Abstract
A variable mix of genetic, epigenetic and environmental factors may result in a “mismatch” sequence of reduced prenatal weight gain (with reduced subcutaneous adipogenesis, and thus a reduced capacity for safe lipid storage) and/or augmented postnatal weight gain (with augmented lipogenesis, thus an augmented need for lipid storage). Such a “mismatch” may lead to ectopic lipid accumulation, particularly in liver and viscera (central obesity), whose endocrine reflection tends to be insulin resistance [1,2].
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