scholarly journals Reducing Pup Litter Size Alters Early Postnatal Calcium Homeostasis and Programs Adverse Adult Cardiovascular and Bone Health in Male Rats

Nutrients ◽  
2019 ◽  
Vol 11 (1) ◽  
pp. 118 ◽  
Author(s):  
Jessica F. Briffa ◽  
Rachael O’Dowd ◽  
Tania Romano ◽  
Beverly S. Muhlhausler ◽  
Karen M. Moritz ◽  
...  
Keyword(s):  
Litter Size ◽  
Calcium Homeostasis ◽  
Milk Quality ◽  
Male Rats ◽  
Cardiometabolic Health ◽  
Postnatal Life ◽  
Male Adult ◽  
Total Body Calcium ◽  
Parathyroid Hormone Related Protein ◽  
Arachidonic Acids

The in utero and early postnatal environments play essential roles in offspring growth and development. Standardizing or reducing pup litter size can independently compromise long-term health likely due to altered milk quality, thus limiting translational potential. This study investigated the effect reducing litter size has on milk quality and offspring outcomes. On gestation day 18, dams underwent sham or bilateral uterine vessel ligation surgery to generate dams with normal (Control) and altered (Restricted) milk quality/composition. At birth, pups were cross-fostered onto separate dams with either an unadjusted or reduced litter size. Plasma parathyroid hormone-related protein was increased in Reduced litter pups, whereas ionic calcium and total body calcium were decreased. These data suggest Reduced litter pups have dysregulated calcium homeostasis in early postnatal life, which may impair bone mineralization decreasing adult bone bending strength. Dams suckling Reduced litter pups had increased milk long-chain monounsaturated fatty acid and omega-3 docosahexaenoic acid. Reduced litter pups suckled by Normal milk quality/composition dams had increased milk omega-6 linoleic and arachidonic acids. Reduced litter male adult offspring had elevated blood pressure. This study highlights care must be taken when interpreting data from research that alters litter size as it may mask subtle cardiometabolic health effects.

Muscle growth, cell number, type and morphometry in single and twin fetal lambs during mid to late gestation

2000 ◽  
Vol 12 (6) ◽  
pp. 319 ◽  
Author(s):  
S. A. McCoard ◽  
W. C. McNabb ◽  
S. W. Peterson ◽  
S. N. McCutcheon ◽  
P. M. Harris
Keyword(s):  
Muscle Mass ◽  
Litter Size ◽  
Muscle Growth ◽  
Cell Number ◽  
Late Gestation ◽  
Postnatal Life ◽  
Cross Sectional ◽  
Hindlimb Muscles ◽  
Full Complement ◽  
Gastrocnemius Muscles

Muscle growth, myofibre number, type and morphometry were studied in large hindlimb muscles of single and twin fetal lambs during mid to late gestation. Placental insufficiency, evident by lower total placentome weight and number per fetus, resulted in reduced fetal weights from 100 to 140 days gestation in twins compared with singletons (at 140 days: 5016 108 g v. 5750 246 g, respectively; P<0.05). However, competition between littermates did not consistently reduce muscle mass (15–22%) until 140 days gestation. Apparent myofibre number increased with age, indicating that the full complement of myofibres in some large hindlimb muscles may be achieved during early postnatal life. Litter size did not impact on apparent myofibre number in the semitendinosus, plantaris or gastrocnemius muscles. However, a transient effect on myofibre number in the adductor femoris muscle was observed from 80–120 days gestation. The phenotypic maturation of myofibres was unaffected by increasing litter size. Smaller muscle mass in twins was associated with smaller myofibre cross-sectional area in the semitendinosus, adductor femoris and gastrocnemius muscles at 140 days gestation. A similar trend was observed for the plantaris muscle. These results indicate that while competition between littermates for nutrients in late gestation can impact on both fetal and muscle mass, the fetus has the capacity to buffer against the effects of restricted nutrient supply on myofibre hyperplasia and phenotypic maturation, but myofibre hypertrophy is compromised.

scholarly journals An Extensive Genetic Program Occurring during Postnatal Growth in Multiple Tissues

