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Myostatin expression and high fat diet effects on skeletal muscle and adipose metabolism in mouse (1102.45)
Author(s) -
Constantinescu Silvana,
Abraham Andrea,
ReiszPorszasz Suzanne
Publication year - 2014
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.28.1_supplement.1102.45
Subject(s) - medicine , endocrinology , adipose tissue , insulin resistance , myostatin , carbohydrate metabolism , skeletal muscle , glycolysis , chemistry , metabolism , insulin , beta oxidation , biology
We explored the effects of myostatin (Mst) expression and high fat diet (HFD) on skeletal muscle (SM) and adipose tissues (AT) metabolic profiles in transgenic mice overexpressing Mst (TG). To investigate the effects of Mst on SM and AT in wild‐type (WT) and TG mice, and the correlation between Mst and insulin resistance, we measured mRNA levels and protein expression of Mst, several intermediates from the insulin signaling pathway and analyzed the metabolic profile of both tissues using METABOLON. Methods: Adult male mice (6 mice/group) were kept on control diet (CD) and HFD for 4 weeks; glucose tolerance was measured before and after the diet; blood, SM and AT were collected. Results: Metabolon heat‐map analysis showed that Mst in TG mice on CD or HFD increased (95%; P<0.05) several glycolytic intermediates in SM suggesting that glycolysis and glucose uptake is elevated by Mst overexpression. TG mice on CD had lower (P>0.05) levels of free fatty acids (FFAs) compared to WT in SM and AT. HFD increased (25%) the levels of FFAs in SM compared to AT in WT and TG. Conclusion: WT‐SM responded to HFD with a rise (62%) in fatty acid oxidation (FAO); TG‐SM with HFD showed no change (P>0.05) in FAO. TG‐AT responded to HFD with a rise in triacylglycerol synthesis (12%) and a decrease in FAO. These data suggest that genetic modification of Mst expression affected primarily SM glucose utilization parallel with decreased FAO in AT in adult mice. Grant Funding Source : NIH/NIGMS: SC1GM089648