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Retinoic Acid Synergizes with Insulin to Induce Glucose Disposal in L6 Rat Skeletal Muscle Cells
Author(s) -
Goff Matthew,
Chen Guoxun
Publication year - 2015
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.29.1_supplement.596.7
Subject(s) - medicine , endocrinology , insulin , glucose uptake , carbohydrate metabolism , skeletal muscle , metabolism , glucose homeostasis , chemistry , retinoic acid , glucose transporter , biology , cell culture , insulin resistance , genetics
Skeletal muscle is the largest body mass for glucose uptake and usage. Alterations of muscle cell number, differentiation, and function can affect glucose homeostasis in the body. As an essential micronutrient, vitamin A plays a critical role in a variety of physiological functions including glucose and lipid metabolism. However, its role in muscle glucose metabolism has not been well established. Therefore, our goal was to investigate the effects of retinoic acid (RA) on glucose usage in rat L6 muscle cell line, a well‐known model for skeletal muscle cell differentiation and metabolism. L6 cells were maintained in DMEM with 10% FBS until ~100% confluence and induced differentiation in medium containing 2% horse serum (HS). The differentiated cells were treated with increasing dosages of RA (0.3, 1, 3, and 10mM) for a period of 6 days. Media were collected every 2 days for the measurements of pH and remaining glucose levels. Compared to cells in the 2% HS control groups, cells treated with 1, 3, and 10mM RA displayed significant decreases in glucose levels at 6 day. Insulin treatments (1 to 100nM) significantly decreased medium glucose levels after 2 days. When RA (1mM) and insulin (0.1nM) were added together, a further decrease of media glucose levels was observed at day 4. At day 4, treatment of 0.1nM insulin alone did not cause a significant decrease in glucose when compared to the control. Therefore, we conclude that RA and insulin signaling pathways work cooperatively to enhance muscle cell glucose utilization.