Endocrinology ◽  
2008 ◽  
Vol 150 (4) ◽  
pp. 1791-1800 ◽  
Author(s):  
Gabriela P. Finkielstain ◽  
Patricia Forcinito ◽  
Julian C. K. Lui ◽  
Kevin M. Barnes ◽  
Rose Marino ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gene Expression Pattern ◽  
Somatic Growth ◽  
Postnatal Growth ◽  
Genetic Program ◽  
Male Rats ◽  
Postnatal Life ◽  
Multiple Organs ◽  
Organ Specific ◽  
Parenchymal Cells

Mammalian somatic growth is rapid in early postnatal life but then slows and eventually ceases in multiple tissues. We hypothesized that there exists a postnatal gene expression program that is common to multiple tissues and is responsible for this coordinate growth deceleration. Consistent with this hypothesis, microarray analysis identified more than 1600 genes that were regulated with age (1 vs. 4 wk) coordinately in kidney, lung, and heart of male mice, including many genes that regulate proliferation. As examples, we focused on three growth-promoting genes, Igf2, Mest, and Peg3, that were markedly down-regulated with age. In situ hybridization revealed that expression occurred in organ-specific parenchymal cells and suggested that the decreasing expression with age was due primarily to decreased expression per cell rather than a decreased number of expressing cells. The declining expression of these genes was slowed during hypothyroidism and growth inhibition (induced by propylthiouracil at 0–5 wk of age) in male rats, suggesting that the normal decline in expression is driven by growth rather than by age per se. We conclude that there exists an extensive genetic program occurring during postnatal life. Many of the involved genes are regulated coordinately in multiple organs, including many genes that regulate cell proliferation. At least some of these are themselves apparently regulated by growth, suggesting that, in the embryo, a gene expression pattern is established that allows for rapid somatic growth of multiple tissues, but then, during postnatal life, this growth leads to negative-feedback changes in gene expression that in turn slow and eventually halt somatic growth, thus imposing a fundamental limit on adult body size.

The role of fetal parathyroid hormone-related protein in transplacental calcium transport

1996 ◽  
Vol 17 (2) ◽  
pp. 159-164 ◽  
Author(s):  
J Tucci ◽  
V Hammond ◽  
P V Senior ◽  
A Gibson ◽  
F Beck
Keyword(s):  
Parathyroid Hormone ◽  
Calcium Pump ◽  
Calcium Deposition ◽  
Related Protein ◽  
Compensatory Mechanisms ◽  
Total Body Calcium ◽  
Parathyroid Hormone Related Protein ◽  
Ionised Calcium ◽  
Total Body

ABSTRACT During pregnancy, a placental calcium pump maintains the fetus in a hypercalcaemic state relative to the mother, a condition which has been thought to facilitate normal development of the fetal skeleton. Based on experiments performed in the sheep, parathyroid hormone-related protein (PTHrP) has been implicated as the hormone responsible for maintaining the placental calcium pump. In the present study on mice in which the PTHrP gene has been ablated by homologous recombination, we have measured both fetal and maternal circulating total and ionised calcium levels, as well as fetal total body calcium, in order to determine whether absence of PTHrP during fetal development has an effect on fetal calcium levels. Our results show that, in fetuses lacking PTHrP, circulating ionised calcium levels are significantly lower than those of heterozygote and wild-type littermates, but circulating total calcium levels show no difference. Total body calcium levels of null mutants are significantly higher than those of normal littermates. The role of PTHrP in maintaining the integrity of the transplacental calcium pump in the rodent thus remains unclear. It may be that the lower levels of fetal blood ionised calcium in mutant animals are due to disruption of the placental pump, but, if this is the case, compensatory mechanisms have operated to allow the excessive calcium deposition seen in the skeletons of these animals. Alternatively, the increased avidity of the bones for calcium may in itself have produced a lower equilibrium level of available ionised calcium.

