Maternal Dietary Supplementation with Oligofructose-Enriched Inulin in Gestating/Lactating Rats Preserves Maternal Bone and Improves Bone Microarchitecture in Their Offspring

Nutrition during pregnancy and lactation could exert a key role not only on maternal bone, but also could influence the skeletal development of the offspring. This study was performed in rats to assess the relationship between maternal dietary intake of prebiotic oligofructose-enriched inulin and its role in bone turnover during gestation and lactation, as well as its effect on offspring peak bone mass/architecture during early adulthood. Rat dams were fed either with standard rodent diet (CC group), calcium-fortified diet (Ca group), or prebiotic oligofructose-enriched inulin supplemented diet (Pre group), during the second half of gestation and lactation. Bone mineral density (BMD) and content (BMC), as well as micro-structure of dams and offspring at different stages were analysed. Dams in the Pre group had significantly higher trabecular thickness (Tb.Th), trabecular bone volume fraction (BV/TV) and smaller specific bone surface (BS/BV) of the tibia in comparison with CC dams. The Pre group offspring during early adulthood had an increase of the lumbar vertebra BMD when compared with offspring of CC and Ca groups. The Pre group offspring also showed significant increase versus CC in cancellous and cortical structural parameters of the lumbar vertebra 4 such as Tb.Th, cortical BMD and decreased BS/BV. The results indicate that oligofructose-enriched inulin supplementation can be considered as a plausible nutritional option for protecting against maternal bone loss during gestation and lactation preventing bone fragility and for optimizing peak bone mass and architecture of the offspring in order to increase bone strength.     

Effects of dietary omega-3 PUFAs on growth and development: Somatic,neurobiological and reproductive functions in a murine model

Omega-3 polyunsaturated fatty acids (ω-3 PUFAs) are relevant to fetal and infant growth and development. Objective: to assess whether long-term exposure to dietary ω-3 PUFA imbalance alters pre- and/or postnatal pups' development and reproductive function later in life. Mice dams were fed with ω-3 PUFA Control (soybean oil, 7%), Deficient (sunflower oil, 7%) or Excess (blend oil; 4.2% cod-liver+2.8% soybean) diet before conception and throughout gestation-lactation and later on, their pups received the same diet from weaning to adulthood. Offspring somatic, neurobiological and reproductive parameters were evaluated. Excess pups were lighter during the preweaning period and shorter in length from postnatal day (PND) 7 to 49, compared to Control pups (P<.05). On PND14, the percentage of pups with eye opening in Excess group was lower than those from Control and Deficient groups (P<.05). In Excess female offspring, puberty onset (vaginal opening and first estrus) occurred significantly later and the percentage of parthenogenetic oocytes on PND63 was higher than Control and Deficient ones (P<.05). Deficient pups were shorter in length (males: on PND14, 21, 35 and 49; females: on PND14, 21 and 42) compared with Control pups (P<.05). Deficient offspring exhibited higher percentage of bending spermatozoa compared to Control and Excess offspring (P<.05). These results show that either an excessively high or insufficient ω-3 PUFA consumption prior to conception until adulthood seems inadvisable because of the potential risks of short-term adverse effects on growth and development of the progeny or long-lasting effects on their reproductive maturation and function.     

Low levels of anterior tibial loading enhance knee extensor reflex response characteristics.

We examined whether neuromuscular reflexes were altered with anterior loads applied to the tibio-femoral joint. A ligament testing device was modified by attaching a reflex hammer to a steel mounted frame to illicit a patellar tendon tap, while anterior directed loads displaced the tibia on the femur. Five trials were acquired while anterior-directed loads (20, 50, 100 N; counterbalanced) were applied to the posterior tibia between 20 N pre (20 N(Pre)) and post (20 N(Post)) baseline conditions on two different days. Surface electromyography (sEMG) recorded mean quadriceps (Q) and hamstring (H) reflex time (R(Time)=ms) and reflex amplitude (R(Amp)=%MVIC). A load cell on the anterior tibia measured the timing (KE(Time)=ms) and amplitude (KE(Amp)=N) of the knee extension force, and was used to calculate electromechanical delay (EMD=ms) and peak knee extension moment (KE(Mom)=Nm/kg). Data from 19 recreationally active subjects revealed good to excellent response consistency between test days and between baseline conditions for R(Time), R(Amp), KE(Time) and KE(Amp). With anterior tibial loading, R(Time) was faster at 50 N vs. 20 N(Post), and R(Amp) was greater at 20 N(Pre) vs. 20 N(Post) (Q and H) and at 50 N vs. 100 N (Q only). KE(Mom) was greater at 20 N(Pre) and 50 N vs. 20 N(Post), and EMD was shorter at 50 N vs. 20 N, 20 N(Pre) and 20 N(Post). These results suggest that knee extensor reflex responses are enhanced with low (50 N) but not moderate (100 N) anterior loading of the knee.     

Premature birth stunts early growth and is a possible driver of stress-induced maternal effects in the guppy Poecilia reticulata

We tested the effects of gestational stress, principally in the form of alarm cue extracted from the skin of conspecifics, on reproduction in female guppies (Poecilia reticulata) and the growth and behaviour of their offspring. Offspring from mothers exposed to alarm cue exhibited stunted growth in the first few days post-partum, which appeared to be mediated by shortening of the gestation period, the length of which directly correlated with growth rate within the first 6 days post-partum. Mature offspring did not differ in behaviour or stress responses compared with controls and so the effects of maternal predation stress did not appear to persist into adulthood. A different form of gestational stress, dietary restriction, did not significantly affect offspring growth, though brood size was reduced, suggesting that the effects of predation stress were not mediated by differences in resource demand or consumption.     

Offspring metabolomic response to maternal protein restriction in a rat model of intrauterine growth restriction (IUGR)

Intrauterine growth restriction (IUGR), along with postnatal growth trajectory, is closely linked with metabolic diseases and obesity at adulthood. The present study reports the time-dependent metabolomic response of male offspring of rat dams exposed to maternal adequate protein diet during pregnancy and lactation (CC) or protein deprivation during pregnancy only (IUGR with rapid catch-up growth, RC) or through pregnancy and lactation (IUGR with slow postnatal growth, RR). Plasma LC-HRMS metabolomic fingerprints for 8 male rats per group, combined with multivariate statistical analysis (PLS-DA and HCA), were used to study the impact of IUGR and postnatal growth velocity on the offspring metabolism in early life (until weaning) and once they reached adulthood (8 months). Compared with CC rats, RR pups had clear-cut alterations in plasma metabolome during suckling, but none at adulthood; in contrast, in RC pups, alterations in metabolome were minimal in early life but more pronounced in the long run. In particular, our results pinpoint transient alterations in proline, arginine, and histidine in RR rats, compared to CC rats, and persistent differences in tyrosine and carnitine, compared to RC rats at adulthood. These findings suggest that the long-term deregulation in feeding behavior and fatty acid metabolism in IUGR rats depends on postnatal growth velocity.     

Prenatal stress in rat causes long-term spatial memory deficit and hippocampus MRI abnormality: differential effects of postweaning enriched environment

Prenatal stress (PS) can cause long-term hippocampus alternations in structure and plasticity in adult offspring. Enriched environment (EE) has an effect in rescuing a variety of neurological disorders. Pregnant dams were left undisturbed (prenatal control, PC) or restrained 6h per day from days 14 to 21 (prenatal stress, PS). Control and prenatal stressed offspring rats were subjected to a standard rearing environment (SE) or an EE on postnatal days 22-120 (PC/SE PC/EE, PS/SE, and PS/EE; n=5, each group). At ～4 months of age, all rats underwent Morris water maze test and brain MRI examination. Hippocampi were then dissected for biochemical analyses, including, Western blot for NMDA receptor (NR) subunits and synaptophysin and RT-PCR forβ1 integrin and tissue-plasminogen activator (t-PA). MRI showed all 5 rats in the PS/SE group and 5 in the PS/EE group exhibited increased signals in bilateral hippocampus and increased T2 time in the PS/SE group. Exposure to EE treatment on postnatal days 22-120 counteracted the deficit in spatial memory and increased NR1 protein expression, but it did not affect the rate of high signals and increased T2 time, decreased NR2, synaptophysin, β1 integrin and t-PA mRNA expressions in PS adult offspring. The results of this study indicate PS in rats causes long-term spatial memory deficits and gross hippocampus pathology. Postnatal EE treatment has differential benefits in terms of spatial learning, signaling molecules, and gross hippocampus pathology.     

Prenatal stress alters seizure thresholds and the development of kindled seizures in infant and adult rats

Stressful events during gestation and in the neonatal period have important effects on the later physical and mental health of the offspring. The present study tested the hypothesis that pre- and/or postnatal stress would affect seizure susceptibility in infant and adult rats, using the hippocampal kindling model. Prenatal stress consisted of daily restraint of the dam under bright light (for 45 min, 3 x / day) during either early gestation or mid/late gestation. Pups were compared to pups born to unstressed dams. Postnatal stress (administered on Days 4 and 5 after birth) consisted of either separation from the dam and placement in the bedding of a strange male for 1 h or injection of dexamethasone. Pups were compared to nonstressed siblings of the same litter. Both early and mid/late-gestation prenatal stress significantly lowered the after-discharge threshold (ADT) in infant, 14-day-old rat offspring, as compared to nonstressed control offspring. This effect on ADT was lost by adulthood. Mid/late-gestation stress increased the rate of kindled seizure development in infant rats and in their adult male, but not female, siblings. Postnatal stress had no significant effect on ADT or kindling rate. These findings indicate that prenatal stress, particularly during the latter half of pregnancy, may play an important role in increasing seizure vulnerability in the unborn offspring. These effects are more pronounced in infancy, but can also extend to adulthood.     

Relationship between exposure to an insecticide and fluctuating asymmetry in a damselfly (Odonata,Coenagriidae)

In this study, we explored the effects of pesticide on fluctuating asymmetry (FA) levels and mortality of Ceriagrion sp. larvae. The results showed that the mortality of larval damselflies treated with pesticide was significantly higher than that treated with tap water which had been aerated for 48 h, but there were no significant differences among mortality of larvae treated with different concentrations of pesticide. Meanwhile, we found that the level of FA of the first tibia length, one of the seven bilaterally symmetrical traits (First femur length, First tibia length, Second femur length, Second tibia length, Third femur length, Third tibia length and Prementum width), differed significantly with different treatments, whereas the others did not show any significant differences. The Bonferroni (Dunn) t Tests revealed that FA of the first tibia length at 15 × 10⁻⁹ mgl⁻¹ was significantly higher than that at 1.5 × 10⁻⁹ mgl⁻¹ and control. There was no significant relationship between trait size and the absolute difference between their right and left sides. There was also no significant relationship between body size and the absolute difference between right and left sides. Trait size was significantly positively correlated with body size. FA was not associated with mortality. Therefore, we concluded that FA of the first tibia length of Ceriagrion sp. larvae may be induced by sublethal doses of pesticides. That is to say, its FA may be regarded as an indicator of reflecting the level of pesticide stress. Handling editor: K. Martens     

α-Tocopherol supplementation reduces 5-nitro-γ-tocopherol accumulation by decreasing γ-tocopherol in young adult smokers

Abstract

γ-Tocopherol (γ-T) scavenges reactive nitrogen species (RNS) to form 5-NO₂-γ-T (NGT). However, α-T supplementation decreases circulating γ-T, which could limit its RNS scavenging activities. We hypothesized that α-T supplementation would mitigate NGT accumulation by impairing γ-T status. Healthy smokers (21 ± 1 y, n = 11) and non-smokers (21 ± 2 y, n = 10) ingested 75 mg/d each of RRR- and all-rac-α-tocopheryl acetate for 6 d. Plasma α-T, γ-T, γ-carboxyethyl hydroxychromanol (CEHC), NGT, and nitrate/nitrite were measured prior to supplementation (Pre), the morning after 6 consecutive evenings of supplementation (Post 1), and on the mornings of d 6 (Post 6) and d 14 (Post 14) during the post-supplementation period. α-T supplementation increased plasma α-T, and decreased γ-T, in both groups and these returned to Pre concentrations on Post 6 regardless of smoking status. Plasma γ-CEHC increased after the first dose of supplementation in both groups, suggesting that α-T supplementation decreased plasma γ-T in part by increasing its metabolism. Plasma NGT and nitrate/nitrite concentrations at Pre were greater in smokers, indicating greater nitrative stress due to cigarette smoking. Plasma NGT concentration was lowered only in smokers on Post 1 and Post 6 and was restored to Pre levels on Post 14. Plasma nitrate/nitrite tended (P = 0.07) to increase post-supplementation only in smokers, supporting decreases in RNS scavenging by γ-T. Plasma NGT concentration was more strongly correlated (P < 0.05) with γ-T in smokers (R = 0.83) compared with non-smokers (R = 0.50), supporting that α-T-mediated decreases in γ-T reduces NGT formation. These data indicate that α-T supplementation limits γ-T scavenging of RNS in smokers by decreasing γ-T availability.     

Developmental exposure to xenoestrogens at low doses alters femur length and tensile strength in adult mice

Developmental exposure to high doses of the synthetic xenoestrogen diethylstilbestrol (DES) has been reported to alter femur length and strength in adult mice. However, it is not known if developmental exposure to low, environmentally relevant doses of xenoestrogens alters adult bone geometry and strength. In this study we investigated the effects of developmental exposure to low doses of DES, bisphenol A (BPA), or ethinyl estradiol (EE(2)) on bone geometry and torsional strength. C57BL/6 mice were exposed to DES, 0.1 μg/kg/day, BPA, 10 μg/kg/day, EE(2), 0.01, 0.1, or 1.0 μg/kg/day, or vehicle from Gestation Day 11 to Postnatal Day 12 via a mini-osmotic pump in the dam. Developmental Xenoestrogen exposure altered femoral geometry and strength, assessed in adulthood by micro-computed tomography and torsional strength analysis, respectively. Low-dose EE(2), DES, or BPA increased adult femur length. Exposure to the highest dose of EE(2) did not alter femur length, resulting in a nonmonotonic dose response. Exposure to EE(2) and DES but not BPA decreased tensile strength. The combined effect of increased femur length and decreased tensile strength resulted in a trend toward decreased torsional ultimate strength and energy to failure. Taken together, these results suggest that exposure to developmental exposure to environmentally relevant levels of xenoestrogens may negatively impact bone length and strength in adulthood.     

Hypothermia after chronic mild stress exposure in rats with a history of postnatal maternal separations

The circadian system develops and changes in a gradual and programmed process over the lifespan. Early in life, maternal care represents an important zeitgeber and thus contributes to the development of circadian rhythmicity. Exposure to early life stress may affect circadian processes and induce a latent circadian disturbance evident after exposure to later life stress. Disturbance of the normal regulation of circadian rhythmicity is surmised to be an etiological factor in depression. We used postnatal maternal separation in rats to investigate how the early life environment might modify the circadian response to later life unpredictable and chronic stress. During postnatal days 2–14, male Wistar rats (n?=?8 per group) were daily separated from their mothers for a period of either 180?min (long maternal separation; LMS) or 10?min (brief maternal separation; BMS). In adulthood, rats were exposed to chronic mild stress (CMS) for 4 weeks. Body temperature, locomotor activity and heart rate were measured and compared before and after CMS exposure. LMS offspring showed a delayed body temperature acrophase compared to BMS offspring. Otherwise, adult LMS and BMS offspring demonstrated similar diurnal rhythms of body temperature, locomotor activity and heart rate. Exposure to CMS provoked a stronger and longer lasting hypothermia in LMS rats than in BMS rats. The thermoregulatory response appears to be moderated by maternal care following reunion, an observation made in the LMS group only. The results show that early life stress (LMS) in an early developmental stage induced a thermoregulatory disturbance evident upon exposure to unpredictable adult life stressors.     

