Mature Offspring Research Articles

Parental micronutrient deficiency distorts liver DNA methylation and expression of lipid genes associated with a fatty-liver-like phenotype in offspring

Micronutrient status of parents can affect long term health of their progeny. Around 2 billion humans are affected by chronic micronutrient deficiency. In this study we use zebrafish as a model system to examine morphological, molecular and epigenetic changes in mature offspring of parents that experienced a one-carbon (1-C) micronutrient deficiency. Zebrafish were fed a diet sufficient, or marginally deficient in 1-C nutrients (folate, vitamin B12, vitamin B6, methionine, choline), and then mated. Offspring livers underwent histological examination, RNA sequencing and genome-wide DNA methylation analysis. Parental 1-C micronutrient deficiency resulted in increased lipid inclusion and we identified 686 differentially expressed genes in offspring liver, the majority of which were downregulated. Downregulated genes were enriched for functional categories related to sterol, steroid and lipid biosynthesis, as well as mitochondrial protein synthesis. Differential DNA methylation was found at 2869 CpG sites, enriched in promoter regions and permutation analyses confirmed the association with parental feed. Our data indicate that parental 1-C nutrient status can persist as locus specific DNA methylation marks in descendants and suggest an effect on lipid utilization and mitochondrial protein translation in F1 livers. This points toward parental micronutrients status as an important factor for offspring health and welfare.

Heterochrony in the evolution of Trinidadian guppy offspring size: maturation along a uniform ontogenetic trajectory.

The size and maturity of Trinidadian guppy (Poecilia reticulata) offspring vary among populations adapted to environments of differential predation. Guppy offspring born to low-predation, high-competition environments are larger and more mature than their high-predation ancestors. Here we ask: what specific changes in developmental or birth timing occur to produce the larger, more mature neonates? We collected specimens across the perinatal window of development from five populations and quantified musculoskeletal maturation. We found that all populations undergo similar ontogenetic trajectories in skeletal and muscle acquisition; the only difference among populations is when neonates emerge along the trajectory. The smallest neonates are born with 20% of their skeleton ossified, whereas the largest neonates are born with over 70% of their skeleton ossified. The area of the major jaw-closing muscle is relatively larger in larger offspring, scaling with length as L2.5. The size range over which offspring are birthed among populations sits along the steepest part of the size–maturity relationship, which provides a large marginal increase in fitness for the high-competition female. Because of the functional effects of producing more mature offspring at birth, offspring size may be the first and most critical life-history trait selected upon in highly competitive environments.

Why does inbreeding reduce male paternity? Effects on sexually selected traits.

Mating with relatives has often been shown to negatively affect offspring fitness (inbreeding depression). There is considerable evidence for inbreeding depression due to effects on naturally selected traits, particularly those expressed early in life, but there is less evidence of it for sexually selected traits. This is surprising because sexually selected traits are expected to exhibit strong inbreeding depression. Here, we experimentally created inbred and outbred male mosquitofish (Gambusia holbrooki). Inbred males were the offspring of matings between full siblings. We then investigated how inbreeding influenced a number of sexually selected male traits, specifically: attractiveness, sperm number and velocity, as well as sperm competitiveness based on a male's share of paternity. We found no inbreeding depression for male attractiveness or sperm traits. There was, however, evidence that lower heterozygosity decreased paternity due to reduced sperm competitiveness. Our results add to the growing evidence that competitive interactions exacerbate the negative effects of the increased homozygosity that arises when there is inbreeding.

