The impact of murine strain and sex on postnatal development after maternal dietary restriction during pregnancy

Knight, Brian S.; Pennell, Craig E.; Adamson, S. Lee; Lye, Stephen J.

doi:10.1113/jphysiol.2006.126573

Cited by 20 publications

(19 citation statements)

References 44 publications

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“…This is consistent with previous findings in rodent models, in which the weanling and adult offspring of HF diet-fed mothers exhibit increased adiposity, adipocyte hypertrophy, and increased hepatic and white adipose tissue expression of lipogenic and adipogenic genes (8,11,12,30,36,53,66). Previous studies have revealed sex differences in the developmental programming of obesity, insulin resistance, and hypertension, with males often being more sensitive to early-life programming events than females (22,38,60,68). In the present experiment, body composition was altered only in the male HF offspring from the first pregnancies; in subsequent pregnancies, this sexually dimorphic response was no longer observed.…”

Section: Discussionsupporting

confidence: 92%

Increased maternal fat consumption during pregnancy alters body composition in neonatal mice

Krasnow

Nguyen

Marks

2011

American Journal of Physiology-Endocrinology and Metabolism

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Krasnow SM, Nguyen MT, Marks DL. Increased maternal fat consumption during pregnancy alters body composition in neonatal mice. Am J Physiol Endocrinol Metab 301: E1243-E1253, 2011. First published September 6, 2011 doi:10.1152/ajpendo.00261.2011Maternal overnutrition prior to and during gestation causes pronounced metabolic dysfunction in the adult offspring. However, less is known about metabolic adaptations in the offspring that occur independently of postnatal growth and nutrition. Therefore, we evaluated the impact of excess maternal dietary lipid intake on the in utero programming of body composition, hepatic function, and hypothalamic development in newborn (P0) offspring. Female mice were fed a low-fat (LF) or high-fat (HF) diet and were mated after 4, 12, and 23 wk. A subset of the obese HF dams was switched to the LF diet during the second (DR2) or third (DR3) pregnancies. The HF offspring accrued more fat mass than the LF pups, regardless of duration of maternal HF diet consumption or prepregnancy maternal adiposity. Increased neonatal adiposity was not observed in the DR3 pups. Liver weights were reduced in the HF offspring but not in the DR2 or DR3 pups. Offspring hepatic triglyceride content was reduced in the HF pups, but hepatic inflammation and expression of lipid metabolism genes were largely unaffected by maternal diet. Maternal diet did not alter the hypothalamic expression of orexigenic and anorexigenic neuropeptides in the offspring. Thus, the intrauterine programming of increased neonatal adiposity and reduced liver size by maternal overnutrition is evident in mice at birth and occurs prior to the development of maternal obesity. These observations demonstrate that dietary intervention during pregnancy minimizes the deleterious effects of maternal obesity on offspring body composition, potentially reducing the offsprings' risk of developing obesity and related diseases later in life. metabolic programming; liver; hypothalamus; inflammation; obesity THE GLOBAL PREVALENCE OF OBESITY has reached epidemic proportions in recent years, not only threatening the health and well-being of affected individuals but also imposing a considerable burden on the economic and health care systems of developed and developing nations (33). In the US, the prevalence of obesity has more than doubled in adults and more than tripled in children and adolescents since the 1970s. According to estimates from the 2007-2008 National Health and Nutrition Examination Survey, 33.8% of adults and 16.9% of children aged 2-19 are obese, and 9.5% of infants and toddlers are at or above the 95th percentile of the weight-for-length growth charts (23,24,45,46). Obese individuals have an increased risk of developing type 2 diabetes mellitus, hypertension, dyslipidemia, and nonalcoholic fatty liver disease. Once restricted to adults, these metabolic diseases and conditions are now being diagnosed in children and adolescents at alarming rates, mirroring the rising rates of juvenile obesity (34,39,47,52,55).The etiology of obesity is...

