Search Results
You are looking at 1 - 3 of 3 items for
- Author: Duane H Keisler x
- Refine by access: All content x
Animal Reproduction Laboratory, Department of Animal Science, Division of Animal Sciences, Texas A&M AgriLife Research Station, 3507 Highway 59E, Beeville, Texas 78102, USA
Search for other papers by Rodolfo C Cardoso in
Google Scholar
PubMed
Search for other papers by Bruna R C Alves in
Google Scholar
PubMed
Animal Reproduction Laboratory, Department of Animal Science, Division of Animal Sciences, Texas A&M AgriLife Research Station, 3507 Highway 59E, Beeville, Texas 78102, USA
Search for other papers by Ligia D Prezotto in
Google Scholar
PubMed
Animal Reproduction Laboratory, Department of Animal Science, Division of Animal Sciences, Texas A&M AgriLife Research Station, 3507 Highway 59E, Beeville, Texas 78102, USA
Search for other papers by Jennifer F Thorson in
Google Scholar
PubMed
Search for other papers by Luis O Tedeschi in
Google Scholar
PubMed
Search for other papers by Duane H Keisler in
Google Scholar
PubMed
Search for other papers by Marcel Amstalden in
Google Scholar
PubMed
Animal Reproduction Laboratory, Department of Animal Science, Division of Animal Sciences, Texas A&M AgriLife Research Station, 3507 Highway 59E, Beeville, Texas 78102, USA
Search for other papers by Gary L Williams in
Google Scholar
PubMed
Feeding a high-concentrate diet to heifers during the juvenile period, resulting in increased body weight (BW) gain and adiposity, leads to early-onset puberty. In this study, we tested the hypothesis that the increase in GnRH/LH release during nutritional acceleration of puberty is accompanied by reciprocal changes in circulating leptin and central release of neuropeptide Y (NPY). The heifers were weaned at 3.5 months of age and fed to gain either 0.5 (Low-gain; LG) or 1.0 kg/day (High-gain; HG) for 30 weeks. A subgroup of heifers was fitted surgically with third ventricle guide cannulas and was subjected to intensive cerebrospinal fluid (CSF) and blood sampling at 8 and 9 months of age. Mean BW was greater in HG than in LG heifers at week 6 of the experiment and remained greater thereafter. Starting at 9 months of age, the percentage of pubertal HG heifers was greater than that of LG heifers, although a replicate effect was observed. During the 6-h period in which CSF and blood were collected simultaneously, all LH pulses coincided with or shortly followed a GnRH pulse. At 8 months of age, the frequency of LH pulses was greater in the HG than in the LG group. Beginning at 6 months of age, concentrations of leptin were greater in HG than in LG heifers. At 9 months of age, concentrations of NPY in the CSF were lesser in HG heifers. These observations indicate that increased BW gain during juvenile development accelerates puberty in heifers, coincident with reciprocal changes in circulating concentrations of leptin and hypothalamic NPY release.
