ECE2013 Poster Presentations Diabetes (151 abstracts)
Elevation of circulating free fatty acids abolishes down-regulation of skeletal muscle adiponectin receptor 1 (AdipoR1) expression caused by insulin infusion
Marek Straczkowski 1, , Monika Karczewska-Kupczewska 1, , Agnieszka Adamska 1 , Magdalena Stefanowicz 1 , Natalia Matulewicz 1 , Irina Kowalska 1 & Agnieszka Nikolajuk 1,
1Medical University of Bialystok, Bialystok, Poland; 2Institute of Animal Reproduction and Food Research, Polish Academy of Sciences, Olsztyn, Poland.
Introduction: Adiponectin is an adipocytokine with insulin-sensitizing and anti-inflammatory properties. In skeletal muscle, it increases fatty acid oxidation and insulin-stimulated glucose uptake through binding with adiponectin receptor 1 (AdipoR1). The aim of our study was to assess the effect of insulin and Intralipid/heparin infusions on muscle AdipoR1 expression in humans.
Methods: Twenty healthy male subjects (age 25.2±3.2 years; BMI, 26.5±4.6 kg/m2) with normal glucose tolerance were studied. Six-hours euglycemic hyperinsulinemic clamp was performed two times: with and without concurrent Intralipid/heparin infusion. Indirect calorimetry was performed at baseline and every 2 h of the clamp. Biopsy of vastus lateralis muscle was performed before and after each clamp. Muscle AdipoR1 and insulin receptor substrate 1 (IRS1) mRNA expression was analyzed with Real Time PCR.
Results: Intralipid/heparin infusion resulted in a decrease in insulin sensitivity by ~40% (P<0.0001). Serum adiponectin concentration decreased similarly during both clamp (~−25%, both P<0.001). Muscle AdipoR1 was positively related to serum adiponectin (r=0.46, P=0.046), insulin sensitivity (r=0.50, P=0.023), muscle IRS1 (r=0.55, P=0.014), but negatively to respiratory quotient in insulin-stimulated conditions (r=−0.45, P=0.046). Insulin infusion decreased muscle AdipoR1 expression by ~30% (P=0.006). This effect was almost completely abolished by concurrent Intralipid/heparin infusion (−7%, P=0.44; the difference between two experiments, P=0.027).
Conclusions: Our data indicate that elevation of circulating free fatty acids abolishes down-regulation of muscle AdipoR1 expression caused by insulin, independently of the changes in serum adiponectin. This may be a potential compensatory mechanism for free fatty acid-induced insulin resistance.
Volume 32
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Endocrine Abstracts
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