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Attenuation of High Glucose/High Insulin‐Induced Muscle Insulin Resistance by Rosemary Extract
Author(s) -
Shamshoum Hesham,
Tsiani Evangelia
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.767.10
Subject(s) - insulin resistance , medicine , glut4 , endocrinology , insulin , glucose uptake , glucose transporter , hyperinsulinemia , protein kinase b , insulin receptor , glucose homeostasis , skeletal muscle , carbohydrate metabolism , chemistry , biology , biochemistry , signal transduction
Insulin is a key hormone affecting metabolism and plays a major role in the regulation of glucose homeostasis. Skeletal muscle accounts for ~80% of postprandial glucose disposal and is thus the major organ of glucose uptake. Insulin increases muscle glucose uptake by increasing the translocation of intracellularly stored GLUT4 glucose transporters to the plasma membrane through the phosphatidylinositol‐3 kinase (PI3K)/Akt signaling pathway. Impaired PI3K/Akt signaling is associated with insulin resistance (IR) in skeletal muscle, leading to chronically elevated blood glucose levels and followed by a compensatory rise in insulin levels. The elevated glucose and insulin levels, in turn, exacerbate IR. Polyphenols are phytochemicals derived from natural plant sources that were found to have antioxidant, anti‐inflammatory, anti‐cancer and anti‐diabetic effects.Rosemary extract (RE), rich in polyphenols, contains carnosic acid (CA), carnosol (COH) and rosmarinic acid (RA), which have been shown to counteract insulin resistance in both in vitro and in vivo animal models. However, the mechanisms involved are not known. Therefore, the aim of this study is to investigate the effects of RE on high glucose (HG)/high insulin (HI)‐induced skeletal muscle insulin resistance and the molecular mechanisms involved. Glucose uptake was assessed using [ 3 H]‐2‐deoxy‐d‐glucose. Total and phosphorylated levels of Akt and IRS‐1 were measured by immunoblotting. Exposure of L6 myotubes to 25mM glucose/100nM insulin for 24 h, to mimic hyperglycemia/hyperinsulinemia, abolished the acute insulin‐stimulated glucose uptake (I: 180±10.43, HG/HI + I: 108 % of basal). In addition, HG/HI attenuated the insulin‐stimulated Akt phosphorylation, while increased IRS‐1 Ser 636/639 phosphorylation indicating insulin resistance. Importantly, treatment with RE (5 μg/ml, 24 h) significantly restored the insulin‐stimulated glucose uptake (HG/HI + RE + I: 184%). Our data indicate a potential of RE to counteract muscle insulin resistance. The focus of our research is to investigate the mechanism involved in mediating this effect of RE. Support or Funding Information Supported by a Natural Sciences and Engineering Research Council of Canada (NSERC) grant to ET This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .