Insulin sensitivity: modulation by nutrients and inflammation.

By S. Schenk, Maziyar Saberi, Jerrold M. Olefsky. Journal of Clinical Investigation, 2008

1,221 citations recorded by the source corpus.

Subfields: Endocrine and Autonomic Systems, Epidemiology, Physiology

View Paper: https://www.semanticscholar.org/paper/25d2f0e8459aef957f1c6a30207c3b25ebb117ef

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In Endocrine and Autonomic Systems

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Citations in the corpus

INFLAMMATION AND LIPID SIGNALING IN THE ETIOLOGY OF INSULIN RESISTANCE (2012, neutral): “Cytokine signaling activates stress kinases such as S6K, IKKb, JNK1, and PKCF, which phosphorylate IRS1 on inhibitory serine residues and results in impaired downstream signaling (Hotamisligil, 2006; Schenk et al., 2008).”
Mitochondrial Fission Contributes to Mitochondrial Dysfunction and Insulin Resistance in Skeletal Muscle (2011, background): “Although many studies demonstrated the effect of hyperglycemia on increased generation of ROS and mitochondrial fission in a variety of cell types (26, 48), elevated circulating lipid and inflammatory cytokines usually occur prior to the development of hyperinsulinemia and hyperglycemia during the p”
Adipokines Mediate Inflammation and Insulin Resistance (2013, background): “…mechanisms of obesity-associated T2D are still unclear, however recent studies have shown that low-grade chronic inflammation is an important factor in the pathogenesis of T2D in humans and rodent animal models (Hotamisligil, 2006; Shoelson et al., 2006; Schenk et al., 2008; Ouchi et al., 2011).”
Inflammation 2010: new adventures of an old flame. (2010, background): “Thus, macrophages infiltrate the adipose tissue of obese animals, a phenomenon with well-appreciated pathological consequences (insulin resistance) but an unknown physiological purpose (Schenk et al., 2008).”
Weight loss and lipolysis promote a dynamic immune response in murine adipose tissue. (2010, background): “Genetic and pharmacologic manipulations that reduce ATM content or alter their inflammatory state in obese rodents modulate local inflammation and are associated with reduced insulin resistance (14).”
Homeostasis, Inflammation, and Disease Susceptibility (2015, neutral): “…skeletal muscle, and white adipose tissue to convert glucose and fatty acids into glycogen and triglycerides, respectively , to export these when necessary for storage in the appropriate organ, and to suppress the mobilization of stored fuels (Schenk et al., 2008; Shulman and Petersen, 2011).”
Obesity, inflammation, and atherosclerosis (2009, background): “Excessive amounts of these lipids overload the oxidation and storage pathways, leading to accumulation of fatty acid intermediates, such as diacylglycerol and ceramide”
Insulin receptor signaling in normal and insulin-resistant states. (2014, background): “Elevated circulating free fatty acids (FFA) are observed in obesity and induce activation of JNK, IKK, and PKC and IRS-1 Ser-307 phosphorylation (Schenk et al. 2008).”
NAFLD: a multisystem disease. (2015, background): “Journal of Hepatology 201 products (particularly DAGs) is very important in causing ‘resistance’ within the hepatic insulin signaling pathway [61], promoting hepatic inflammation [62–65] and increasing risk of progressive liver disease that occurs with NASH.”
Obesity and Its Metabolic Complications: The Role of Adipokines and the Relationship between Obesity, Inflammation, Insulin Resistance, Dyslipidemia and Nonalcoholic Fatty Liver Disease (2014, background): “inhibitor of nuclear factor κB kinase β [54].”
Hepatic lipotoxicity and the pathogenesis of nonalcoholic steatohepatitis: The central role of nontriglyceride fatty acid metabolites (2010, background): “A view has emerged from recent studies that the formation of lipid droplets may actually be a protective response that prevents lipotoxicity from other fatty acid–derived species.(4,5,10,12,34) Early studies of lipotoxicity demonstrated this in cardiomyocytes,(35) and subsequently, a protective effe”
Regulation of insulin sensitivity by serine/threonine phosphorylation of insulin receptor substrate proteins IRS1 and IRS2 (2012, background): “Additionally, the expanded adipose compartment in diabetes/obesity produces proinflammatory cytokines such as TNFα and IL1β that can contribute to insulin resistance systemically (reviewed in [79]).”
GPR120 is an omega-3 fatty acid receptor mediating potent anti-inflammatory and insulin-sensitizing effects. (2010, neutral): “Since chronic macrophage-mediated tissue inflammation is a key mechanism for insulin resistance in obesity, we fed obese WT and GPR120 knockout mice a high-fat diet with or without u-3 FA supplementation.”