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Short communication: Manipulation of neonatal leptin profile via exogenous glucocorticoids in beef calves

Published online by Cambridge University Press:  25 January 2019

L. K. Lewis ,
R. E. Ricks  and
N. M. Long Open the ORCID record for N. M. Long [Opens in a new window]
L. K. Lewis
Affiliation:
Department of Animal and Veterinary Sciences, Clemson University, Clemson, SC 29634, USA
R. E. Ricks
Affiliation:
Department of Animal and Veterinary Sciences, Clemson University, Clemson, SC 29634, USA
N. M. Long*
Affiliation:
Department of Animal and Veterinary Sciences, Clemson University, Clemson, SC 29634, USA
*
†E-mail: [email protected]
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Abstract

The link between circulating glucocorticoids and leptin in beef calves has not been explored but has been noted in several studies. The aim of this study is to determine the effects of exogenous glucocorticoids given at birth and 1 day of age on serum leptin concentrations in beef calves. Ruminant animals secrete leptin, which is thought to be important for the programming of the hypothalamic appetite centers. Angus crossbred cows (n = 31) bred via natural service were utilized for this experiment. At parturition (day 0), calf BW was recorded and each calf was infused intravenously with either a hydrocortisol sodium succinate solution (HC, 8 males and 8 females) at a dosage of 3.5 μg/kg of BW or a similar volume of saline solution (CONT, 7 males and 8 females). Each calf was given a second infusion of its respective treatment 24 h postpartum at 1.5 μg/kg of BW for HC treatment. Calf treatment was blocked by sex, dam body condition score (BCS), and dam age. Blood samples were taken via jugular venipuncture before infusion, daily from days 0 to 5, then every other day up to day 17. Serum leptin and cortisol concentrations were analyzed via radioimmunoassay. Dam age, dam BCS, calf BW, and serum leptin and cortisol concentrations were analyzed using MIXED procedure of SAS. Dam age was not different (P = 0.81) among HC and CONT calves (4.9±0.5 and 4.7±0.5, respectively). Dam BCS was not different between treatments (5.7±0.2 and 5.6±0.2 HC and CONT, respectively; P = 0.66). There was no difference in calf birth BW between treatments (P = 0.87) and averaged 38.3±1.4 kg. Cortisol concentrations were not different between both treatments (P = 0.23) from birth to day 4 of age. Calves that received the HC treatment showed significantly reduced (P = 0.03) leptin concentrations on days 1 to 13. Calf BW from 60 to 150 days of age was not different between CONT and HC treated calves (P = 0.65). These data indicate that exogenous glucocorticoids can be used to suppress neonatal leptin levels in calves. This could lead to changes in voluntary feed intake of treated calves.

Keywords

bos taurusnewborn calfcortisolpostnataldam age
Type
Short Communication
Information
animal , Volume 13 , Issue 9 , September 2019 , pp. 1982 - 1985
Copyright
© The Animal Consortium 2019 

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References

Beef Improvement Federation 2010. Guidelines for uniform Beef Improvement Programs, 9th edition. Retrieved on 17 January 2018 from http://beefimprovement.org/content/uploads/2015/08/REVISED-MasterEd-BIF-GuidelinesFinal-08-2015.pdf.Google Scholar
Blum, JW, Zbinden, Y, Hammon, HM and Chilliard, Y 2005. Plasma leptin status in young calves: effects of pre-term birth, age, glucocorticoid status, suckling, and feeding with an automatic feeder or bucket. Domestic Animal Endocrinology 28, 119–133.CrossRefGoogle ScholarPubMed
Bouret, SG, Draper, SJ and Simerly, RB 2004. Formation of projection pathways from the arcuate nucleus of the hypothalamus to hypothalamic regions implicated in the neural control of feeding behavior in mice. Journal of Neuroscience 24, 2797–2805.CrossRefGoogle ScholarPubMed
Desai, M, Li, T and Ross, MG 2011. Hypothalamic neurosphere progenitor cells in low birth-weight rat newborns: neurotrophic effects of leptin and insulin. Journal of Brain Research 1378, 29–42.CrossRefGoogle ScholarPubMed
Lewis, LK, Ricks, RE and Long, NM 2016. Manipulations of neonatal leptin profile via exogenous cortisol in beef calves. Journal of Animal Science 95 (suppl. 1), 38.CrossRefGoogle Scholar
Long, NM, Ford, SP and Nathanielsz, PW 2011. Maternal obesity eliminates the neonatal lamb plasma leptin peak. Journal of Physiology 589, 1455–1462.CrossRefGoogle ScholarPubMed
Long, NM and Schafer, DW 2013. Sex effects on plasma leptin concentrations in newborn and postnatal beef calves. Professional Animal. Scientist. 29, 601–605.Google Scholar
Long, NM, Smith, DT, Ford, SP and Nathanielsz, PW 2013. Elevated glucocorticoids during ovine pregnancy increase appetite and produce glucose dysregulation and adiposity in their granddaughters in response to ad libitum feeding at 1 year of age. Journal of Obstetrics and Gynecology 209, 353.e1–353.e9.Google ScholarPubMed
Sloboda, DM, Challis, JRG, Moss, TJM and Newnham, JP 2005. Synthetic glucocorticoids: antenatal administration and long-term implications. Current Pharmaceutical Design 11, 1459–1472.CrossRefGoogle ScholarPubMed
Tipton, JE, Ricks, RE, LeMaster, CT and Long, NM 2018. The effects of late gestation nutrient restriction of dams on heifer offspring intake, metabolites and hormones during an ad libitum feeding trial. Journal of Animal Physiology and Animal Nutrition 102, e877–e884.CrossRefGoogle ScholarPubMed
United States department of Agriculture 2016. Economic research service: cattle & beef. Retrieved 12 January 2016 from https://www.ers.usda.gov/topics/animal-products/cattle-beef/background.aspx.Google Scholar
Yura, S, Itoh, H, Sagawa, N, Yamamoto, H, Masuzaki, H, Nakao, K, Kawamura, M, Takemura, M, Kakui, K, Ogawa, Y and Fujii, S 2005. Role of premature leptin surge in obesity resulting from intrauterine undernutrition. Cell Metabolism. 1, 371–378.CrossRefGoogle ScholarPubMed