Early nutritional changes induce sexually dimorphic long-term effects on body weight gain and the response to sucrose intake in adult rats

ABSTRACT The acute and long-term effects of pituitary-testis suppression with a gonadotrophin-releasing hormone (GnRH) agonist, d-Ser(But)6des-Gly10-GnRH N-ethylamide (buserelin; 0·02, 0·1, 1·0 or 10 mg/kg body weight per day s.c.) or antagonist, N-Ac-d-Nal(2)1,d-p-Cl-Phe2,d-Trp3,d-hArg(Et2)6,d-Ala10-GnRH (RS 68439; 2 mg/kg body weight per day s.c.) were studied in male rats treated on days 1–15 of life. The animals were killed on day 16 (acute effects) or as adults (130–160 days; long-term effects). Acutely, the lowest dose of the agonist decreased pituitary FSH content and testicular LH receptors, but with increasing doses pituitary and serum LH concentrations, intratesticular testosterone content and weights of testes were also suppressed (P< 0·05–0·01). No decrease was found in serum FSH or in weights of accessory sex organs even with the highest dose of the agonist, the latter finding indicating continuing secretion of androgens. The GnRH antagonist treatment suppressed pituitary LH and FSH contents and serum LH (P< 0·05–0·01) but, as with the agonist, serum FSH remained unaltered. Testicular testosterone and testis weights were decreased (P <0·01) but testicular LH receptors remained unchanged. Moreover, the seminal vesicle and ventral prostate weights were reduced, in contrast to the effects of the agonists. Pituitary LH and FSH contents had recovered in all adult rats treated neonatally with agonist and there was no effect on serum LH and testosterone concentrations or on fertility. In contrast, in adult rats treated neonatally with antagonist, weights of testis and accessory sex organs remained decreased (P <0·01–0·05) but hormone secretion from the pituitary and testis had returned to normal except that serum FSH was increased by 80% (P <0·01). Interestingly, 90% of the antagonist-treated animals were infertile. It is concluded that treatment with a GnRH agonist during the neonatal period does not have a chronic effect on pituitary-gonadal function. In contrast, GnRH antagonist treatment neonatally permanently inhibits the development of the testis and accessory sex organs and results in infertility. Interestingly, despite the decline of pituitary FSH neonatally, neither of the GnRH analogues was able to suppress serum FSH values and this differs from the concomitant changes in LH and from the effects of similar treatments in adult rats. Journal of Endocrinology (1989) 123, 83–91

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Long term differentiated phosphorus supply from below to above requirement affects nutrient balance and retention, body weight gain and bone growth in growing-finishing pigs

Livestock Science ◽

10.1016/j.livsci.2018.03.002 ◽

2018 ◽

Vol 211 ◽

pp. 14-20 ◽

Cited By ~ 11

Author(s):

K.U. Sørensen ◽

A.-H. Tauson ◽

H.D. Poulsen

Keyword(s):

Body Weight ◽

Weight Gain ◽

Bone Growth ◽

Body Weight Gain ◽

Nutrient Balance ◽

Finishing Pigs

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Effects of neonatal treatment with Tyr-MIF-1 and naloxone on the long-term body weight gain induced by repeated postnatal stressful stimuli

Peptides ◽

10.1016/s0196-9781(99)00152-7 ◽

1999 ◽

Vol 20 (12) ◽

pp. 1425-1430 ◽

Cited By ~ 3

Author(s):

Antonio d’Amore ◽

Alberto Loizzo

Keyword(s):

Body Weight ◽

Weight Gain ◽

Body Weight Gain ◽

Neonatal Treatment

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Combined Deletion of Y1, Y2, and Y4 Receptors Prevents Hypothalamic Neuropeptide Y Overexpression-Induced Hyperinsulinemia despite Persistence of Hyperphagia and Obesity

Endocrinology ◽

10.1210/en.2006-0097 ◽

2006 ◽

Vol 147 (11) ◽

pp. 5094-5101 ◽

Cited By ~ 43

Author(s):

En-Ju D. Lin ◽

Amanda Sainsbury ◽

Nicola J. Lee ◽

Dana Boey ◽

Michelle Couzens ◽

...