Sociodemographic variation in foraging behavior and the adaptive significance of worker production in the facultatively social small carpenter bee, Ceratina calcarata

Provisioning for young offspring is an archetypical form of parental investment. Ceratina calcarata bees provide extended maternal care to their young and demonstrate an unusual strategy of dual-phase pollen provisioning. Most bees first gather provisions as they establish nests in spring. However, C. calcarata mothers will also feed their newly eclosed young a second time, perhaps ensuring their survival during a long winter diapause. Some mothers rear a small, worker-like daughter to assist them during this second provisioning phase. We studied provisioning behavior in C. calcarata to examine patterns of maternal investment and foraging dynamics throughout the breeding season. Mothers typically made a high number of short-duration foraging trips each day, whereas late-season females tended to make fewer and longer trips. This difference in foraging duration may indicate a lower risk of brood loss in those nests where mature offspring are present. Nest demographic data revealed that an offspring laid in the first brood cell position is typically female and usually smaller than her siblings. In 29% of the nests, this small daughter was observed to adopt a forager role at maturity and provisioned for her siblings. Dwarf daughters had a higher number of active days and foraging trips per day in orphaned nests than in nests where a mother was present. The foraging behaviors of worker-like daughters were similar in length of foraging trip and handling time to mothers during this second provisioning period. We hypothesize that incipiently social foraging by this smallest daughter may act as a form of insurance against brood loss during occasions when a mother is unable to sufficiently provision for her eclosed offspring during the second phase. Parental investment in the size and sex of offspring is under strong selection for assured fitness returns. For example, many social insect mothers make an initial investment in small offspring to take on risky foraging behavior while they specialize on future reproduction. Solitary and facultatively social species provide an important baseline to understand the evolution of social complexity from natural variation in maternal care and foraging behavior. Here, we characterize the parental investment strategies of a subsocial small carpenter bee and reveal the potential adaptive significance of prolonged maternal care and worker production in this species. Mothers provide an initial investment that is extended by workers providing alloparental care to siblings. Maternal manipulation of dwarf eldest daughters may serve as an insurance mechanism in the event of maternal mortality to assure the survival of siblings.

Maternal obesity programs reduced leptin signaling in the pituitary and altered GH/IGF1 axis function leading to increased adiposity in adult sheep offspring.

Studies in rodents highlight a role for leptin in stimulation of pituitary growth hormone (GH) secretion, with an impact on body composition regulation. We have reported that maternal obesity (MO) during ovine pregnancy results in hyperphagia, glucose-insulin dysregulation, increased adiposity, hypercortisolemia and hyperleptinemia in mature offspring subjected to a bout of ad libitum feeding. We hypothesized that MO reduces leptin signaling in the pituitary and down regulates the GH/IGF1 axis and increases circulating cortisol leading to increased adiposity in their adult offspring. Male lambs born to MO (n = 6) or control (CON, n = 6) ewes were fed only to requirements until placed on a 12 week ad libitum feeding trial at maturity. The pituitary, hypothalamic arcuate nucleus, and liver were collected at necropsy and mRNA and protein expression determined. Plasma cortisol concentrations were increased (P<0.05) in MO vs. CON offspring at the end of the feeding trial. Further, serum concentrations of IGF1 decreased (P<0.01) and GH tended to decrease (P<0.08) in MO vs. CON offspring. Pituitary mRNA and leptin receptor protein expression were decreased in MO vs. CON offspring in association with decreased GH mRNA expression, and decreased IGF1 mRNA and protein expression in liver. Liver 11β-hydroxysteroid dehydrogenase 1 (11βHSD1) expression was increased (P<0.01) and its cofactor hexose-6-phosphate dehydrogenase tended to increase (P<0.06) in MO vs. CON offspring. 11βHSD2 expression remained unchanged. These data indicate that MO induced an increase in liver conversion of cortisone to cortisol in adult offspring and support a role for leptin signaling in the pituitary in mediating offspring adiposity.