Prenatal stress causes dendritic atrophy of pyramidal neurons in hippocampal CA3 region by glutamate in offspring rats

A substantial number of human epidemiological data, as well as experimental studies, suggest that adverse maternal stress during gestation is involved in abnormal behavior, mental, and cognition disorder in offspring. To explore the effect of prenatal stress (PS) on hippocampal neurons, in this study, we observed the dendritic field of pyramidal neurons in hippocampal CA3, examined the concentration of glutamate (Glu), and detected the expression of synaptotagmin‐1 (Syt‐1) and N‐methyl‐D ‐aspartate receptor 1 (NR1) in hippocampus of juvenile female offspring rats. Pregnant rats were divided into two groups: control group (CON) and PS group. Female offspring rats used were 30‐day old. The total length of the apical dendrites of pyramidal neurons in hippocampal CA3 of offspring was significantly shorter in PS than that in CON (p < 0.01). The number of branch points of the apical dendrites of pyramidal neurons in hippocampal CA3 of offspring was significantly less in PS (p < 0.01). PS offspring had a higher concentration of hippocampal Glu compared with CON (p < 0.05). PS offspring displayed increased expression of Syt‐1 and decreased NR1 in hippocampus compared with CON (p < 0.001 and p < 0.01, respectively). The expression of NR1 in different hippocampus subfields of offspring was significantly decreased in PS than that in CON (p < 0.05‐0.01). This study shows that PS increases the Glu in hippocampus and causes apical dendritic atrophy of pyramidal neurons of hippocampal CA3 in offspring rats. The decline of NR1 in hippocampus may be an adaptive response to the increased Glu. © 2009 Wiley Periodicals, Inc. Develop Neurobiol, 2010     

Studies of the teratogenic potential of exposure of rats to 6000-MHz microwave radiation. II. Postnatal psychophysiologic evaluations

Wistar rats (36) were exposed daily throughout pregnancy to a power density level of 35 mW/cm2 of 6000-MHz microwave radiation (11), sham irradiated (10), or used as control animals (15). Litters were culled to a maximum of eight F1a offspring/litter (total = 124) on Postnatal Day 1 and subjected to a series of reflex tests beginning Day 3. Mothers were rebred 10 days after weaning. Teratologic evaluations were completed on 263 F1b offspring. Weekly weights were recorded for 298 F1a offspring. At 60 days, behavioral testing was initiated on 121 offspring. At 90 days, offspring were bred within/across groups. Teratologic evaluations were completed on 659 F2 term fetuses. Organ weight analyses were completed on 17 mothers and 181 F1a adult offspring, and blood analyses on 21 mothers and 131 offspring. Sex differences within groups were observed in four behavioral tests and in blood data. Significant differences between groups were observed for: F1b term fetal weight; F1a eye opening, postnatal growth to the fifth week, water T-maze and open field test results; and several organ/body weight ratios. These results indicate that exposure to 6000-MHz radiation at this power density level may result in subtle long-term neurophysiologic alterations not detectable at term using conventional morphologic teratologic procedures.     

Prenatal Exposure to Nicotine Causes Postnatal Obesity and Altered Perivascular Adipose Tissue Function

Objective: Recent epidemiological studies have shown that there is an increased risk of obesity and hypertension in children born to women who smoked during pregnancy. The aim of this study was to examine the effect of fetal and neonatal exposure to nicotine, the major addictive component of cigarette smoke, on postnatal adiposity and blood vessel function. Research Methods and Procedures: Female Wistar rats were given nicotine or saline (vehicle) during pregnancy and lactation. Postnatal growth was determined in the male offspring from weaning until 26 weeks of age. At 26 weeks of age, fat pad weight and the function of the perivascular adipose tissue (PVAT) in the thoracic aorta and mesenteric arteries were examined. Results: Exposure to nicotine resulted in increased postnatal body weight and fat pad weight and an increased amount of PVAT in the offspring. Contraction of the aorta induced by phenylephrine was significantly attenuated in the presence of PVAT, whereas this effect was not observed in the aortic rings from the offspring of nicotine‐exposed dams. Phenylephrine‐induced contraction without PVAT was not different between saline‐ and nicotine‐exposed rats. Transfer of solution incubated with PVAT‐intact aorta to PVAT‐free aorta induced a marked relaxation response in the rats from saline‐exposed dams, but this relaxation response was significantly impaired in the rats from nicotine‐exposed dams. Discussion: Our results showed that prenatal nicotine exposure increased adiposity and caused an alteration in the modulatory function of PVAT on vascular relaxation response, thus providing insight into the mechanisms underlying the increased prevalence of obesity and hypertension in children exposed to cigarette smoke in utero.     

