Limits...
Maternal regulation of offspring development in mammals is an ancient adaptation tied to lactation ☆

View Article: PubMed Central - PubMed

ABSTRACT

The developmental origins of health and disease (DOHaD) is a paradigm for understanding metabolic diseases of modern humans. Vulnerability to disease is linked to perturbations in development during critical time periods in fetal and neonatal life. These perturbations are caused by environmental signals, often generated or transduced by the mother. The regulation of mammalian development depends to a large extent on maternal biochemical signals to her offspring. We argue that this adaptation is ancient, and originated with the evolution of lactation. Lactation evolved earlier than live birth and before the extensive placental development of modern eutherian mammals. Milk contains a host of signaling molecules including nutrients, immunoglobulins, growth factors and metabolic hormones. As evidenced by marsupials, lactation originally served to supply the biochemical factors for growth and development for what is essentially a fetus to a weanling transitioning to independent existence. In placental mammals maternal signaling in earliest life is accomplished through the maternal–placental–fetal connection, with more of development shifted to in utero life. However, significant development occurs postpartum, supported by milk. Mothers of all taxa provide biochemical signals to their offspring, but for non-mammalian mothers the time window is short. Developing mammals receive maternal biochemical signals over an extended period. These signals serve to guide normal development, but also can vary in response to environmental conditions. The ancient adaptation of lactation resulted in a lineage (mammals) in which maternal regulation of offspring development evolved to a heightened degree, with the ability to modify development at multiple time points. Modern metabolic diseases may arise due to a mismatch between maternal regulation and eventual circumstances of the offspring, and due to a large proportion of mothers that exceed past evolutionary norms in body fat and pregnancy weight gain such that maternal signals may no longer be within the adaptive range.

No MeSH data available.


Related in: MedlinePlus

Body mass at 90 days for rat pups born to either a lean genotype dam (L) or an obese phenotype dam (O) and cross fostered to either a lean or obese genotype dam. L–L = lean–lean; O–L = lean–obese; O–O = obese–obese; L–O = lean–obese. Pup phenotype matched the nursing dam genotype, although O–O males were significantly larger than O–L males.
© Copyright Policy - CC BY-NC-ND
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC5121250&req=5

f0005: Body mass at 90 days for rat pups born to either a lean genotype dam (L) or an obese phenotype dam (O) and cross fostered to either a lean or obese genotype dam. L–L = lean–lean; O–L = lean–obese; O–O = obese–obese; L–O = lean–obese. Pup phenotype matched the nursing dam genotype, although O–O males were significantly larger than O–L males.

Mentions: Recent evidence suggests that mothers may pass on their metabolic history to their infants. Maternal obesity predisposes offspring to obesity and metabolic dysfunction in rodent models. Cross fostering mouse pups from lean dams to obese dams during lactation results in those pups becoming vulnerable to obesity and metabolic disease (Gorski et al., 2006, Oben et al., 2010). Cross fostering mouse pups that are predisposed to obesity onto lean dams lowers the extent of obesity in the pups (Reifsnyder et al., 2000) and improves insulin sensitivity (Gorski et al., 2006). Obesity-prone and obesity-resistant rat pups displayed a phenotype consistent with the foster (nursing) dam's genotype prior to weaning rather than to their own genotype (Fig. 1), although after weaning their food intake and weight gain reflected their own genotype (Schroeder et al., 2010). There was an effect of sex, as male obesity-prone pups fostered to obesity-resistant dams, although still becoming obese post-weaning, had significantly lower body weight and fat mass than obesity-prone male pups nursed by obesity prone dams (Fig. 1; Schroeder et al., 2010). Important aspects of early postnatal development appear to be regulated to a significant extent via milk, though what bioactive factors are most important are not yet known.


Maternal regulation of offspring development in mammals is an ancient adaptation tied to lactation ☆
Body mass at 90 days for rat pups born to either a lean genotype dam (L) or an obese phenotype dam (O) and cross fostered to either a lean or obese genotype dam. L–L = lean–lean; O–L = lean–obese; O–O = obese–obese; L–O = lean–obese. Pup phenotype matched the nursing dam genotype, although O–O males were significantly larger than O–L males.
© Copyright Policy - CC BY-NC-ND
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5121250&req=5

f0005: Body mass at 90 days for rat pups born to either a lean genotype dam (L) or an obese phenotype dam (O) and cross fostered to either a lean or obese genotype dam. L–L = lean–lean; O–L = lean–obese; O–O = obese–obese; L–O = lean–obese. Pup phenotype matched the nursing dam genotype, although O–O males were significantly larger than O–L males.
Mentions: Recent evidence suggests that mothers may pass on their metabolic history to their infants. Maternal obesity predisposes offspring to obesity and metabolic dysfunction in rodent models. Cross fostering mouse pups from lean dams to obese dams during lactation results in those pups becoming vulnerable to obesity and metabolic disease (Gorski et al., 2006, Oben et al., 2010). Cross fostering mouse pups that are predisposed to obesity onto lean dams lowers the extent of obesity in the pups (Reifsnyder et al., 2000) and improves insulin sensitivity (Gorski et al., 2006). Obesity-prone and obesity-resistant rat pups displayed a phenotype consistent with the foster (nursing) dam's genotype prior to weaning rather than to their own genotype (Fig. 1), although after weaning their food intake and weight gain reflected their own genotype (Schroeder et al., 2010). There was an effect of sex, as male obesity-prone pups fostered to obesity-resistant dams, although still becoming obese post-weaning, had significantly lower body weight and fat mass than obesity-prone male pups nursed by obesity prone dams (Fig. 1; Schroeder et al., 2010). Important aspects of early postnatal development appear to be regulated to a significant extent via milk, though what bioactive factors are most important are not yet known.

View Article: PubMed Central - PubMed

ABSTRACT

The developmental origins of health and disease (DOHaD) is a paradigm for understanding metabolic diseases of modern humans. Vulnerability to disease is linked to perturbations in development during critical time periods in fetal and neonatal life. These perturbations are caused by environmental signals, often generated or transduced by the mother. The regulation of mammalian development depends to a large extent on maternal biochemical signals to her offspring. We argue that this adaptation is ancient, and originated with the evolution of lactation. Lactation evolved earlier than live birth and before the extensive placental development of modern eutherian mammals. Milk contains a host of signaling molecules including nutrients, immunoglobulins, growth factors and metabolic hormones. As evidenced by marsupials, lactation originally served to supply the biochemical factors for growth and development for what is essentially a fetus to a weanling transitioning to independent existence. In placental mammals maternal signaling in earliest life is accomplished through the maternal–placental–fetal connection, with more of development shifted to in utero life. However, significant development occurs postpartum, supported by milk. Mothers of all taxa provide biochemical signals to their offspring, but for non-mammalian mothers the time window is short. Developing mammals receive maternal biochemical signals over an extended period. These signals serve to guide normal development, but also can vary in response to environmental conditions. The ancient adaptation of lactation resulted in a lineage (mammals) in which maternal regulation of offspring development evolved to a heightened degree, with the ability to modify development at multiple time points. Modern metabolic diseases may arise due to a mismatch between maternal regulation and eventual circumstances of the offspring, and due to a large proportion of mothers that exceed past evolutionary norms in body fat and pregnancy weight gain such that maternal signals may no longer be within the adaptive range.

No MeSH data available.


Related in: MedlinePlus