Investigating the Prenatal Exposure of Hydro-Alcoholic Extract of Ginger on the Function of Pituitary : Gonad Axis in Male Mature Offspring Rats

Investigating the Prenatal Exposure of Hydro-Alcoholic Extract of Ginger on the Function of Pituitary : Gonad Axis in Male Mature Offspring Rats

Diet-dependent retinoid effects on liver gene expression include stellate and inflammation markers and parallel effects of the nuclear repressor Shp

For mice, a maternal vitamin A (VA)-deficient diet initiated from midgestation (GVAD) produces serum retinol deficiency in mature offspring. We hypothesize that the effects of GVAD arise from preweaning developmental changes. We compare the effect of this GVAD protocol in combination with a postweaning high-fat diet (HFD) or high-carbohydrate diet (LF12). Each is compared to an equivalent VA-sufficient combination. GVAD extensively decreased serum retinol and liver retinol, retinyl esters, and retinoid homeostasis genes (Lrat, Cyp26b1 and Cyp26a1). These suppressions were each more effective with LF12 than with HFD. Postweaning initiation of VA deficiency with LF12 depleted liver retinoids, but serum retinol was unaffected. Liver retinoid depletion, therefore, precedes serum attenuation. Maternal LF12 decreased the obesity response to the HFD, which was further decreased by GVAD. LF12 fed to the mother and offspring extensively stimulated genes marking stellate activation (Col1a1, Timp2 and Cyp1b1) and novel inflammation markers (Ly6d, Trem2 and Nupr1). The GVAD with LF12 diet combination suppressed these responses. GVAD in combination with the HFD increased these same clusters. A further set of expression differences on the HFD when compared to a high-carbohydrate diet was prevented when GVAD was combined with HFD. Most of these GVAD gene changes match published effects from deletion of Nr0b2/Shp, a retinoid-responsive, nuclear co-repressor that modulates metabolic homeostasis. The stellate and inflammatory increases seen with the high-carbohydrate LF12 diet may represent postprandial responses. They depend on retinol and Shp, but the regulation reverses with an HFD.

Parental preferences for the facial traits of their offspring's partners can enhance parental inclusive fitness

Physical appearance provides a wealth of information concerning an individual's biological fitness and reproductive quality, but we do not know whether parents make use of this information when evaluating potential partners for their offspring. This is critical to our understanding of human mate choice, because parents frequently influence their offspring's mating decisions, either directly, for instance through arranged marriages, or indirectly, through manipulating their offspring's partner choice. Here, we used facial images that varied in attractiveness, masculinity, health, and symmetry to assess both reproductively-aged daughters' and their parents' preferences in potential mates for the daughters. In line with our predictions, both daughters and their parents had clear preferences for markers of genetic quality, although the daughters showed significantly stronger preferences for these markers than their parents. Contrary to previous research, parents and daughters did not have stronger preferences for markers of genetic quality if they perceived the daughter to be more attractive. Parents' preferences for the facial markers of genetic quality in their offspring's partner may help maximize inclusive fitness.

Breast milk MSCs: An explanation of tissue growth and maturation of offspring.

Exciting advances are revealing that breast milk harbors populations of stem and progenitor cells, and much attention is now intensified on delineating their properties and functions. The aim of this study is to isolate a mesenchymal stem cell (MSC)-like population from rabbit breast milk and track their integration into the different organs of the breastfed rabbits after taken by oral route and to explore the functional role of stem cells in the breastfed newborn babies. Ten newborn rabbits 2 weeks old fed on 2 × 106 PKH26-labeled rabbit milk derived-MSCs suspended in 2 mL Dulbecco's modified Eagle's medium (DMEM) and 10 newborn baby rabbits fed with 2 mL DMEM solution or with rabbit fibroblasts as a control group were used in the study. All rabbits were sacrificed after 1 week. We found that PKH26-labeled MSCs were engrafted into the offspring organs as liver, cartilage, bone and duodenum. Histologically, there was proliferation of cells in some organs. Moreover, there was overexpression of both PCNA and cyclin D1 genes in all organs from milk derived MSCs fed rabbits compared to the control group. Our results confirmed the presence of MSC-like population in the breast milk. We first showed that milk derived-MSCs were engrafted into the offspring organs when were taken orally. Milk derived-MSCs may elucidate the functional benefits to the newborn babies by increasing cell proliferation and growth. © 2016 IUBMB Life, 68(12):935-942, 2016.