Body adiposity and bone parameters of male rats from mothers fed diet containing flaxseed flour during lactation

2015 ◽  
Vol 7 (3) ◽  
pp. 314-319 ◽  
Author(s):  
C. A. S. da Costa ◽  
P. C. A. da Silva ◽  
D. C. Ribeiro ◽  
A. D. D. Pereira ◽  
A. d. S. d. Santos ◽  
...  
Keyword(s):  
Body Mass ◽  
Density Lipoprotein ◽  
Male Rats ◽  
Skeletal Structure ◽  
Male Rat ◽  
Postnatal Life ◽  
Lactation Period ◽  
Body Adiposity ◽  
Maximal Load ◽  
Flaxseed Flour

Obesity and osteoporosis may have their origins in early postnatal life. This study was designed to evaluate whether flaxseed flour use during lactation period bears effect on body adiposity and skeletal structure of male rat pups at weaning. At birth, male Wistar rats were randomly assigned to control and experimental (FF) groups, whose dams were treated with control or flaxseed flour diet, respectively, during lactation. At 21 days of age, pups were weaned to assess body mass, length and composition by dual-energy X-ray absorptiometry. The animals were then sacrificed to carry out analysis of serum profile, intra-abdominal adipocyte morphology and femur characteristics. Differences were considered significant when P<0.05. The FF group displayed the following characteristics (P<0.05): higher body mass, length, bone mineral content, bone area and concentrations of osteoprotegerin, osteocalcin and high-density lipoprotein cholesterol; higher levels of stearic, α-linolenic, eicosapentaenoic and docosapentaenoic acids and lower levels of arachidonic acid and cholesterol; smaller adipocyte area; and higher mass, epiphysis distance, diaphysis width, maximal load, break load, resilience and stiffness of femur. Flaxseed flour intake during lactation period promoted adipocyte hypertrophy down-regulation and contributed to pup bone quality at weaning.

scholarly journals Prenatal exposure to paracetamol/acetaminophen and precursor aniline impairs masculinisation of male brain and behaviour

Reproduction ◽  
2017 ◽  
Vol 154 (2) ◽  
pp. 145-152 ◽  
Author(s):  
Anders Hay-Schmidt ◽  
Olivia T Ejlstrup Finkielman ◽  
Benjamin A H Jensen ◽  
Christine F Høgsbro ◽  
Jacob Bak Holm ◽  
...  
Keyword(s):  
Prenatal Exposure ◽  
Sexual Behaviour ◽  
Reproductive Tract ◽  
Reproductive Behaviour ◽  
Postnatal Life ◽  
Similar Reduction ◽  
Foetal Development ◽  
Male Adult ◽  
Male Sexual Behaviour ◽  
Neuronal Number

Paracetamol/acetaminophen (N-Acetyl-p-Aminophenol; APAP) is the preferred analgesic for pain relief and fever during pregnancy. It has therefore caused concern that several studies have reported that prenatal exposure to APAP results in developmental alterations in both the reproductive tract and the brain. Genitals and nervous system of male mammals are actively masculinised during foetal development and early postnatal life by the combined actions of prostaglandins and androgens, resulting in the male-typical reproductive behaviour seen in adulthood. Both androgens and prostaglandins are known to be inhibited by APAP. Through intrauterine exposure experiments in C57BL/6 mice, we found that exposure to APAP decreased neuronal number in the sexually dimorphic nucleus (SDN) of the preoptic area (POA) in the anterior hypothalamus of male adult offspring. Likewise, exposure to the environmental pollutant and precursor of APAP, aniline, resulted in a similar reduction. Decrease in neuronal number in the SDN-POA is associated with reductions in male sexual behaviour. Consistent with the changes, male mice exposed in uteri to APAP exhibited changes in urinary marking behaviour as adults and had a less aggressive territorial display towards intruders of the same gender. Additionally, exposed males had reduced intromissions and ejaculations during mating with females in oestrus. Together, these data suggest that prenatal exposure to APAP may impair male sexual behaviour in adulthood by disrupting the sexual neurobehavioral programming. These findings add to the growing body of evidence suggesting the need to limit the widespread exposure and use of APAP by pregnant women.

