Puberty onset is delayed following uteroplacental insufficiency and occurs earlier with improved lactation and growth for pups born small

2017 ◽  
Vol 29 (2) ◽  
pp. 307 ◽  
Author(s):  
Tania Romano ◽  
Deanne H. Hryciw ◽  
Kerryn T. Westcott ◽  
Mary E. Wlodek
Keyword(s):  
Sex Steroids ◽  
Postnatal Growth ◽  
Growth Restriction ◽  
Uterine Vessel ◽  
Risk Of Disease ◽  
Puberty Onset ◽  
Accelerated Growth ◽  
Wistar Kyoto ◽  
Plasma Leptin ◽  
And Control

Being born small programs adult diseases later in life, with the early postnatal growth rate in growth-restricted offspring playing a role in the reduction of the risk of disease in adulthood. In addition, early postnatal growth is critical for puberty onset (PO). Using cross-fostering, we determined the effects of growth restriction and prenatal and postnatal environments on PO and sex steroids. Bilateral uterine vessel ligation (Restricted) or sham surgery (Control), performed on Gestational Day 18 in Wistar-Kyoto rats induced fetal growth restriction. Control, Reduced (Control litter size reduced to five pups) and Restricted pups were cross-fostered onto different Control (normal lactation) or Restricted (impaired lactation) mothers on Day 1. The day of vaginal opening (females) and balanopreputial separation (males) characterised PO. Blood was sampled for sex steroid and leptin analysis. Restricted pups were born lighter than Controls (P < 0.05). PO was delayed by 3.4–4 days in Restricted-on-Restricted males and females (P < 0.05). Plasma leptin concentrations at PO were lower in both sexes in all groups compared with Restricted-on-Control and Control-on-Control (P < 0.05). PO occurred earlier in Restricted-on-Control (~2 days) with normal leptin concentrations and accelerated growth compared with Restricted-on-Restricted (P < 0.05). Testosterone concentrations were lower in male Restricted-on-Restricted than Control-on-Control at 6 months (P < 0.05). Restricted-on-Restricted females had lower progesterone at PO compared with Control-on-Control (P < 0.05). Female Restricted-on-Restricted had lower oestradiol, with Restricted-on-Control having higher testosterone concentrations at 6 months than Control-on-Control (P < 0.05). Growth restriction reduced postnatal growth and leptin concentrations, delaying PO in both sexes and programming altered sex steroids. This highlights the importance of the interaction between prenatal and postnatal growth in the programming of adult reproductive status.

Effects of uteroplacental insufficiency and reducing litter size on maternal mammary function and postnatal offspring growth

2008 ◽  
Vol 294 (2) ◽  
pp. R539-R548 ◽  
Author(s):  
Rachael O'Dowd ◽  
Jacqueline C. Kent ◽  
Jane M. Moseley ◽  
Mary E. Wlodek
Keyword(s):  
Birth Weight ◽  
Litter Size ◽  
Intrauterine Growth Restriction ◽  
Postnatal Growth ◽  
Milk Composition ◽  
Mammary Development ◽  
Growth Restriction ◽  
Intrauterine Growth ◽  
Parathyroid Hormone Related Protein ◽  
Wistar Kyoto

Human intrauterine growth restriction is often associated with uteroplacental insufficiency and a decline in nutrient and oxygen supply to the fetus. This study investigated the effects of uteroplacental insufficiency and intrauterine growth restriction (Restricted) or reducing litter size for normally grown pups (Reduced Litter) on maternal mammary development and function, milk composition, offspring milk intake, and their resultant effects on postnatal growth. Uteroplacental insufficiency was surgically induced by bilateral uterine vessel ligation on day 18 of gestation in the Wistar Kyoto rat. At birth, a group of sham control rats had their litter size reduced to five (Reduced Litter) to match that of the Restricted group. Cohorts of rats were terminally anesthetized on day 20 of gestation or day 6 of lactation, and a third group was studied throughout lactation. Restricted pups had a lower birth weight (by 16%) and litter size (by 36%) compared with controls, as well as reduced mammary parathyroid hormone-related protein content and milk ionic calcium concentrations associated with reduced total pup calcium. Restricted dams with lower circulating progesterone experienced premature lactogenesis, producing less milk per pup with altered composition compared with controls, further slowing growth during lactation. Reducing litter size of pups born of normal birth weight (Reduced Litter) was associated with decreased pup growth, highlighting the importance of appropriate controls. The present study demonstrates that uteroplacental insufficiency impairs mammary function, compromises milk quality and quantity, and reduces calcium transport into milk, further restraining postnatal growth.

