Mitochondrial dysfunction and type 2 diabetes

By R. Parish, K. Petersen. Current Diabetes Reports, 2005

1,081 citations recorded by the source corpus.

Subfields: Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/b73fed4f3a251ddfd7686f6401d0f28ed5de0728

How researchers see this paper

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

In Molecular Biology

In Physiology

Citations in the corpus

The PI3K/AKT pathway in obesity and type 2 diabetes (2018, background): “Excessive fatty acid oxidation in the mitochondria via the tricarboxylic acid (TCA) cycle and the electron transport chain (ETC) increases the production of fatty acid metabolites and reactive oxygen species (ROS), subsequently activated intracellular stress kinases to inhibit IRS-1 and possibly exe”
Inflammation and metabolic disorders (2006, background): “However, recent evidence indicates that oxidative stress and mitochondrial dysfunction also have important roles in type 2 diabete”
Mitochondrial Dysfunction in Diabetes: From Molecular Mechanisms to Functional Significance and Therapeutic Opportunities (2010, positive): “Mitochondrial dysfunction should lead to impaired fatty acid oxidation, resulting in increased intracellular fatty acyl-CoA and diacylglycerol content, with consequent activation of protein kinase C (1, 204).”
Metabolic control through the PGC-1 family of transcription coactivators. (2005, background): “The mitochondrial electron transport chain is a major site of ROS production in the cell (Lenaz et al., 2002; Lowell and Shulman, 2005).”
Pathogenesis of Insulin Resistance in Skeletal Muscle (2010, background): “[20] B.”
Peroxisome proliferator-activated receptor gamma coactivator 1 coactivators, energy homeostasis, and metabolism. (2006, background): “In recent years, strong evidence for mitochondrial dysregulation in type 2 diabetes has been found (69).”
Diabetes and mitochondrial function: role of hyperglycemia and oxidative stress. (2006, background): “Hyperglycemia-induced superoxide production by mitochondria is an important aspect in β-cell glucose toxicity (Brownlee, 2003; Lowell and Shulman, 2005).”
Mitochondrial dysfunction results from oxidative stress in the skeletal muscle of diet-induced insulin-resistant mice. (2008, background): “Cumulative evidences strongly suggest that alterations of mitochondrial density and function in skeletal muscle are associated with both insulin resistance and type 2 diabetes (9).”
Exercise metabolism and the molecular regulation of skeletal muscle adaptation. (2013, background): “Dysfunctional mitochondria have been implicated in sarcopenia (Bua et al., 2002) and insulin resistance (Lowell and Shulman, 2005), Transcription factors and coregulator proteins can be activated or induced in response to specific cellular signals, cocomplex with a variety of other factors, and/ or…”
Endothelial dysfunction - a major mediator of diabetic vascular disease. (2013, background): “However, under conditions of oxidative stress, these antioxidant systems are overwhelmed, allowing ROS to exert their deleterious effects and ultimately change mitochondrial function [116,131,134].”
Fiber types in mammalian skeletal muscles. (2011, background): “ity, may contribute to insulin resistance and type 2 diabetes (492, 590).”
MITOCHONDRIAL DNA MUTATIONS IN HUMAN DISEASE (2005, neutral): “A good example of a common condition in which mtDNA is a potential cause is diabetes, the most common metabolic disease to affect human”
SIRT1 is required for AMPK activation and the beneficial effects of resveratrol on mitochondrial function (2012, background): “…2006; Lagouge et al., 2006) and mitochondrial dysfunction is known to play an important role in the development of glucose imbalance in diabetes (Lowell and Shulman, 2005), we sought to determine whether the ability of resveratrol to improve glucose homeostasis was lost in our inducible SIRT1…”