Suboptimal fetal environments due to inadequate maternal nutrition,
obesity,
inflammation or
gestational diabetes expose the fetus to humoral cues that alter metabolism and growth parameters leading to metabolic disturbances later in life. The fetal stage is crucial for the development of skeletal muscle, a tissue playing an important role in metabolism.
Maternal obesity induces
inflammation in the fetus causing modifications in the development of fetal skeletal muscle. Changes in the normal course of myogenesis may arise through several mechanisms: changes in WNT/β-
catenin signaling pathway, decreased AMPK activity evoked by TNF-α, increased activity of NF-κB in response to
inflammation, which leads to a decrease in myogenic
factor MyoD, and increased expression of TGF β1. Modification in fetal development associated with
maternal obesity is attributed to epigenetic changes.
Polyunsaturated fatty acids supplied in the diet did affect the development of
insulin-sensitive tissues during both the fetal and postnatal period. The specific phenotype of skeletal muscle fibers may play a role in the development of
obesity, i.e. fiber phenotype I (slow, oxidative) may protect against
obesity and
insulin resistance. Exploring the mechanisms of direct impact of
maternal obesity on the development of tissues in the offspring may help to reduce the occurrence of
metabolic diseases in later life.