The cardiac phenotype induced by PPARalpha overexpression mimics that caused by diabetes mellitus.

By B. Finck, J. J. Lehman, T. Leone, M. Welch, M. Bennett, A. Kovács, Xianlin Han, R. Gross, R. Kozak, G. Lopaschuk and 1 more. Journal of Clinical Investigation, 2002

1,002 citations recorded by the source corpus.

Subfields: Cardiology and Cardiovascular Medicine, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/d1a0b2546b1bfae153a9f65aaddab405f9f3402f

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. M. Hill
2. Guanghong Jia
3. J. Sowers
4. Rong Tian
5. Christoph Handschin
6. E. Dale Abel
7. Bart Staels
8. B. Spiegelman

In Molecular Biology

1. B. Spiegelman
2. Christoph Handschin
3. Johan Auwerx
4. Jiandie D. Lin
5. M. Hill
6. Guanghong Jia
7. J. Sowers
8. Mitchell A. Lazar

In Physiology

1. B. Spiegelman
2. Christoph Handschin
3. Jiandie D. Lin
4. Johan Auwerx
5. Mitchell A. Lazar
6. L. Michalik
7. W. Wahli
8. S. O’Rahilly

Citations in the corpus

• The Randle cycle revisited: a new head for an old hat. (2009, background): “Similarly, overexpression of PPAR in muscle and in heart also favors fatty acid uptake and oxidation and induces triglyceride accumulation as well as glucose intolerance and insulin resistance (57), whereas PPAR deletion downregulates fatty acid oxidation but increases glucose oxidation and glycolys”
• Cardiac remodeling in obesity. (2008, background): “PPAR, peroxisome proliferator-activated receptor; KO, knockout; FAO, fatty acid oxidation; ROS, reactive oxygen species; FA, fatty acid.”
• Cardiac Metabolism and Its Interactions with Contraction, Growth, and Survival of the Cardiomyocte (2013, background): “Additional studies show that increases of lipid supply in animal models of cardiac lipotoxicity exceed the increases in the rate of oxidation, which eventually leads to downregulation of FAO, accumulation of toxic lipid intermediates, and contractile failure.(112,113) Genetic manipulations in mice t”
• Diabetic cardiomyopathy: an update of mechanisms contributing to this clinical entity (2018, background): “FFA uptake and triacylglycerol accumulation and reducing glucose use, also characteristic of diabetic cardiomyopathy.(59)”
• Metabolic control through the PGC-1 family of transcription coactivators. (2005, background): “PGC-1α mRNA levels are elevated in the myocardium of streptozotocin-treated and db/db mice (Finck et al., 2002), suggesting that this coactivator may play a role in the development of diabetic cardiomyopathy.”
• Diabetic cardiomyopathy: a hyperglycaemia- and insulin-resistance-induced heart disease (2017, background): “Additionally, in diabetes, the heart often displays increased expression of peroxisome proliferator-activated receptor-α (PPAR-α), associated with increased fatty acid uptake, triacylglycerol accumulation and reduced glucose utilisation [25].”
• International Union of Pharmacology. LXI. Peroxisome Proliferator-Activated Receptors (2006, background): “77,78 ; overexpression in muscle leads to the development of glucose intolerance, increased fatty acid oxidation rates, reduced AMP-activated protein kinase activity, reduced insulin-stimulated glucose uptake, repression of GLUT4 gene {Mm} (cid:2) transgenesis (cid”