Impaired mitochondrial activity in the insulin-resistant offspring of patients with type 2 diabetes.
By K. Petersen, S. Dufour, D. Befroy, R. Garcia, Gerald I. Shulman. New England Journal of Medicine, 2004
2,223 citations recorded by the source corpus.
Subfields: Endocrinology, Diabetes and Metabolism, Epidemiology, Physiology
View Paper: https://www.semanticscholar.org/paper/9816067e1308da31e5584238782e06a507061643
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Endocrinology, Diabetes and Metabolism
- Gerald I. Shulman
- V. Samuel
- K. Petersen
- M. Karin
- Nir Barzilai
- Jerrold M. Olefsky
- Douglas C. Wallace
- B. K. Pedersen
In Epidemiology
- Gerald I. Shulman
- V. Samuel
- Jerrold M. Olefsky
- K. Petersen
- M. Komatsu
- A. M. Petersen
- A. Hevener
- Jamal Naderi
In Physiology
- Gerald I. Shulman
- V. Samuel
- R. Scarpulla
- Johan Auwerx
- K. Petersen
- Douglas C. Wallace
- M. Qatanani
- Mitchell A. Lazar
Citations in the corpus
- The anti-inflammatory effect of exercise. (2005, background): “In humans, circulating IL-6 levels may (6, 107) or may not (18, 106) be associated with insulin resistance.”
- Mechanisms of obesity-associated insulin resistance: many choices on the menu. (2007, background): “Plasma IL-6 concentrations predict the development of T2DM (Vozarova et al. 2001), and peripheral administration of IL-6 induces hyperlipidemia, hyperglycemia, and insulin resistance in rodents and humans (Stith and Luo 1994; Tsigos et al. 1997; Petersen et al. 2005).”
- Mitochondrial Dynamics in the Regulation of Nutrient Utilization and Energy Expenditure (2013, background): “…favor the hypothesis that inherited or induced transcriptional downregulation of mitochondrial transcripts (Mootha et al., 2003; Patti et al., 2003, Petersen et al., 2004) is a protective mechanism which counteracts insulin resistance, rather than a pathogenic mechanism contributing to insulin…”
- Metabolic control of muscle mitochondrial function and fatty acid oxidation through SIRT1/PGC‐1α (2007, background): “In fact, there is a strong correlation between the presence of intramyocellular lipid in skeletal muscle and liver and progression of type II diabetes (Guan et al, 2002; Kelley et al, 2002; Petersen et al, 2004).”
- AMPK: an emerging drug target for diabetes and the metabolic syndrome. (2009, background): “More recently, defects in fatty acid oxidation have been considered the primary causal factors in the development of muscle insulin resistance (Petersen et al., 2004).”
- Current approaches for assessing insulin sensitivity and resistance in vivo: advantages, limitations, and appropriate usage. (2008, methodology): “In addition, (31)P magnetic resonance spectroscopy may be used in conjunction with the glucose clamp to assess rates of insulin-stimulated muscle mitochondrial ATP synthase flux and insulin-stimulated increases in concentrations of intramyocellular inorganic phosphate (75).”
- Transcriptional paradigms in mammalian mitochondrial biogenesis and function. (2008, background): “ficiency has been found in the insulin-resistant offspring of patients with type 2 diabetes (164).”
- Regulation of mitochondrial biogenesis (2010, background): “In further studies, Petersen and co-workers [47,49] measured basal rates of mitochondrial function in human skeletal muscle of young, lean and sedentary insulin-resistant offspring of parents with Type 2 diabetes.”
- Membrane fatty acid transporters as regulators of lipid metabolism: implications for metabolic disease. (2010, background): “In individuals with type 2 diabetes, whole muscle fatty acid oxidation also appears to be reduced (18), and basal mitochondrial oxidative phosphorylation was reduced in insulin-resistant offspring of patients with type 2 diabetes (331).”