Effects of Maternal Hyperhomocysteinemia on the Early Physical Development and Neurobehavioral Maturation of Rat Offspring

During pregnancy, several complications have been associated with hyperhomocysteinemia (HHcy) and elevated homocysteine (Hcy) levels have been shown to play a role in the etiology of preeclampsia, placental abruption, intrauterine growth retardation, and neural tube defects and associated with the neurological consequences. In the present work, we investigated the effects of chronic maternal HHcy on the development and neurobehavioral maturation of the offspring. We analyzed classical parameters of development such as body weight, eyelid opening, ear unfolding, incisor eruption, and the appearance of hair, and subjected the pups to various tests that reflected the neurobehavioral maturation extending from 4th to 20th postnatal days (righting reflex, negative geotaxis, cliff avoidance, head shake, acoustic startle reflex, free-fall righting, cliff avoidance caused by visual stimulus, olfactory discrimination). We have shown that newborn animals were characterized by lower body weight and higher mortality. Besides, the delay in neurobehavioral maturation of the pups from the Hcy group was observed. The obtained results indicate that early developmental impairments of brain maturation induced by prenatal HHcy may underlie long-term deficits in the learning and memory behaviors.

Prenatal androgen exposure and parental care interact to influence timing of reproductive maturation in marmosets.

The timing of reproductive maturation is susceptible to hormonal and environmental influences, and variation in this timing can be partially attributed to the prenatal and post-natal environment. We examined associations between prenatal steroid exposure and the post-natal family environment on the variability in reproductive maturation timing in young marmosets (Callithrix geoffroyi). Urine samples from pregnant females were analyzed for cortisol (CORT) and androgens (uA). Post-natal uA was measured in males to determine age (in days) of adult-like levels of androgens associated with spermatogenesis; post-natal pregnanediol glucuronide (PdG) was measured in females to determine age (in days) of first ovulation. Maternal, paternal, alloparental, and total care (carrying, grooming, and rejection/removals) of offspring were observed. Female offspring exposed to lower prenatal uA levels and higher paternal grooming and lower maternal rejection/removals showed later first ovulation, whereas female offspring exposed to higher prenatal uA showed earlier first ovulation. Male offspring showed earlier reproductive maturation as paternal grooming increased, regardless of first trimester uA exposure. Male offspring exposed to low prenatal uA levels showed earlier reproductive maturation as maternal rejections/removals increased. In offspring exposed to low prenatal CORT, high total carrying predicted earlier first ovulation in females, but later reproductive maturation in males. Total carrying duration did not affect timing of reproductive maturation in offspring exposed to high third trimester CORT levels. Our findings expand the evolutionary theory of socialization by demonstrating that the effect of post-natal family environment on timing of reproductive maturation depends on prenatal uA exposure and also influences reproductive maturation timing in male offspring.

Developmental cigarette smoke exposure II: Hepatic proteome profiles in 6 month old adult offspring.

Utilizing a mouse model of 'active' developmental cigarette smoke exposure (CSE) [gestational day (GD) 1 through postnatal day (PD) 21] characterized by offspring low birth weight, the impact of developmental CSE on liver proteome profiles of adult offspring at 6 months of age was determined. Liver tissue was collected from Sham- and CSE-offspring for 2D-SDS-PAGE based proteome analysis with Partial Least Squares-Discriminant Analysis (PLS-DA). A similar study conducted at the cessation of exposure to cigarette smoke documented decreased gluconeogenesis coupled to oxidative stress in weanling offspring. In the current study, exposure throughout development to cigarette smoke resulted in impaired hepatic carbohydrate metabolism, decreased serum glucose levels, and increased gluconeogenic regulatory enzyme abundances during the fed-state coupled to decreased expression of SIRT1 as well as increased PEPCK and PGC1α expression. Together these findings indicate inappropriately timed gluconeogenesis that may reflect impaired insulin signaling in mature offspring exposed to 'active' developmental CSE.