EFFECT OF ESTRADIOL AND TESTOSTERONE ON THE FATTY ACIDS OF PLASMA CHOLESTERYL ESTERS AND PHOSPHOLIPIDS IN THE CASTRATED RAT

1964 ◽  
Vol 42 (3) ◽  
pp. 365-376 ◽  
Author(s):  
R. L. Lyman ◽  
Angela Shannon ◽  
Rosemarie Ostwald ◽  
P. Miljanich
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Palmitic Acid ◽  
Phospholipid Fatty Acid ◽  
Male Rats ◽  
Cholesteryl Esters ◽  
Phospholipid Fatty Acid Composition ◽  
Plasma Phospholipids ◽  
Plasma Cholesteryl Ester ◽  
Arachidonic Acids

The effects of physiological doses of estradiol and testosterone on plasma cholesteryl ester and phospholipid fatty acid composition were investigated in castrated male rats. The animals were killed after 3 weeks on experiment, and their plasma cholesteryl esters and phospholipids were analyzed and compared with those of intact female and male rats.Estradiol appeared to be responsible for the increased proportion of plasma cholesteryl arachidonate seen in the female or estrogen-injected rats since the proportion of cholesteryl arachidonate in castrated control rats was lower and similar to that of male or testosterone-treated rats. Plasma phospholipids of female and estradiol-injected rats had a higher percentage of stearic acid relative to palmitic acid. On the other hand, male, castrated control and testosterone-treated rats had higher proportions of palmitic acid. Fractionation of the plasma phospholipids into cephalins, lecithins, sphingomyelins, and lysolecithins, and analyses of their fatty acids, revealed that a principal effect of estradiol was to increase proportions and amounts of stearic and arachidonic acids in the lecithin fraction.The results suggest that estradiol may influence the synthesis of a lecithin rich in stearic and arachidonic acid. A possible relationship between the arachidonic-acid-rich lecithin and the higher percentage of cholesteryl arachidonate in estradiol-treated rats is discussed.

scholarly journals Oestradiol decreases rat apolipoprotein AI transcription via promoter site B

2000 ◽  
Vol 25 (2) ◽  
pp. 207-219 ◽  
Author(s):  
AH Taylor ◽  
AE Fox-Robichaud ◽  
C Egan ◽  
J Dionne ◽  
DE Lawless ◽  
...  
Keyword(s):  
Promoter Activity ◽  
Target Genes ◽  
Inhibitory Effect ◽  
Male Rats ◽  
Sprague Dawley ◽  
Male Adult ◽  
Nuclear Extracts ◽  
Major Mode ◽  
Apo Ai

Oestrogens protect against ischaemic heart disease in the post-menopausal female by increasing serum concentrations of apolipoprotein (apo) AI and the abundance of high-density lipoprotein particles. In men and experimental male animals, the administration of oestrogen has variable effects on apo AI expression. As the major mode of oestrogen action on target genes involves regulating promoter activity and hence transcription, oestrogen is expected to alter transcription of the apo AI gene. To test this hypothesis, the effect of 17beta-oestradiol (E(2)), on rat apo AI promoter activity in male hepatoma HuH-7 cells, was tested by co-transfecting a reporter template, pAI.474.CAT containing-474 to-7 of the rat apo AI promoter and an oestrogen receptor (ER) expression vector, pCMV-ER. Transfected cells exposed to E(2) showed a dose-dependent decrease in chloramphenicol acetyltransferase (CAT)-activity, with a maximum 91+/-1.5% reduction at 1 microM E(2). Deletional analysis of the promoter localized the inhibitory effect of ER and E(2) to site B (-170 to-144) with an adjacent 5' contiguous motif, site S (-186 to-171) acting as an amplifier. HuH-7 cell nuclear extracts showed binding activities with both sites S and B, but recombinant human ER did not. Furthermore, nuclear extracts from E(2)-treated HuH-7 cells showed weaker binding activity to site B, but not to site S. In summary, the inhibitory effect of ER and E(2) on rat apo AI gene activity is mediated by a promoter element, site B. This inhibitory effect arises from a mechanism that does not involve direct ER binding to the B-element. The conclusion that E(2) inhibits apo AI transcription was confirmed in vivo. Treatment of male adult Sprague-Dawley rats with up to 200 microg E(2) for 7 days decreased apo AI protein and hepatic mRNA by 72+/-21% and 68+/-1.4% respectively. Results of 'run-on' transcription of the apo AI gene in isolated hepatic nuclei showed a 55% decrease in hormone-treated male rats. These findings suggest that E(2) exerts primarily an inhibitory effect within male hepatic nuclei.

scholarly journals Effects of the Aqueous Extract ofEremomastax speciosa(Acanthaceae) on Sexual Behavior in Normal Male Rats