Somatic growth and the risks of bronchopulmonary dysplasia and pulmonary hypertension: connecting epidemiology and physiology

2019 ◽  
Vol 97 (3) ◽  
pp. 197-205 ◽  
Author(s):  
Mark A. Underwood ◽  
Stephen Wedgwood ◽  
Satyan Lakshminrusimha ◽  
Robin H. Steinhorn
Keyword(s):  
Pulmonary Hypertension ◽  
Bronchopulmonary Dysplasia ◽  
Somatic Growth ◽  
Postnatal Growth ◽  
Pulmonary Complications ◽  
Growth Restriction ◽  
Extreme Prematurity ◽  
Poor Growth ◽  
Increased Risk ◽  
Poor Nutrition

In the premature infant, poor growth in utero (fetal growth restriction) and in the first weeks of life (postnatal growth restriction) are associated with increased risk for bronchopulmonary dysplasia and pulmonary hypertension. In this review, we summarize the epidemiologic data supporting these associations, present a novel rodent model of postnatal growth restriction, and review 5 promising mechanisms by which poor nutrition may affect the developing lung. These observations support the hypothesis that nutritional and (or) pharmacologic interventions early in life may be able to decrease risk of the pulmonary complications of extreme prematurity.

scholarly journals Redundancy in the central tachykinin systems safeguards puberty onset and fertility

2018 ◽  
Author(s):  
Silvia León ◽  
Chrysanthi Fergani ◽  
Rajae Talbi ◽  
Serap Simavli ◽  
Caroline A. Maguire ◽  
...  
Keyword(s):  
Substance P ◽  
Reproductive Success ◽  
Sex Steroids ◽  
Delayed Puberty ◽  
Neurokinin A ◽  
Neurokinin B ◽  
Female Mice ◽  
Gnrh Release ◽  
Lh Release ◽  
Puberty Onset

ABSTRACTThe tachykinin neurokinin B (NKB, Tac2) is critical for GnRH release. NKB signaling deficiency leads to infertility in humans. However, some patients reverse this hypogonadism resembling the fertile phenotype of Tac2KO and Tacr3KO (encoding NKB receptor, NK3R) mice despite the absence of NKB signaling. Here, we demonstrate that in the absence of NKB signaling, other tachykinins (substance P and neurokinin A [NKA], encoded by Tac1) may take over to preserve fertility. The complete absence of tachykinins in Tac1/Tac2KO mice leads to delayed puberty onset in both sexes and infertility in 80% of females (but not males), in contrast to the 100% fertile phenotype of Tac1KO and Tac2KO mice separately. Furthermore, we demonstrate that NKA controls puberty onset and LH release through NKB-independent mechanisms in the presence of sex steroids and NKB-dependent mechanisms in their absence. In summary, tachykinins interact in a coordinated manner to ensure reproductive success in female mice.

Diabetes-induced endothelial dysfunction in streptozotocin-treated rats: role of prostaglandin endoperoxides and free radicals.

1993 ◽  
Vol 4 (6) ◽  
pp. 1327-1336
Author(s):  
F X Dai ◽  
A Diederich ◽  
J Skopec ◽  
D Diederich
Keyword(s):  
Free Radicals ◽  
Endothelial Dysfunction ◽  
Diabetic Rats ◽  
Renal Arteries ◽  
Radical Scavenger ◽  
Wistar Kyoto ◽  
And Control ◽  
A2 Receptors

The vasoactive responses of renal arteries from diabetic and control rats were compared in vitro in arteriograph assemblies. Diabetes was established by an iv injection of streptozotocin (55 mg/kg) in Wistar-Kyoto rats. Endothelium-dependent relaxations mediated by nitric oxide (EDNO) were impaired in arteries from the diabetic rats; the impairment in endothelial function increased with duration of the diabetic state. After 6 and 16 wk, the concentrations of acetylcholine required to produce 50% relaxation of norepinephrine preconstriction were 3.2 and 25 microM for arteries from diabetic rats and 0.4 microM in control arteries, representing 8- and 62-fold decreases in sensitivity to the endothelium-dependent vasodilator in the diabetic arteries. After 6 wk of diabetes, renal arteries also became 20-fold less sensitive to relaxation induced by histamine, another agonist that induces EDNO-mediated relaxations. The inhibition of EDNO production with L-NG-nitroarginine produced greater impairments in acetylcholine relaxations in arteries from diabetic rats than from control rats. Relaxations in response to acetylcholine were impaired in arteries from diabetic rats because of increased production of factors that opposed the vasorelaxant effects of EDNO, rather than from decreased production of EDNO. Pretreatment of the diabetic arteries with the hydroxyl radical scavenger dimethylthiourea normalized relaxations in response to acetylcholine. The blockade of prostaglandin H2-thromboxane A2 receptors with SQ 29548 also improved relaxations in response to acetylcholine in diabetic arteries. These data indicate that endothelial dysfunction in the renal arteries of diabetic rats may be mediated by the increased production of free radicals and of prostaglandin endoperoxides, which oppose the vasorelaxant effects of EDNO.