Biparental immune priming in the pipefish Syngnathus typhle

The transfer of immunity from parents to offspring (trans-generational immune priming (TGIP)) boosts offspring immune defence and parasite resistance. TGIP is usually a maternal trait. However, if fathers have a physical connection to their offspring, and if offspring are born in the paternal parasitic environment, evolution of paternal TGIP can become adaptive. In Syngnathus typhle, a sex-role reversed pipefish with male pregnancy, both parents invest into offspring immune defence. To connect TGIP with parental investment, we need to know how parents share the task of TGIP, whether TGIP is asymmetrically distributed between the parents, and how the maternal and paternal effects interact in case of biparental TGIP. We experimentally investigated the strength and differences but also the costs of maternal and paternal contribution, and their interactive biparental influence on offspring immune defence throughout offspring maturation. To disentangle maternal and paternal influences, two different bacteria were used in a fully reciprocal design for parental and offspring exposure. In offspring, we measured gene expression of 29 immune genes, 15 genes associated with epigenetic regulation, immune cell activity and life-history traits. We identified asymmetric maternal and paternal immune priming with a dominating, long-lasting paternal effect. We could not detect an additive adaptive biparental TGIP impact. However, biparental TGIP harbours additive costs as shown in delayed sexual maturity. Epigenetic regulation may play a role both in maternal and paternal TGIP.

Cohort effects and proximal versus distal metrics for lifetime reproductive success in Richardson’s ground squirrels

Lifetime reproductive success (LRS) in the form of number of descendants is a commonly used measure of individual fitness, but the life stage at which descendants are counted varies among studies. Conceptual and logistical trade-offs exist along the gradient of proximal-to-distal LRS metrics. Although proximal metrics, such as number of offspring weaned, are logistically easier to collect than distal metrics, such as number of reproductively mature offspring or grandoffspring, they may be of little evolutionary significance if stochastic events heavily influence the realized number of descendants. We use a 25-year demographic data set based on 954 adult female Richardson’s ground squirrels ( Urocitellus richardsonii ) from 22 annual cohorts to characterize and compare 6 metrics for LRS: lifetime production of litters, numbers of weanlings, weanling daughters, adult daughters, weanling matrilineal granddaughters, and adult matrilineal granddaughters. Most adult females weaned only 0 (21%), 1 (47%), or 2 (22%) lifetime litters. All LRS distributions were right skewed, with 53% and 77% of adult female Richardson’s ground squirrels having no adult female matrilineal descendants after 1 and 2 generations, respectively. Survival of daughters and mothers covaried with calendar year, and LRS was strongly influenced by the calendar year in which females recruited into the breeding population as yearlings. Catastrophic flooding in 2005 killed nearly all descendants from the 2004 and 2005 cohorts. Daughter survival to adulthood explained more variance in lifetime production of adult daughters and granddaughters than number, size, or sex ratio of litters. Overall, to have a ≥ 50% chance of 1 adult granddaughter, a female needed to produce 2 litters, 7 weanling daughters, or 2 adult daughters. All distal (response) versus proximal (predictor) LRS metrics had significantly positive relationships, but variability increased with each distal step in the response variable. Our long-term study highlights sampling issues with LRS studies, variability within and among cohorts, and the role of stochastic events in uncoupling a mammal’s reproductive effort from realized number of descendants.

