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Partial hepatic resistance to IL-6-induced inflammation develops in type 2 diabetic mice, while the anti-inflammatory effect of AMPK is maintained

Artikel i vetenskaplig tidskrift
Författare Emmelie Cansby
Annika Nerstedt
Manoj Amrutkar
Esther Nuñez Durán
Ulf Smith
Margit Mahlapuu
Publicerad i Molecular and Cellular Endocrinology
Volym 393
Nummer/häfte 1-2
Sidor 143-151
ISSN 0303-7207
Publiceringsår 2014
Publicerad vid Institutionen för medicin, avdelningen för molekylär och klinisk medicin
Sidor 143-151
Språk en
Länkar dx.doi.org/10.1016/j.mce.2014.06.01...
Ämnesord IL-6, AMPK, Inflammation, Liver, Type 2 diabetes, ACTIVATED PROTEIN-KINASE, ACUTE-PHASE RESPONSE, INDUCED, GLUCOSE-INTOLERANCE, ADULT-RAT HEPATOCYTES, HUMAN SKELETAL-MUSCLE, STIMULATORY FACTOR-II, TUMOR-NECROSIS-FACTOR, FATTY-ACID OXIDATION, C-REACTIVE PROTEIN, INSULIN-RESISTANCE, Cell Biology, Endocrinology & Metabolism, GA T, 1989, CELL, V58, P573, GA T, 1987, JOURNAL OF EXPERIMENTAL MEDICINE, V166, P967, EWARD AR, 1985, MOLECULAR PHARMACOLOGY, V27, P125
Ämneskategorier Klinisk medicin

Sammanfattning

Interleukin-6 (IL-6) induces hepatic inflammation and insulin resistance, and therapeutic strategies to counteract the IL-6 action in liver are of high interest. In this study, we demonstrate that acute treatment with AMP-activated protein kinase (AMPK) agonists AICAR and metformin efficiently repressed IL-6-induced hepatic proinflammatory gene expression and activation of STAT3 in a mouse model of diet-induced type 2 diabetes, bringing it back to basal nonstimulated level. Surprisingly, the inflammatory response in liver induced by IL-6 administration in vivo was markedly blunted in the mice fed a high-fat diet, compared to lean chow-fed controls, while this difference was not replicated in vitro in primary hepatocytes derived from these two groups of mice. In summary, our work reveals that partial hepatic IL-6 resistance develops in the mouse model of type 2 diabetes, while the anti-inflammatory action of AMPK is maintained. Systemic factors, rather than differences in intracellular IL-6 receptor signaling, are likely mediating the relative impairment in IL-6 effect.

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