Adequate but not supplemental folic acid combined with soy isoflavones during early life improves bone health at adulthood in male mice

Previous investigations from our laboratory have demonstrated that neonatal exposure to soy isoflavones (ISO) improves bone outcomes in CD-1 mice at adulthood with greater benefits in females than males. This study determined whether early-life exposure to supplemental folic acid (FA) — that may enhance DNA methylation of target genes — in combination with ISO provides greater benefits to male bone development than ISO alone. CD-1 dams were randomized to a low (0 mg/kg diet), adequate (2 mg/kg diet) or supplemental (8 mg/kg diet) level of FA during pregnancy and lactation. Offspring received corn oil or ISO (7 mg/kg of body weight per day) from postnatal day 1–10. From weaning, males were fed adequate FA and studied to age 4 months. Offspring exposed to adequate FA+ISO had multiple benefits to bone health: higher (P<.05) bone mineral density (BMD) and greater (P<.05) resistance to fracture at the femur and lumbar spine than mice exposed to adequate FA alone. Exposure to supplemental FA+ISO resulted in higher (P<.05) serum osteoprotegerin (OPG), and a higher ratio of OPG to receptor activator for nuclear factor κβ ligand (RANKL) but did not result in greater BMD or strength at the femur or lumbar spine than supplemental FA alone. In conclusion, early-life exposure to adequate FA+ISO provided functional benefits to male bone development, while improvements induced by supplemental FA+ISO were limited to a higher level of serum OPG. Mechanistic studies are needed to better understand how FA and ISO improve bone development in male offspring.     

The effects of prenatal stress on Alpha4 Beta2 and Alpha7 hippocampal nicotinic acetylcholine receptor levels in adult offspring

Prenatal stress in humans is associated with psychiatric problems in offspring such as anxiety, depression, and schizophrenia. These same illnesses are also associated with neuronal nicotinic acetylcholine receptor (nAChR) dysfunction. Despite the known associations between prenatal stress exposure and offspring mental illness, and between mental illness and nAChR dysfunction, it is not known whether prenatal stress exposure impacts neuronal nAChRs. Thus, we tested the hypothesis that maternal stress alters the development of hippocampal alpha4 beta2 (α4β2^?) and alpha7 (α7^?) nicotinic receptor levels in adult offspring. Female Sprague‐Dawley rats experienced unpredictable variable stressors two to three times daily during the last week of gestation. At weaning (21 days) the offspring of prenatally stressed (PS) and nonstressed (NS) dams were assigned to same‐sex PS or NS groups. In young adulthood (56 days), the brains of offspring were collected and adjacent sections processed for quantitative autoradiography using [¹²⁵I]‐epibatidine (α4β2* nicotinic receptor‐selective) and [¹²⁵I]‐α‐bungarotoxin (α‐BTX; α7* nicotinic receptor‐selective) ligands. We found that PS significantly increased hippocampal α4β2* nAChRs of males and females in all subfields analyzed. In contrast, only females showed a trend toward PS‐induced increases in α7* nAChRs in the dentate gyrus. Interestingly, NS females displayed a significant left‐biased lateralization of α7* nAChRs in the laconosum moleculare of area CA1, whereas PS females did not, suggesting that PS interfered with normal lateralization patterns of α7* nAChRs during development. Taken together, our results suggest that PS impacts the development of hippocampal nAChRs, which may be an important link between PS exposure and risk for neuropsychiatric illness. © 2013 Wiley Periodicals, Inc. Develop Neurobiol 73:806–814, 2013     

Gestational Heat Stress Alters Postnatal Offspring Body Composition Indices and Metabolic Parameters in Pigs

