Ceramides in insulin resistance and lipotoxicity.
By S. Summers. Progress in lipid research, 2006
860 citations recorded by the source corpus.
Subfields: Epidemiology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/9120455800fa1e68499c3b90c931644833560dcd
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Epidemiology
- Ralph DeFronzo
- M. Wymann
- LM Obeid
- Sushil Kumar Jain
- Mark P. Mattson
- Yusuf A. Hannun
- R. Schneiter
- A. Achari
In Molecular Biology
- Yusuf A. Hannun
- LM Obeid
- Ralph DeFronzo
- M. Wymann
- Sushil Kumar Jain
- Mark P. Mattson
- R. Schneiter
- Christopher B. Newgard
Citations in the corpus
- Cellular Stress Responses, The Hormesis Paradigm, and Vitagenes: Novel Targets for Therapeutic Intervention in Neurodegenerative Disorders (2010, neutral): “Ceramides generated in response to membrane-associated oxidative stress are implicated in the dysfunction and death of cells in a range of disorders, including diabetes (428), emphysema (352), ischemic stroke (476), Alzheimer’s disease (141), and amyotrophic lateral sclerosis (142).”
- Plasma Ceramides Are Elevated in Obese Subjects With Type 2 Diabetes and Correlate With the Severity of Insulin Resistance (2009, background): “In addition, the measures of plasma ceramide subspecies were obtained in the postabsorptive state, and it should be noted that feeding has been shown to influence plasma ceramide levels (5,51,52).”
- Metabolic Syndrome and Insulin Resistance: Underlying Causes and Modification by Exercise Training (2013, neutral): “Despite being a relatively small component of the total lipid pool, sphingolipids, such as ceramide and glucosylceramide, are considered the most pathogenic (618) and are elevated almost twofold in insulin-resistant obese compared with lean, sedentary or exercise-trained subjects (19).”
- Adiponectin, a Therapeutic Target for Obesity, Diabetes, and Endothelial Dysfunction (2017, background): “Since accumulation of ceramide in skeletal muscle has been reported to be associated with impaired insulin sensitivity [61], decreased ceramide concentration by adiponectin may be a mechanism for increasing insulin sensitivity in skeletal muscles.”
- Mechanisms linking obesity with cardiovascular disease (2006, background): “When adipocytes exceed their storage capacity and the process of fat-cell proliferation fails, fat begins to accumulate in tissues not suited for lipid storage, leading to the formation of specific metabolites that inhibit insulin signal transductio”
- Alternate day calorie restriction improves clinical findings and reduces markers of oxidative stress and inflammation in overweight adults with moderate asthma. (2007, background): “Ceramides are liberated from membrane sphingomyelin in response to inflammatory cytokine receptor activation and oxidative stress and levels of ceramides are elevated in affected tissues and body fluids in several inflammatory and infectious diseases [34] [35] [36].”
- Homeostasis, Inflammation, and Disease Susceptibility (2015, neutral): “Similarly, the abnormal accumulation of harmful lipid mediators (lipotoxicity) in adipocytes, liver, and muscle in obesity leads to cellular stress and tissue dysfunction, and consequently to inflammation (DeFronzo, 2010; Samuel and Shulman, 2012; Summers, 2006).”
- Principles of bioactive lipid signalling: lessons from sphingolipids (2008, background): “These cellular roles extend to organismal function and pathobiology and have implications for the understanding of cancer biology, arthritis and inflammation, diabetes, immune function and neurodegenerative disorder”
- A Branched-Chain Amino Acid-Related Metabolic Signature that Differentiates Obese and Lean Humans and Contributes to Insulin Resistance (2009, background): “…via glutamate transamination to alanine. contributing to accumulation of lipid-derived metabolites such as diacylglyerols, ceramides, ketones, prostaglandins, and incompletely oxidized lipids that can impact insulin signaling (Muoio and Newgard, 2008; Morino et al., 2006; Summers, 2006).”
- Lipid signalling in disease (2008, background): “Ceramide activates protein phosphatase-2A (PP2A), which, in turn, inactivates PKB/Akt and thereby attenuates the insulin respons”
- Disordered lipid metabolism and the pathogenesis of insulin resistance. (2007, neutral): “(110) recently argued that ceramides may be a key factor in the pathogenesis of insulin resistance.”