Differential genotypic effects of sexual trait size on offspring mating success and viability

Indicator models of sexual selection predict that females mating with the most ornamented males should produce offspring with enhanced expression of fitness-related traits, such as overall vigor and viability. Empirical support for this prediction, however, is limited. We quantified the effects of a heritable and condition-dependent secondary sexual trait on offspring performance traits in Drosophila bipectinata Duda (Diptera: Drosophilidae). Forty-eight genetic (isofemale) lines were extracted from a natural population, reared in a common environment, and characterized in terms of sex comb size. We measured pupal viability and adult mating success among the progeny of the 5 lines with the largest combs (high line category) and the 5 lines with the smallest combs (low line category). The high line category produced offspring that were significantly more viable than the low line category, and this advantage held across 2 developmental temperatures. In contrast, there was no effect of line category on male mating success, although at the individual-level, comb size was significantly positively correlated with mating success. Our results indicate that the relative size of the D. bipectinata sex comb taps genotypic properties that enhance offspring fitness in a trait-specific manner. Thus, distinct proximate mechanisms likely underlie relationships between secondary sexual trait expression and different performance traits in offspring, offering a possible explanation for inconsistent support for the existence of indirect benefits in sexual selection.

Reproductive competition and inbreeding avoidance in a primate species with habitual female dispersal

As in other highly sexually dimorphic, group-living animals, reproduction in gorillas has been largely viewed as the outcome of competition among males. However, females may exert choice via dispersal decisions or choice of partner in multimale groups, and males may also mate selectively. Here, we examine the paternity of 79 wild mountain gorilla offspring born into four groups characterized by stable dominance hierarchies and the presence of mature offspring of the dominant male. We found that on average the dominant male sires the majority (72 %) of the offspring in stable multimale groups and subordinate males also produce offspring, particularly when dominant males become older or the number of competing males increases. Although expected to disperse to avoid inbreeding, only half of the maturing daughters of dominant males left the group in which their father maintained dominance. However, in all five cases of reproduction by a resident daughter of a dominant male, a subordinate male was the sire of the offspring. As females commonly initiate and end copulations, and dominant males may prefer mating with fully mature females, both male and female mate preferences in addition to male competition apparently play a role in reproductive patterns in multimale groups, emphasizing the complexity of social dynamics in one of our closest living relatives.

Characteristic of sperm motility in mature offspring of females with experimental liver diseases of various origins.

We studied the effect of experimental liver injury of various origins (toxic, autoimmune, alcoholic, and mesenchymal) in the females on motility of spermatozoa in the offspring. The number of infertile (jerking and immotile) spermatozoa increased, whereas the number of fertile spermatozoa (progressive motile and slow motile) was reduced. Changes in the ratio of fertile and infertile germ cells resulted in a significant decrease in sperm motility index.

The multidrug resistance 1 gene Abcb1 in brain and placenta: comparative analysis in human and guinea pig.

The Multidrug Resistance 1 (MDR1; alternatively ABCB1) gene product P-glycoprotein (P-gp), an ATP binding cassette transporter, extrudes multiple endogenous and exogenous substrates from the cell, playing an important role in normal physiology and xenobiotic distribution and bioavailability. To date, the predominant animal models used to investigate the role of P-gp have been the mouse and rat, which have two distinct genes, Abcb1a and Abcb1b. In contrast, the human has a single gene, ABCB1, for which only a single isoform has been validated. We and others have previously shown important differences between Abcb1a and Abcb1b, limiting the extrapolation from rodent findings to the human. Since the guinea pig has a relatively long gestation, hemomonochorial placentation and neuroanatomically mature offspring, it is more similar to the human, and may provide a more comparable model for investigating the regulation of P-gp in the brain and placenta, however, to date, the Abcb1 gene in the guinea pig remains to be characterized. The placenta and fetal brain are barrier sites that express P-gp and that play a critical role of protection of the fetus and the fetal brain from maternally administered drugs and other xenobiotics. Using RNA sequencing (RNA-seq), reverse transcription-polymerase chain reaction (RT-PCR) and quantitative PCR (QPCR) to sequence the expressed isoforms of guinea pig Abcb1, we demonstrate that like the human, the guinea pig genome contains one gene for Abcb1 but that it is expressed as at least three different isoforms via alternative splicing and alternate exon usage. Further, we demonstrate that these isoforms are more closely related to human than to rat or mouse isoforms. This striking, overall similarity and evolutionary relatedness between guinea pig Abcb1 and human ABCB1 indicate that the guinea pig represents a relevant animal model for investigating the function and regulation of P-gp in the placenta and brain.

