“…Indeed, it stimulates the theca cells to produce androgens and exert a growth stimulatory effect on GCs cells, thus priming the production of estradiol [ 3 ]. Overstimulation of the insulin pathway due to a high-fat diet reinforces the activity of LH on theca cells causing excessive androgen production which in turn contributes to the dysregulation of GCs differentiation in female mice [ 36 , 41 , 46 , 70 , 74 , 75 , 94 , 95 , 96 , 97 ], rats [ 19 , 25 , 26 , 32 , 42 , 71 , 72 , 84 , 98 ], ruminants [ 20 ], pigs [ 28 , 29 , 45 ], rabbits [ 18 ], humans [ 79 ], and non-human primates [ 57 , 86 , 87 ], compromising the follicular progression [ 23 , 99 , 100 ]. As a consequence of GCs dysregulation, a poor follicular vascularization, which at a molecular level is attributable to dysfunctional behavior of the angiogenic factors, such as the vascular–endothelial growth factor A (VEGFA) [ 101 , 102 , 103 ], vascular–endothelial growth factor receptor 1 (VEGFR1) [ 104 ], PDGF [ 105 ], transforming growth factor beta (TGF-β) [ 106 , 107 ], basic fibroblast growth factor (bFGF) [ 108 ], angiopoietin 1 and 2 [ 105 , 109 ], and placent...…”