Selective versus total insulin resistance: a pathogenic paradox.

By Michael S. Brown, J. Goldstein. Cell Metabolism, 2008

965 citations recorded by the source corpus.

Subfields: Cardiology and Cardiovascular Medicine, Endocrinology, Diabetes and Metabolism, Surgery

View Paper: https://www.semanticscholar.org/paper/05d76ab4f391198b654494f8aa9d3888db9e00ec

How researchers see this paper

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

In Cardiology and Cardiovascular Medicine

1. G. Hotamışlıgil
2. K. Bornfeldt
3. Gerald I. Shulman
4. S. Friedman
5. V. Samuel
6. I. Tabas
7. R. Loomba
8. B. Spiegelman

In Endocrinology, Diabetes and Metabolism

1. Gerald I. Shulman
2. V. Samuel
3. I. Tabas
4. B. Spiegelman
5. S. Friedman
6. A. Okunade
7. B. Patterson
8. K. Bornfeldt

In Surgery

1. Gerald I. Shulman
2. G. Hotamışlıgil
3. V. Samuel
4. K. Bornfeldt
5. B. Manning
6. S. Friedman
7. I. Tabas
8. B. Spiegelman

Citations in the corpus

• Homeostasis, Inflammation, and Disease Susceptibility (2015, neutral): “Interestingly, not all of these functions are reduced during the insulin resistant state (Brown and Goldstein, 2008), nor are all organs equally affected.”
• Mechanisms and disease consequences of nonalcoholic fatty liver disease (2021, background): “Direct hepatic insulin action activates SREBP1c by increasing mRNA expression and proteolytic cleavage of the SREBP1c precursor protein into a mature nuclear transcription factor (Brown and Goldstein, 2008).”
• Insulin resistance drives hepatic de novo lipogenesis in nonalcoholic fatty liver disease. (2019, background): “Studies conducted in primary hepatocytes and in rodent models of obesity and diabetes support the notion of selective pathway-specific insulin resistance in the liver (31-34).”
• Non-Alcoholic Fatty Liver Disease as a Nexus of Metabolic and Hepatic Diseases (2017, positive): “Direct hepatic insulin action activates SREBP1c by increasing mRNA expression and proteolytic cleavage of the SREBP1c precursor protein into a mature nuclear transcription factor (Brown and Goldstein, 2008).”
• Insulin Resistance, Hyperglycemia, and Atherosclerosis (2011, positive): “…can mean either defective insulin receptor signaling or, ironically, overstimulation of insulin receptor pathways caused by hyperinsulinemia (Brown and Goldstein, 2008); and (b) systemic risk factors induced by these syndromes versus direct processes acting at the level of the arterial…”
• Molecular mechanisms of cancer development in obesity (2011, background): “In the diabetic liver, the gluconeogenic pathway becomes insulin resistant, and insulin-stimulated lipogenesis remains sensitiv”