Developmental Programming in Response to Intrauterine Growth Restriction Impairs Myoblast Function and Skeletal Muscle Metabolism

Figure 2

Impact of placental insufficiency on endocrine responsiveness in fetal myoblasts and myofibers. Adrenergic activity increases due to greater circulating catecholamines. Adrenergic receptor β subtype-specific desensitization results in a greater proportion of signaling through Adrβ1 and Adrβ3 because Adrβ2 expression is reduced. Insulin signaling is reduced due to adrenergic suppression of insulin secretion in pancreatic β-cells and by muscle adrenergic signaling that negatively influences the insulin-Akt2 intercellular signaling pathway. These developmental adaptations reduce rates of myoblast proliferation and differentiation as well as glucose metabolism in skeletal muscle.