Transgenerational plasticity in marine sticklebacks: maternal effects mediate impacts of a warming ocean

Summary Our study addresses the role of non‐genetic and genetic inheritance in shaping the adaptive potential of populations under a warming ocean scenario. We used a combined experimental approach [transgenerational plasticity (TGP) and quantitative genetics] to partition the relative contribution of maternal vs. paternal (additive genetic) effects to offspring body size (a key component of fitness), and investigated a potential physiological mechanism (mitochondrial respiration capacities) underlying whole‐organism growth/size responses. In very early stages of growth (up to 30 days), offspring body size of marine sticklebacks benefited from maternal TGP: offspring of mothers acclimated to 17 °C were larger when reared at 17 °C, and offspring of mothers acclimated to 21 °C were larger when reared at 21 °C. The benefits of maternal TGP on body size were stronger and persisted longer (up to 60 days) for offspring reared in the warmer (21 °C) environment, suggesting that maternal effects will be highly relevant for climate change scenarios in this system. Mitochondrial respiration capacities measured on mature offspring (F1 adults) matched the pattern of TGP for juvenile body size, providing an intuitive mechanistic basis for the maternal acclimation persisting into adulthood. Size differences between temperatures seen at early growth stages remained in the F1 adults, linking offspring body size to maternal inheritance of mitochondria. Lower maternal variance components in the warmer environment were mostly driven by mothers acclimated to ambient (colder) conditions, further supporting our tenet that maternal effects were stronger at elevated temperature. Importantly, all parent–offspring temperature combination groups showed genotype × environment (G × E) interactions, suggesting that reaction norms have the potential to evolve. To summarize, TGP and G × E interactions work in concert to mediate impacts of ocean warming on metabolic capacity and early growth of marine sticklebacks. TGP can buffer short‐term detrimental effects of climate warming and may buy time for genetic adaptation to catch up, therefore markedly contributing to the evolutionary potential and persistence of populations under climate change.

Maternal quercetin administration during gestation and lactation decrease endoplasmic reticulum stress and related inflammation in the adult offspring of obese female rats

Maternal obesity is a risk factor for metabolic diseases in offspring. The aim of this study was to investigate whether quercetin administration during gestation and lactation could have any protective effect against the impact of maternal obesity on increased sensitivity to obesity and metabolic disorders in offspring. Female Sprague-Dawley rats were fed a high-fat diet to induce obesity. Obese dams were administered 0, 50, 100 or 200 mg/kg body weight (BW) quercetin intragastrically during gestation and lactation. Normal weight dams were used as controls. The F1 generation was fed with a standard diet after weaning, and blood glucose, lipids and inflammatory factors were assessed. Expression of biomarkers involved endoplasmic reticulum (ER) stress, and related inflammatory pathways in liver and adipose tissues were analyzed at postnatal day 100. Maternal obesity resulted in increased birth weight, postnatal BW gain, hyperglycemia, hyperlipemia, hyperinsulinemia, increased serum levels of inflammatory factors, and up-regulated biomarkers involved in ER stress and related inflammatory pathways in the offspring. Maternal quercetin intervention (QI) had significant ameliorating effects on maternal blood lipids, especially cholesterol, which resulted in improved glucose metabolism and insulin sensitivity and alleviated ER stress and related inflammation in the grown offspring of obese dams. Maternal QI in obese dams during gestation and lactation reduced birth weight and postnatal BW gain in the offspring, and helped to improve insulin sensitivity and lipid metabolism of the mature offspring via reducing ER stress and related inflammation in the liver and adipose tissue.