Oxidative stress and stress-activated signaling pathways: a unifying hypothesis of type 2 diabetes.

By Joseph L. Evans, I. Goldfine, B. Maddux, G. Grodsky. Endocrine reviews, 2002

2,265 citations recorded by the source corpus.

Subfields: Biochemistry, Clinical Biochemistry, Physiology

View Paper: https://www.semanticscholar.org/paper/7d0950189b167583f411196224c713ac061a215e

How researchers see this paper

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

In Biochemistry

1. Ralph DeFronzo
2. P. Havel
3. Sushil Kumar Jain
4. Prasenjit Manna
5. D. Mozaffarian
6. A. Fardet
7. Haiming Cao

In Clinical Biochemistry

1. Ralph DeFronzo
2. P. Havel
3. A. Fardet
4. A. Kappas
5. Nader G. Abraham

In Physiology

1. M. Qatanani
2. Ralph DeFronzo
3. P. Havel
4. Sushil Kumar Jain
5. A. Meijer
6. P. Codogno
7. Mitchell A. Lazar
8. D. Mozaffarian

Citations in the corpus

• Glucose toxicity in beta-cells: type 2 diabetes, good radicals gone bad, and the glutathione connection. (2003, background): “in 54,55) imply that ROS levels need to be finely regulated to keep good radicals from going bad and thereby avoid oxidative damage to cellular processes (56).”
• Endothelial Dysfunction and Diabetes: Effects on Angiogenesis, Vascular Remodeling, and Wound Healing (2012, background): “ROS causes loss of insulin type 1 diabetes by destructing the β cells but it causes insulin resistance in type 2 diabetes by β cell dysfunction of [49, 55, 56].”
• Mitochondrial dysfunction results from oxidative stress in the skeletal muscle of diet-induced insulin-resistant mice. (2008, background): “Because increased ROS levels also play an important role in altered insulin secretion by pancreas (33), oxidative stress might contribute to the two prominent features of type 2 diabetes, insulin resistance”
• The perfect storm: obesity, adipocyte dysfunction, and metabolic consequences. (2008, background): “ROS also appears to adversely affect insulin production by the pancreas and may lead to -cell apoptosis (27), further exacerbatingglucose-insulinhomeostasis.Additionally,once peripheral glucose homeostasis is compromised by skeletal muscle insulin resistance, hyperglycemia can lead to a further mito”
• Obesity, Oxidative Stress, Adipose Tissue Dysfunction, and the Associated Health Risks: Causes and Therapeutic Strategies (2015, background): “Activation of the polyol pathway causes NADPH depletion and increases the conversion of glucose to sorbitol, which activates several stress genes and causes oxidative stress, as evidenced in several animal studies.(37) Formation of glucosamine-6-phosphate in the hexosamine pathway inhibits thioredox”
• Insulin resistance, lipotoxicity, type 2 diabetes and atherosclerosis: the missing links. The Claude Bernard Lecture 2009 (2010, background): “Multiple stimuli [152], including lipids, activate IkB kinase/NFkB, causing insulin resistance in cultured myocytes [160] and muscle from rodents [155, 161] and humans [162].”
• Mitochondrial dysfunction and molecular pathways of disease. (2007, background): “0% of all oxygen consumed is converted in mitochondria to the superoxide (O2 ) radical (Shigenaga et al., 1994; Evans et al., 2002; Carreras et al., 2004).”
• New hypotheses for the health-protective mechanisms of whole-grain cereals: what is beyond fibre? (2010, background): “Whole-grain cereals can protect the body against the increased oxidative stress that is involved and/or associated with all the major chronic diseases: metabolic syndrome((124)), obesity((125,126)), diabetes((127,128)), cancers((91)) and CVD((129,130)).”