Interleukin-6 Increases Insulin-Stimulated Glucose Disposal in Humans and Glucose Uptake and Fatty Acid Oxidation In Vitro via AMP-Activated Protein Kinase

By A. Carey, G. Steinberg, S. Macaulay, W. Thomas, A. Holmes, G. Ramm, O. Prelovsek, C. Hohnen-Behrens, M. Watt, D. James and 3 more. Diabetes, 2006

885 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/aebddb2c4d3a258bd55e0631e9bcba2bc071f572

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Citations in the corpus

Exercise is the real polypill. (2013, background): “IL-6 has “leptin-like” actions: through AMPK activation in both skeletalmuscle and adipose tissue (6, 61, 145, 224), it increases glucose uptake (126) and intra-muscle (50, 61, 373) or whole-body (486) lipid oxidation (61, 214).”
Brain-derived neurotrophic factor is produced by skeletal muscle cells in response to contraction and enhances fat oxidation via activation of AMP-activated protein kinase (2009, methodology): “Palmitate oxidation and glucose uptake experiments were performed as previously described [10].”
Muscles and their myokines (2011, background): “Taken together, these data demonstrate that BDNF is a protein, produced in skeletal muscle cells, that is increased by contraction to enhance fat oxidation in an AMPK-dependent fashion, most probably by acting in an autocrine and/or paracrine manner within skeletal muscle.”
Interleukin-6 enhances insulin secretion by increasing glucagon-like peptide-1 secretion from L cells and alpha cells (2011, neutral): “During exercise, it is proposed that IL-6 promotes nutrient availability and improves whole-body insulin sensitivit”
Biochemistry of adipose tissue: an endocrine organ (2013, background): “It is also possible that RAAS peptides secreted by adipose tissue act on the vasculature and distant targets to regulate blood pressure and cardiovascular responses in obese individuals [32].”
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): “Treatment of IL-6 enhances insulin-stimulated glucose disposal in humans in vivo, and it increases glucose uptake and fatty acid oxidation in cultured L6 myotubes via activation of adenosine monophosphate-activated protein kinase (AMPK), as well as having an anti-inflammatory effect [101,102], where”
AMPK: an emerging drug target for diabetes and the metabolic syndrome. (2009, background): “IL-6 also rapidly and markedly increased AMPK activity in myotubes, enhancing fatty acid oxidation as well as basal and insulin-stimulated glucose uptake (Carey et al., 2006).”
AMPK in Health and Disease. (2009, methodology): “The mammalian AMPK domain limits were established experimentally by partial proteolysis (395), and a stable rat 1(68-163) fragment was expressed and crystallized in the presence of -cyclodextrin (an 1-4 linked heptaglucan), as had previously been performed for other starch binding domain structural ”
Adipocytes as regulators of energy balance and glucose homeostasis (2006, background): “Other cytokines, including interleukin-6, are produced by adipocytes, and there is conflicting evidence suggesting that they have both insulin-resistance-promoting and insulin-sensitizing effect”