Marion Martin's research while affiliated with Université de Lille and other places

... Shortening the standard (21 days) lactation period (usually by the last 3 days, comparable to 1 month in humans [16]) results in obesity (on a regular diet), dyslipidemia, resistance to leptin and insulin, anxiety, aggressive behavior, and preference for fat and palatable foods in the adult offspring (15). On the contrary, delayed weaning protects rat offspring from obesity (17). Hence, animal models may recapitulate to some extent the human situations. ...

... The proposed mechanism that underlies this protective effect involves the liver, specifically by promoting elevated expression and secretion of hepatic FGF21. This molecule is able to access the central nervous system, where it regulates systemic effects and reprograms hypothalamic circuitries, rendering the descendants additionally resistant to diet-induced obesity later in life [56]. On the other hand, a comparison of serum biochemistry between breastfed children and formula-fed children revealed significant differences in molecules directly related to liver metabolism. ...

... Finally, in light of the unusual vulnerability of fetal GnRH neurons, particular attention must also be paid to the consequences of maternal or perinatal COVID-19 infection in neonates. 88 Indeed, the growing evidence that some neonates born to infected mothers may be COVID-19-positive 89 is especially concerning since the first postnatal activation of the HPG axis, i.e., minipuberty, a phenomenon that plays a key role in the later maturation of the reproductive system 45,90 and likely also in brain development in a broader sense, 49 occurs shortly after birth. The impairment of minipuberty, 91,92 for example by premature birth, 93,94 may be correlated with the incidence of a range of age-related noncommunicable diseases or metabolic dysfunction, 49,93,94 and early reports already indicate that antenatal or neonatal exposure to SARS-CoV-2 may lead to neurodevelopmental delays. ...

... These epigenetic alterations were discovered to be heritable, as they also appeared in the F1 and F2 generation of these mice [83]. However, Lopez-Rodriguez and colleagues [33] reached a slightly different outcome, as their study concluded that delayed pubertal onset and altered folliculogenesis was inherited by F2 and F3 mice, but not by F1 ones, after gestation exposition to a combination of EDCs, including BPA and phthalates (DEHP and DNBP), among others. These effects were identified as a result of an epigenetic alteration of hypothalamic genes controlling puberty and ovulation. ...