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Section: Discussionsupporting

confidence: 92%

Increased maternal fat consumption during pregnancy alters body composition in neonatal mice

Krasnow

Nguyen

Marks

2011

American Journal of Physiology-Endocrinology and Metabolism

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“…Maternal calorie restriction in C57Bl/6J and A/J mice leads to reduced whole body BMC in B6 but not A/J offspring at 6 months of age [60], suggesting strain differences in sensitivity to maternal diet. Rats exposed to intrauterine growth restriction via uterine artery ligation are shorter, with narrower bones, lower whole body and femoral BMC, and lower bone strength in adulthood [61–62].…”

Section: Maternal Body Composition Diet and Offspring Bone Massmentioning

confidence: 99%

Influence of pre- and peri-natal nutrition on skeletal acquisition and maintenance

Devlin

Bouxsein

2012

Bone

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Early life nutrition has substantial influences on postnatal health, with both under-and overnutrition linked with permanent metabolic changes that alter reproductive and immune function and significantly increase metabolic disease risk in offspring. Since perinatal nutrition depends in part on maternal metabolic condition, maternal diet during gestation and lactation is a risk factor for adult metabolic disease. Such developmental responses may be adaptive, but might also result from constraints on, or pathological changes to, normal physiology. The rising prevalence of both obesity and osteoporosis, and the identification of links among bone, fat, brain, and gut, suggest that obesity and osteoporosis may be related, and moreover that their roots may lie in early life. Here we focus on evidence for how maternal diet during gestation and lactation affects metabolism and skeletal acquisition in humans and in animal models. We consider the effects of overall caloric restriction, and macronutrient imbalances including high fat, high sucrose, and low protein, compared to normal diet. We then discuss potential mechanisms underlying the skeletal responses, including perinatal developmental programming via disruption of the perinatal leptin surge and/or epigenetic changes, to highlight unanswered questions and identify the most critical areas for future research.

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“…Gene-by-environment interactions in sheep was evidenced in a study in which pregnant sheep from two breeds subjected to the same nutrient restriction resulted in offspring with different metabolic outcomes (Vonnahme et al, 2006). Similarly, studies in mice that tested gene-by-environment interactions found two strains of mice to have different metabolic outcomes to exposures during prenatal life (Knight et al, 2007). Because homogeneity of the genetic background of the Suffolk breed used in our studies was not controlled for, the genetic background is likely to differ within this breed between our earlier (Savabiesfahani et al, 2006) and this study; hence, this may account for the differences seen in preovulatory LH surge amplitude observed in the current study.…”

Section: Discussionmentioning

confidence: 99%

Developmental programming: Prenatal BPA treatment disrupts timing of LH surge and ovarian follicular wave dynamics in adult sheep

Veiga-López

Beckett

Salloum

et al. 2014

Toxicology and Applied Pharmacology

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Developmental exposure to BPA adversely affects reproductive function. In sheep, prenatal BPA treatment induces reproductive neuroendocrine defects, manifested as LH excess and dampened LH surge and perturbs early ovarian gene expression. In this study we hypothesized that prenatal BPA treatment will also disrupt ovarian follicular dynamics. Pregnant sheep were treated from days 30 to 90 of gestation with 3 different BPA doses (0.05, 0.5, or 5 mg/kg BW/day). All female offspring were estrus synchronized and transrectal ultrasonography was performed daily for 22 days to monitor ovarian follicular and corpora lutea dynamics. Blood samples were collected to assess hormonal preovulatory changes and luteal progesterone dynamics. Statistical analysis revealed that the time interval between the estradiol rise and the preovulatory LH surge was shortened in the BPA-treated females. None of the three BPA doses had an effect on corpora lutea, progestogenic cycles, and mean or duration of ovulatory and non-ovulatory follicles. However, differences in follicular count trajectories were evident in all three follicular size classes (2–3 mm, 4–5 mm, and ≥ 6 mm) of prenatal BPA-treated animals compared to controls. Number of follicular waves tended also to be more variable in the prenatal BPA-treated groups ranging from 2 to 5 follicular waves per cycle, while this was restricted to 3 to 4 waves in control females. These changes in ovarian follicular dynamics coupled with defects in time interval between estradiol rise and preovulatory LH release are likely to lead to subfertility in prenatal BPA-treated females.

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The impact of murine strain and sex on postnatal development after maternal dietary restriction during pregnancy

Cited by 20 publications

References 44 publications

Increased maternal fat consumption during pregnancy alters body composition in neonatal mice

Increased maternal fat consumption during pregnancy alters body composition in neonatal mice

Influence of pre- and peri-natal nutrition on skeletal acquisition and maintenance

Developmental programming: Prenatal BPA treatment disrupts timing of LH surge and ovarian follicular wave dynamics in adult sheep

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