Banting lecture 2001: dysregulation of fatty acid metabolism in the etiology of type 2 diabetes.

By J. McGarry. Diabetes, 2002

1,506 citations recorded by the source corpus.

Subfields: Endocrinology, Diabetes and Metabolism, Genetics, Physiology

View Paper: https://www.semanticscholar.org/paper/754111460942e97b4b2dbac834caf8ded29802d7

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In Endocrinology, Diabetes and Metabolism

In Genetics

In Physiology

Citations in the corpus

A high-fat diet coordinately downregulates genes required for mitochondrial oxidative phosphorylation in skeletal muscle. (2005, background): “One common feature of diverse insulin-resistant states is an elevation in nonesterified fatty acids (11).”
Pathogenesis of Insulin Resistance in Skeletal Muscle (2010, background): “The important role of elevated plasma FFA in the pathogenesis of insulin resistance is now well established [12, 14, 57].”
A Branched-Chain Amino Acid-Related Metabolic Signature that Differentiates Obese and Lean Humans and Contributes to Insulin Resistance (2009, background): “This would lead to increased tissue malonyl CoA levels and suppression of fatty acid oxidation in liver (McGarry, 2002), partitioning lipids toward esterification pathways.”
Disordered lipid metabolism and the pathogenesis of insulin resistance. (2007, neutral): “MRS measurements of intramyocellular lipids (IMCL) correlate more closely with insulin resistance than any other commonly measured indices including body mass index (BMI), waist-hip ratios, or total body fat (58, 67).”
Overproduction of large VLDL particles is driven by increased liver fat content in man (2006, background): “Indeed, increased delivery of NEFA to the liver in humans is associated with fatty liver [29, 30] and has been linked to hepatic insulin resistance [31–33].”
Are oxidative stress-activated signaling pathways mediators of insulin resistance and beta-cell dysfunction? (2003, background): “FFA-induced activation of NF- B can be prevented by vitamin E (72), suggesting that the alteration in cellular redox status is a contributory component of the proinflammatory effects of FFAs.”
Insulin resistance in non-diabetic patients with non-alcoholic fatty liver disease: sites and mechanisms (2005, neutral): “conservative, through substrate competition [41].”
Inhibition of ceramide synthesis ameliorates glucocorticoid-, saturated-fat-, and obesity-induced insulin resistance. (2007, background): “Second, excess lipids may be delivered to nonadipose tissues that are not suited for fat storage (i.e., skeletal muscle and the liver), thus leading to the formation of specific metabolites that directly antagonize insulin action (McGarry, 2002; Schmitz-Peiffer, 2000).”
Diabetes associated cell stress and dysfunction: role of mitochondrial and non‐mitochondrial ROS production and activity (2007, background): “Increased plasma concentration of free fatty acid (FFA) leads to intramyocellular lipid accumulation in humans, and this has also been proposed to play a critical role in initiating and developing insulin resistance and also pancreaticβ-cell death (McGarry, 2002; Azevedo-Martins et al. 2006).”