Keyword(s):

Body Weight ◽

Weight Gain ◽

Neuropeptide Y ◽

Energy Homeostasis ◽

Viral Vector ◽

Body Weight Gain ◽

Hormonal Changes ◽

Obesity Syndrome ◽

Y Receptors

Neuropeptide Y (NPY) is a key regulator of energy homeostasis and is implicated in the development of obesity and type 2 diabetes. Whereas it is known that hypothalamic administration of exogenous NPY peptides leads to increased body weight gain, hyperphagia, and many hormonal and metabolic changes characteristic of an obesity syndrome, the Y receptor(s) mediating these effects is disputed and unclear. To investigate the role of different Y receptors in the NPY-induced obesity syndrome, we used recombinant adeno-associated viral vector to overexpress NPY in mice deficient of selective single or multiple Y receptors (including Y1, Y2, and Y4). Results from this study demonstrated that long-term hypothalamic overexpression of NPY lead to marked hyperphagia, hypogonadism, body weight gain, enhanced adipose tissue accumulation, hyperinsulinemia, and other hormonal changes characteristic of an obesity syndrome. NPY-induced hyperphagia, hypogonadism, and obesity syndrome persisted in all genotypes studied (Y1−/−, Y2−/−, Y2Y4−/−, and Y1Y2Y4−/− mice). However, triple deletion of Y1, Y2, and Y4 receptors prevented NPY-induced hyperinsulinemia. These findings suggest that Y1, Y2, and Y4 receptors under this condition are not crucially involved in NPY’s hyperphagic, hypogonadal, and obesogenic effects, but they are responsible for the central regulation of circulating insulin levels by NPY.

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Postnatal intracerebroventricular exposure to neuropeptide Y causes weight loss in female adult rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00557.2001 ◽

2003 ◽

Vol 284 (6) ◽

pp. R1560-R1566 ◽

Cited By ~ 14

Author(s):

Amit Varma ◽

Jing He ◽

Lisa Weissfeld ◽

Sherin U. Devaskar

Keyword(s):

Body Weight ◽

Weight Gain ◽

Food Intake ◽

Neuropeptide Y ◽

Body Weight Gain ◽

Sprague Dawley ◽

Adult Rats ◽

Sprague Dawley Rats ◽

Old Adult ◽

Arcuate Nuclei

We investigated the effect of repetitive postnatal (2–7 days) intracerebroventricular administration of neuropeptide Y (NPY) on food intake and body weight gain in the 3- to 120-day-old Sprague-Dawley rats. NPY caused a 32% transient increase in body weight gain with elevated circulating insulin concentrations within 24 h. This early intervention led to the persistence of hyperinsulinemia and relative hyperleptinemia with euglycemia in the 120-day-old female alone. This perturbation was associated with 50% suppression in adult female hypothalamic NPY concentrations and a 50–85% decline in NPY immunoreactivity in the paraventricular and arcuate nuclei. This change was paralleled by a ∼20% decline in food intake and body weight gain at 60 and 120 days. However, when exogenous NPY was stereotaxically reinjected into the paraventricular nucleus of the ∼120-day-old adult females who were pretreated with NPY postnatally, an increase in food intake and body weight gain was noted, attesting to no disruption in the NPY end-organ responsivity. We conclude that postnatal intracerebroventricular NPY has long-lasting effects that predetermine the resultant adult phenotype in a sex-specific manner.

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Long-term reductions in GH, insulin-like growth factor-I and body weight gain in rats treated neonatally with antibodies to rat GH

Journal of Endocrinology ◽

10.1677/joe.0.1240381 ◽

1990 ◽

Vol 124 (3) ◽

pp. 381-386 ◽

Cited By ~ 11

Author(s):

M. J. Gardner ◽

D. J. Flint

Keyword(s):

Body Weight ◽

Weight Gain ◽

Growth Factor ◽

Body Weight Gain ◽

Female Rats ◽

Serum Prolactin ◽

Insulin Like Growth Factor ◽

Factor I ◽

Growth Factor I

ABSTRACT Treatment of neonatal rats on days 2–5 with antibodies against rat GH (rGH) markedly reduced body weight gain and serum concentrations of insulin-like growth factor-I for 6–8 weeks in both females and males, after which weight gain normalized without evidence of catch-up growth. There were no significant effects on serum prolactin, tri-iodothyronine or corticosterone. Testis and ovarian weights were reduced, although only in proportion to body size. In females, but not males, the treated rats, though lighter, had increased fat deposition in the parametrial depot. Pituitary weight was considerably reduced over 100 days later, as was the pituitary content of GH, but not prolactin. The response to GH-releasing factor of both male and female rats was also greatly reduced at this time. Taken together with the fact that these rGH antibodies can bind directly to somatotrophs, we propose that the long-term effects of the antibodies are induced by specific somatotroph destruction. Journal of Endocrinology (1990) 124, 381–386

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