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
B. Nchegang ◽  
C. Mezui ◽  
F. Longo ◽  
Z. E. Nkwengoua ◽  
A. P. Amang ◽  
...  
Keyword(s):  
Sexual Behavior ◽  
Aqueous Extract ◽  
Male Rats ◽  
Normal Male ◽  
Adult Rats ◽  
Male Adult ◽  
Positive Effects ◽  
Posttreatment Period ◽  
And Performance ◽  
Behavior Of Rats

Objective. We studied prosexual effects ofEremomastax speciosaaqueous extract in male adult rats.Materials and Methods. 100 and 500 mg/kg of extract were administered orally (days 0, 1, 4, 7, 14, and 28 (posttreatment)). The sexual behavior of rats receiving a single dose (500 mg/kg) was also evaluated after pretreatment with Lω-NAME (10 mg/kg), haloperidol (1 mg/kg), or atropine (5 mg/kg). Controls received distilled water or testosterone enanthate (20 mg/kg/day/3 days(s.c.)before the test).Results. The extract (days 1–14) had no significant effect on mount, intromission, and ejaculation frequencies but on day 28 (14 days after treatment), it increased frequency of mounts and intromissions at 500 mg/kg. Mount, intromission, and ejaculation latencies reduced and postejaculatory intervals decreased but the effect did not persist 2 weeks after treatment. Extract prosex effects were greatly reduced by atropine and completely abolished by haloperidol, while Lω-NAME increased mount latency and potentiated extract effect on intromission and ejaculation latencies.Conclusion. In summary,E. speciosaextract can have positive effects on male sexual motivation and performance when administered for two weeks at the dose of 500 mg/kg. The effects (dopaminergic and/or cholinergic dependent) tend to appear during the posttreatment period.

scholarly journals Royal Jelly ameliorates 6-mercaptopurine induced spermatogenesis impairment and testicular apoptosis by regulating PI3K/AKT pathway in male rats

2020 ◽  
Author(s):  
khalid Hashem ◽  
Ahmed Z. Abdelazem ◽  
Naglaa W. Abdelbaky
Keyword(s):  
Adverse Effect ◽  
Mrna Expression ◽  
Sex Hormones ◽  
Caspase 3 ◽  
Royal Jelly ◽  
Male Rats ◽  
Akt Pathway ◽  
Albino Rats ◽  
Male Adult ◽  
Spermatogenesis Impairment

Abstract Testicular apoptosis is an obvious adverse effect of many chemotherapeutic agents.one of these chemotherapeutic drugs is 6-mercaptopurine (6MP) which has a powerful anticancer effect. On the contrary, it has an adverse effect on the male reproductive system. This study aimed to evaluate the prospective ameliorative effects of Royal Jelly (RJ) on 6MP induced testicular apoptosis and investigate the mechanistic pathway of protection. For this aim, forty male adult albino rats were divided into four equal groups (n= 10): control rats, RJ group (200 mg/kg.b.wt. of RJ for 30 day P.o.), 6MP group (5 mg/kg.b.wt of 6MP for 20 day P.o.), and RJ+6MP group pretreated with RJ (200 mg/kg.b.wt. for 10 day P.o.), and continued with 6MP (5 mg/kg.b.wt, P.o) for 20 day. After 30 days blood samples, epididymis and testis were collected to investigate sex hormones, sperm parameters, histological and molecular changes of testicular tissues, that include anti-oxidants activity, caspase-3, TNF-α, gene expression of Androgen receptors (AR) and P53 also protein concentration of PI3K, AKT, Nrf2 and HO1were estimated. The results of our study revealed that Pretreatment of Royal Jelly (RJ) abrogated 6MP induced spermatogenesis impairment by ameliorating sperm count, motility and morphology, regulating AR mRNA expression and sex hormones levels. RJ ameliorated testicular damage of 6MP exposed rats through restoring testicular antioxidant/oxidative redox, inhibiting caspase-3 activity and P53 mRNA expression as well as regulation of PI3K, AKT, Nrf2 and HO1 protein levels. Our data concluded that RJ protected testicular tissue from 6MP induced apoptosis by regulation PI3K/AKT pathway.

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