The study objectives were to test the hypothesis that heat stress (HS) during gestational development alters postnatal growth, body composition, and biological response to HS conditions in pigs. To investigate this, 14 first parity crossbred gilts were exposed to one of four environmental treatments (TNTN, TNHS, HSTN, or HSHS) during gestation. TNTN and HSHS dams were exposed to thermal neutral (TN, cyclical 18–22°C) or HS conditions (cyclical 28–34°C) during the entire gestation, respectively. Dams assigned to HSTN and TNHS treatments were heat-stressed for the first or second half of gestation, respectively. Postnatal offspring were exposed to one of two thermal environments for an acute (24 h) or chronic (five weeks) duration in either constant TN (21°C) or HS (35°C) environment. Exposure to chronic HS during their growth phase resulted in decreased longissimus dorsi cross-sectional area (LDA) in offspring from HSHS and HSTN treated dams whereas LDA was larger in offspring from dams in TNTN and TNHS conditions. Irrespective of HS during prepubertal postnatal growth, pigs from dams that experienced HS during the first half of gestation (HSHS and HSTN) had increased (13.9%) subcutaneous fat thickness compared to pigs from dams exposed to TN conditions during the first half of gestation. This metabolic repartitioning towards increased fat deposition in pigs from dams heat-stressed during the first half of gestation was accompanied by elevated blood insulin concentrations (33%; P = 0.01). Together, these results demonstrate HS during the first half of gestation altered metabolic and body composition parameters during future development and in biological responses to a subsequent HS challenge.     

Neonatal exposure to leptin augments diet-induced obesity in leptin-deficient Ob/Ob mice

Objective: Epidemiological evidence has revealed that undernutrition in utero is closely associated with obesity and related detrimental metabolic sequelae in adulthood. Recently, using a wild‐type (wt) mouse model in which offspring were exposed to intrauterine undernutrition (UN offspring), we reported that the premature leptin surge during neonatal growth promotes lifelong changes in energy regulating circuitry in the hypothalamus, thus playing an important role in the development of pronounced obesity on a high‐fat diet (HFD) in adulthood. Here, we further evaluate the essential involvement of leptin in the developmental origins of obesity using leptin‐deficient ob/ob mice. Methods and Procedures: We assessed the progression of obesity on an HFD in adult leptin‐deficient ob/ob male mice that were exposed to intrauterine undernutrition by maternal food restriction (ob/ob UN offspring) or to leptin treatment during the neonatal period; this treatment is comparable to the premature leptin surge observed in the wt‐UN offspring. Results: On an HFD, the body weight of the male ob/ob UN offspring paralleled that of the ob/ob offspring exposed to normal intrauterine nutrition (ob/ob NN offspring). In contrast, early exposure to leptin in the ob/ob NN offspring during early neonatal growth reproduced the development of pronounced obesity on an HFD in adulthood. Discussion: The presence of leptin and associated energy regulation are indispensable in the acceleration of obesity on an HFD caused by undernutrition in utero. The premature leptin surge plays an essential role in the developmental origins of obesity as a programming signal during the early neonatal period.     

Scaling of the appendicular skeleton of the giraffe (Giraffa camelopardalis)

Giraffes have remarkably long and slender limb bones, but it is unknown how they grow with regard to body mass, sex, and neck length. In this study, we measured the length, mediolateral (ML) diameter, craniocaudal (CC) diameter and circumference of the humerus, radius, metacarpus, femur, tibia, and metatarsus in 10 fetuses, 21 females, and 23 males of known body masses. Allometric exponents were determined and compared. We found the average bone length increased from 340 ± 50 mm at birth to 700 ± 120 mm at maturity, while average diameters increased from 30 ± 3 to 70 ± 11 mm. Fetal bones increased with positive allometry in length (relative to body mass) and in diameter (relative to body mass and length). In postnatal giraffes bone lengths and diameters increased iso‐ or negatively allometric relative to increases in body mass, except for the humerus CC diameter which increased with positive allometry. Humerus circumference also increased with positive allometry, that of the radius and tibia isometrically and the femur and metapodials with negative allometry. Relative to increases in bone length, both the humerus and femur widened with positive allometry. In the distal limb bones, ML diameters increased isometrically (radius, metacarpus) or positively allometric (tibia, metatarsus) while the corresponding CC widths increased with negative allometry and isometrically, respectively. Except for the humerus and femur, exponents were not significantly different between corresponding front and hind limb segments. We concluded that the patterns of bone growth in males and females are identical. In fetuses, the growth of the appendicular skeleton is faster than it is after birth which is a pattern opposite to that reported for the neck. Allometric exponents seemed unremarkable compared to the few species described previously, and pointed to the importance of neck elongation rather than leg elongation during evolution. Nevertheless, the front limb bones and especially the humerus may show adaptation to behaviors such as drinking posture. J. Morphol. 276:503–516, 2015. © 2014 Wiley Periodicals, Inc.