Early Life Research Unit, INRA and University of Nantes, School of Veterinary Medicine and Science, Institute of Health Sciences, Oniris, Department of Animal Science, Academic Division of Child Health, Obstetrics and Gynaecology, School of Medicine, Queen's Medical Centre, The University of Nottingham, Nottingham NG7 2UH, UK
Search for other papers by Neele S Dellschaft in
Google Scholar
PubMed
Search for other papers by Marie-Cecile Alexandre-Gouabau in
Google Scholar
PubMed
Search for other papers by David S Gardner in
Google Scholar
PubMed
Search for other papers by Jean-Philippe Antignac in
Google Scholar
PubMed
Search for other papers by Duane H Keisler in
Google Scholar
PubMed
Search for other papers by Helen Budge in
Google Scholar
PubMed
Search for other papers by Michael E Symonds in
Google Scholar
PubMed
Early Life Research Unit, INRA and University of Nantes, School of Veterinary Medicine and Science, Institute of Health Sciences, Oniris, Department of Animal Science, Academic Division of Child Health, Obstetrics and Gynaecology, School of Medicine, Queen's Medical Centre, The University of Nottingham, Nottingham NG7 2UH, UK
Search for other papers by Sylvain P Sebert in
Google Scholar
PubMed
Maternal caloric restriction during late gestation reduces birth weight, but whether long-term adverse metabolic outcomes of intra-uterine growth retardation (IUGR) are dependent on either accelerated postnatal growth or exposure to an obesogenic environment after weaning is not established. We induced IUGR in twin-pregnant sheep using a 40% maternal caloric restriction commencing from 110 days of gestation until term (∼147 days), compared with mothers fed to 100% of requirements. Offspring were reared either as singletons to accelerate postnatal growth or as twins to achieve standard growth. To promote an adverse phenotype in young adulthood, after weaning, offspring were reared under a low-activity obesogenic environment with the exception of a subgroup of IUGR offspring, reared as twins, maintained in a standard activity environment. We assessed glucose tolerance together with leptin and cortisol responses to feeding in young adulthood when the hypothalamus was sampled for assessment of genes regulating appetite control, energy and endocrine sensitivity. Caloric restriction reduced maternal plasma glucose, raised non-esterified fatty acids, and changed the metabolomic profile, but had no effect on insulin, leptin, or cortisol. IUGR offspring whose postnatal growth was enhanced and were obese showed insulin and leptin resistance plus raised cortisol. This was accompanied by increased hypothalamic gene expression for energy and glucocorticoid sensitivity. These long-term adaptations were reduced but not normalized in IUGR offspring whose postnatal growth was not accelerated and remained lean in a standard post-weaning environment. IUGR results in an adverse metabolic phenotype, especially when postnatal growth is enhanced and offspring progress to juvenile-onset obesity.
Veterinary Medicine and Surgery,
Animal Sciences, University of Missouri-Columbia, Columbia, Missouri 56211, USA
Search for other papers by Preston R Buff in
Google Scholar
PubMed
Veterinary Medicine and Surgery,
Animal Sciences, University of Missouri-Columbia, Columbia, Missouri 56211, USA
Search for other papers by Nat T Messer IV in
Google Scholar
PubMed
Veterinary Medicine and Surgery,
Animal Sciences, University of Missouri-Columbia, Columbia, Missouri 56211, USA
Search for other papers by Andria M Cogswell in
Google Scholar
PubMed
Veterinary Medicine and Surgery,
Animal Sciences, University of Missouri-Columbia, Columbia, Missouri 56211, USA
Search for other papers by David A Wilson in
Google Scholar
PubMed
Veterinary Medicine and Surgery,
Animal Sciences, University of Missouri-Columbia, Columbia, Missouri 56211, USA
Search for other papers by Philip J Johnson in
Google Scholar
PubMed
Veterinary Medicine and Surgery,
Animal Sciences, University of Missouri-Columbia, Columbia, Missouri 56211, USA
Search for other papers by Duane H Keisler in
Google Scholar
PubMed
Veterinary Medicine and Surgery,
Animal Sciences, University of Missouri-Columbia, Columbia, Missouri 56211, USA
Search for other papers by Venkataseshu K Ganjam in
Google Scholar
PubMed
Endocrine characteristics of Quarter Horse-type mares were determined during a 68 h feed deprivation and again in the same mares following surgical thyroidectomy (THX). A crossover experimental design was implemented, in which mares received brome hay available ad libitum (FED) or were food deprived (RES) for 68 h. Blood samples were collected every 20 min for 48 h, beginning 20 h after the onset of food deprivation. Concentrations of triiodothyronine and thyroxine were undetectable post-THX. Plasma concentrations of thyrotropin were greater post-THX versus pre-THX (P<0.001). Plasma concentrations of leptin were greater in the THX FED group than in the THX RES group (P< 0.01). The existence of leptin pulse secretion was found only in post-THX compared with the same horses pre-THX (P = 0.02). We theorize that non-pulsatile secretion of leptin may have contributed to the survival of this species, as it evolved in the regions of seasonal availability of food. Lack of pulsatile secretion of leptin may contribute to the accumulation of energy stores by modulating leptin sensitivity.
