Figure 1.

Main routes by which maternal obesity impacts on hypothalamic development and function in the offspring. Animal models have shown that exposure to maternal obesity impacts on hypothalamic development throughout fetal development. Maternal obesity is associated with reduced proliferation of hypothalamic progenitor cells in the fetal and neonatal hypothalamus, whether this is a permanent reduction or a delay in the normal neurogenic process is unknown. The formation of intra- hypothalamic projections- particularly in the melanocortin system- is also disrupted in offspring exposed to maternal obesity. This may be due to altered signalling of neurotrophic factors such as leptin, resulting in a reduction in neurite projections, or altered expression of axon guidance cues, resulting in incorrect targets of growing neurites. The offspring of obese mothers also show reduced nutrient sensing, which is one of the primary functions of the hypothalamus and required for the correct regulation of energy homeostasis.