|
| HPA axis development and function | |
| (i) Altered placental 11betaHSD activity and cortisol : cortisone in fetal circulation [20, 21] | |
| (ii) Accelerated activation of fetal HPA axis in late gestation [22–25] | |
| (iii) Preterm birth [23–25] | |
| (iv) Enhanced HPA axis response to CRH stimulation at 2 months [26] | |
| (v) Blunted cortisol response to CRH and AVP stimulation in adult offspring [27] | |
| (vi) Increased adrenal gland size in males and females and greater stress response in adult female offspring accompanied by epigenetic changes to adrenal IGF2/H19 gene [28] | |
|
| Growth, body composition, and energy regulating pathways | |
| (i) Altered relationships between maternal weight and fetoplacental growth in early pregnancy [29] | |
| (ii) Altered fetal growth response to late gestation stressors [30] | |
| (iii) Epigenetic changes in POMC and GR genes in fetal hypothalamus [31] | |
| (iv) Reduced fat mass in offspring of overweight ewes [32] | |
| (v) Greater percent fat mass and smaller relative heart, lungs, and adrenals in male offspring [33] | |
| (vi) Decreased voluntary physical activity in adult offspring [34] | |
|
| Glucose-insulin axis | |
| (i) Impaired pregnancy insulin resistance [35] | |
| (ii) Increased fetal insulin response to glucose in late gestation [36] | |
| (iii) Altered thermogenic, insulin, and fatty acid oxidation signalling in fetal perirenal fat depot [37] | |
| (iv) Altered glucose-insulin metabolism in adult males [38] | |
| (v) Epigenetic modification of hepatic insulin-signalling molecules [39] | |
| (vi) Impaired glucose tolerance in adult offspring [40] | |
|
| Cardiovascular function | |
| (i) Increased late gestation fetal blood pressure [41] | |
| (ii) Enhanced vasoconstriction in adult female coronary arteries and endothelial dysfunction in femoral resistance vessels [42] | |
|
