic Syndrome as a Predictor of Nonalcoholic Fatty Liver Disease (2006, background): “The metabolic syndrome is now proposed to reflect a failure of normal partitioning of surplus fat exclusively into adipose tissue (21, 22).”
• Triglyceride metabolism in the liver (2017, neutral): “The overflow of FA derived from excessive lipolysis in the adipose tissue contributes to the pathogenesis of insulin resistance in mice and humans (159), leading to both type 2 diabetes (213) and NAFLD (27, 171).”
• Molecular mediators of hepatic steatosis and liver injury. (2004, neutral): “13).”
• The multiple-hit pathogenesis of non-alcoholic fatty liver disease (NAFLD). (2016, background): “[31] Lewis GF, Carpentier A, Adeli K, et al.”
• Pathogenesis of non-alcoholic fatty liver disease (2009, background): “However, in situations of IR, such as NAFLD, this suppression is impaired resulting in an increased efflux of FFA from adipose tissue.(38) The hyperinsulinaemia associated with IR leads to: (i) up-regulation of the transcription factor sterol regulatory element binding protein-1c (SREBP-1c), which i”