Inaugural Article: The role of skeletal muscle insulin resistance in the pathogenesis of the metabolic syndrome

By K. Petersen, S. Dufour, D. Savage, S. Bilz, J. Solomon, S. Yonemitsu, G. Cline, D. Befroy, L. Zemany, B. Kahn and 3 more. 2007

725 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/e303f3c1f75cbc6f3b455e305e60c2d8efb46daa

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Citations in the corpus

• Mitochondrial dysfunction: mechanisms and advances in therapy (2024, background): “300,301 As NAFLD progresses to nonalcoholic steatohepatitis (NASH), mitochondria evidence a distinct shift to metabolic maladaptation, indicated by ultrastructural damage, compromised ETC activity, upregulated uncoupling protein content, and increased ROS production.”
• Metabolic flexibility in health and disease (2017, unknown): “, 2012), and an enormous body of work supports a causal role for skeletal muscle insulin resistance in type 2 diabetes (DeFronzo and Tripathy, 2009; Petersen et al., 2007).”
• Mechanisms and disease consequences of nonalcoholic fatty liver disease (2021, background): “Othermetabolic causes of NAFLD andNASH, which are most often genetically related, include (1) defects in intrahepatic lipolysis (e.g., decreased ATGL/CGI-58 activity); (2) defects in triglyceride export (e.g., defective Apo-B 100, MTTP activity); (3) increased glucokinase activity, resulting in incr”
• Regulation of insulin sensitivity by serine/threonine phosphorylation of insulin receptor substrate proteins IRS1 and IRS2 (2012, background): “Frequent sampling of postprandial blood in these individuals—in combination with more sophisticated tracer/ imaging techniques to monitor metabolism—reveals the redirection of dietary carbohydrate away from glycogen synthesis in muscle and toward the insulin-driven synthesis of TAG in the liver [75,”
• Increased de novo Lipogenesis is a Distinct Characteristic of Individuals with Nonalcoholic Fatty Liver Disease (2013, unknown): “Previously, indirect evidence of elevated lipogenesis in NAFLD has come from the findings of Fabbrini et al(7) and Sevastianova et al(30) andmuscle insulin resistance has been hypothesized to contribute to NAFLD by shifting dietary carbohydrate away from muscle glycogen synthesis and into hepatic li”
• Current approaches for assessing insulin sensitivity and resistance in vivo: advantages, limitations, and appropriate usage. (2008, background): “Insulin resistance plays a major pathophysiological role in type 2 diabetes and is tightly associated with major public health problems including obesity, hypertension, coronary artery disease, dyslipidemias, and a cluster of metabolic and cardiovascular abnormalities that define the metabolic syndr”
• Non Alcoholic Fatty Liver Disease, Hepatic Insulin Resistance and Type 2 Diabetes (2014, background): “In individuals with selective IR in skeletal muscle, as observed in healthy, young, lean, individuals in the bottom quartile of whole-body insulin sensitivity, ingested carbohydrates are diverted away from muscle glycogen synthesis and toward hepatic de novo lipogenesis, predisposing these individua”