Deficiency of subsarcolemmal mitochondria in obesity and type 2 diabetes.

By V. Ritov, Elizabeth V. Menshikova, Jing He, R. Ferrell, B. Goodpaster, D. Kelley. Diabetes, 2005

904 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/e99e3263d3bc1999be848b216cbcc4f473f67930

How researchers see this paper

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

In Cell Biology

1. Ralph DeFronzo
2. Gerald I. Shulman
3. B. Goodpaster
4. J. Luiken
5. A. Bonen
6. J. Glatz

In Molecular Biology

1. Gerald I. Shulman
2. Ralph DeFronzo
3. K. Petersen
4. Muhammad Abdul-Ghani
5. M. White
6. D. Befroy
7. K. Morino
8. S. Dufour

In Physiology

1. Gerald I. Shulman
2. Ralph DeFronzo
3. K. Petersen
4. K. Morino
5. Muhammad Abdul-Ghani
6. B. Goodpaster
7. J. Luiken
8. A. Bonen

Citations in the corpus

• Mitochondrial Fission Contributes to Mitochondrial Dysfunction and Insulin Resistance in Skeletal Muscle (2011, background): “For example, the activity of the electron transport chain in subsarcolemmal mitochondria is dramatically reduced in type 2 diabetic and obese subjects, compared with that in lean subjects (36).”
• Membrane fatty acid transporters as regulators of lipid metabolism: implications for metabolic disease. (2010, background): “In obese individuals, the reduction in fatty acid oxidation appears to be correlated with the extent of obesity (BMI) (430) and has also been attributed to a reduced mitochondrial content (202, 246, 384), as fatty acid oxidation by isolated mitochondria of obese individuals was normal (202) and not ”
• Mitochondrial Dysfunction in Diabetes: From Molecular Mechanisms to Functional Significance and Therapeutic Opportunities (2010, neutral): “The SLM are larger, lamellar shaped, and located below the sarcolemma (169, 268).”
• Reduced mitochondrial density and increased IRS-1 serine phosphorylation in muscle of insulin-resistant offspring of type 2 diabetic parents. (2005, positive): “Previous studies have shown that insulin per se stimulates mitochondrial biogenesis (11, 12) and that mitochondrial morphology is altered in obese insulin-resistant and type 2 diabetic individuals (13).”
• Metabolic Syndrome and Insulin Resistance: Underlying Causes and Modification by Exercise Training (2013, positive): “LCFA entry into the mitochondria, carnitine palmitoyltransferase-1 (CPT1), and impaired mitochondrial function (decreased mitochondrial number, lower levels of oxidative enzymes, and lower ATP synthetic rates) are found in insulin-resistant skeletal muscle and coincide with muscle lipid accumulation”
• Increased Levels of Plasma Acylcarnitines in Obesity and Type 2 Diabetes and Identification of a Marker of Glucolipotoxicity (2010, positive): “In support of this hypothesis, impaired FAO and accumulation of intramuscular triglyceride correlates with abnormalities in the ETC and in the redox state (low NAD+/NADH ratios) within the mitochondrial matrix (11,12).”
• Pathogenesis of Insulin Resistance in Skeletal Muscle (2010, background): “Electron microscopic studies have revealed a significant reduction (∼40%) in mitochondrial density in skeletal muscle in lean NGT offspring of type 2 diabetic parents, in obese nondiabetic individuals and in T2DM subjects compared to lean insulin-sensitive, age-matched controls [111, 112].”