Dietary sodium restriction and development of hypertension in spontaneously hypertensive rats

1983 ◽  
Vol 245 (6) ◽  
pp. H1081-H1084 ◽  
Author(s):  
C. B. Toal ◽  
F. H. Leenen
Keyword(s):  
Blood Pressure ◽  
Control Diet ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Spontaneously Hypertensive ◽  
Basal Blood Pressure ◽  
Blood Pressures ◽  
Dietary Sodium Restriction ◽  
Wistar Kyoto ◽  
And Control

Blood pressure and body weight of conscious spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats were measured up to 16 wk of age in animals started at birth on five different sodium-containing diets. SHR on 9 mumol sodium/g food did not show a rise in basal blood pressure; however, when stressed the SHR still exhibited slightly higher blood pressures than WKY. In SHR on 17 mumol sodium/g food the development of hypertension was blunted compared with that of control (101 mumol/g) diet animals. SHR on 26 or 44 mumol sodium/g diet exhibited a development of hypertension similar to that of SHR on control diet. The 26 mumol/g, 44 mumol/g, and control sodium diet groups, regardless of strain, had similar growth rates. By contrast, on 17 mumol sodium/g food both SHR and WKY showed a substantially reduced growth rate, and all animals on 9 mumol sodium/g diet were severely retarded in growth. The results indicate that dietary sodium restriction can ameliorate the development of hypertension in SHR, but only when the sodium levels are so low as to affect overall growth.

When early life growth restriction in rats is followed by attenuated postnatal growth: effects on cardiac function in adulthood

2014 ◽  
Vol 54 (5) ◽  
pp. 743-750 ◽  
Author(s):  
Vladislava Zohdi ◽  
James T. Pearson ◽  
Michelle M. Kett ◽  
Paul Lombardo ◽  
Michal Schneider ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Early Life ◽  
Postnatal Growth ◽  
Growth Restriction ◽  
Growth Effects

scholarly journals Postnatal Growth after Intrauterine Growth Restriction Alters Central Leptin Signal and Energy Homeostasis

PLoS ONE ◽  
2012 ◽  
Vol 7 (1) ◽  
pp. e30616 ◽  
Author(s):  
Bérengère Coupé ◽  
Isabelle Grit ◽  
Philippe Hulin ◽  
Gwenaëlle Randuineau ◽  
Patricia Parnet
Keyword(s):  
Intrauterine Growth Restriction ◽  
Energy Homeostasis ◽  
Postnatal Growth ◽  
Growth Restriction ◽  
Intrauterine Growth

scholarly journals Bilateral uterine vessel ligation as a model of intrauterine growth restriction in mice

2014 ◽  
Vol 12 (1) ◽  
pp. 62 ◽  
Author(s):  
Mathilde Janot ◽  
Marie-Laure Cortes-Dubly ◽  
Stéphane Rodriguez ◽  
Uyen Huynh-Do
Keyword(s):  
Intrauterine Growth Restriction ◽  
Growth Restriction ◽  
Intrauterine Growth ◽  
Uterine Vessel ◽  
Vessel Ligation

scholarly journals Superimposition of Postnatal Calorie Restriction Protects the Aging Male Intrauterine Growth- Restricted Offspring from Metabolic Maladaptations

Endocrinology ◽  
2012 ◽  
Vol 153 (9) ◽  
pp. 4216-4226 ◽  
Author(s):  
Yun Dai ◽  
Shanthie Thamotharan ◽  
Meena Garg ◽  
Bo-Chul Shin ◽  
Sherin U. Devaskar
Keyword(s):  
Physical Activity ◽  
Insulin Sensitivity ◽  
Postnatal Growth ◽  
Growth Restriction ◽  
Fine Tuning ◽  
Whole Body ◽  
Aging Male ◽  
Intrauterine Growth ◽  
Euglycemic Clamp ◽  
Hyperinsulinemic Euglycemic Clamp

Intrauterine growth restriction (IUGR) results in dysregulated glucose homeostasis and adiposity in the adult. We hypothesized that with aging, these perturbations will wane, and superimposition of postnatal growth restriction (PNGR) on IUGR [intrauterine and postnatal growth restriction (IPGR)] will reverse the residual IUGR phenotype. We therefore undertook hyperinsulinemic-euglycemic clamp, energy balance, and physical activity studies during fed, fasted, and refed states, in light and dark cycles, on postweaned chow diet-fed more than 17-month aging male IUGR, PNGR, and IPGR vs. control (CON) rat offspring. Hyperinsulinemic-euglycemic clamp revealed similar whole-body insulin sensitivity and physical activity in the nonobese IUGR vs. CON, despite reduced heat production and energy expenditure. Compared with CON and IUGR, IPGR mimicking PNGR was lean and growth restricted with increased physical activity, O2 consumption (VO2), energy intake, and expenditure. Although insulin sensitivity was no different in IPGR and PNGR, skeletal muscle insulin-induced glucose uptake was enhanced. This presentation proved protective against the chronologically earlier (5.5 months) development of obesity and dysregulated energy homeostasis after 19 wk on a postweaned high-fat diet. This protective role of PNGR on the metabolic IUGR phenotype needs future fine tuning aimed at minimizing unintended consequences.

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