Authors:
Andrea Győrffy Szent István University Department of Physiology and Biochemistry István u. 2 H-1078 Budapest Hungary

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Mónika Keresztes Szent István University Department and Clinic of Obstetrics and Reproduction István u. 2 H-1078 Budapest Hungary

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Vera Faigl Szent István University Department and Clinic of Obstetrics and Reproduction István u. 2 H-1078 Budapest Hungary

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Vilmos Frenyó Szent István University Department of Physiology and Biochemistry István u. 2 H-1078 Budapest Hungary

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Margit Kulcsár Szent István University Department and Clinic of Obstetrics and Reproduction István u. 2 H-1078 Budapest Hungary

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Tibor Gaál Szent István University Department and Clinic of Internal Medicine, Faculty of Veterinary Science István u. 2 H-1078 Budapest Hungary

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Miklós Mézes Szent István University Department of Animal Nutrition, Faculty of Agriculture Gödöllő Hungary

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Attila Zsarnovszky Szent István University Department of Physiology and Biochemistry István u. 2 H-1078 Budapest Hungary

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Gyula Huszenicza Szent István University Department and Clinic of Obstetrics and Reproduction István u. 2 H-1078 Budapest Hungary

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Tibor Bartha Szent István University Department of Physiology and Biochemistry István u. 2 H-1078 Budapest Hungary

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In the regulation of energy metabolism, the liver plays an important role in the reinforcement of energy production. In periparturient cows the energy homeostasis turns into a negative energy balance that may shift the physiological regulation of energy balance towards pathological processes. Propylene glycol (PG), as a complementary source of energy used in the nutrition of dairy cows, alters systemic thyroid hormone economy; however, the exact mechanism through which highly glycogenic feed supplements impact liver metabolism is little known. Previous studies showed that only leptin receptors are expressed in the liver of cows, and now we report that leptin mRNA is expressed in the liver of cows as well. The present results show that the mRNA of leptin and its receptors are differentially modulated by the increased energy content of the feed consumed. Simultaneous changes in hepatic type I deiodinase activity suggest that hepatic modulation of the leptin system by PG supplementation may be mediated by an increased local thyroxine-triiodothyronine conversion. Since PG supplementation with simultaneous T4–T3 turnover and increased hepatic leptin- and short-form leptin receptor mRNA were not associated with a significant change in hepatic total lipid levels, it is suggested that the leptin system, directly or indirectly modulated by thyroid hormones, may represent a local defence mechanism to prevent fatty liver formation.

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Senior editors

Editor-in-Chief: Ferenc BASKA

Editorial assistant: Szilvia PÁLINKÁS

 

Editorial Board

  • Mária BENKŐ (Acta Veterinaria Hungarica, Budapest, Hungary)
  • Gábor BODÓ (University of Veterinary Medicine, Budapest, Hungary)
  • Béla DÉNES (University of Veterinary Medicine, Budapest Hungary)
  • Edit ESZTERBAUER (Veterinary Medical Research Institute, Budapest, Hungary)
  • Hedvig FÉBEL (University of Veterinary Medicine, Budapest, Hungary)
  • László FODOR (University of Veterinary Medicine, Budapest, Hungary)
  • János GÁL (University of Veterinary Medicine, Budapest, Hungary)
  • Balázs HARRACH (Veterinary Medical Research Institute, Budapest, Hungary)
  • Peter MASSÁNYI (Slovak University of Agriculture in Nitra, Nitra, Slovak Republic)
  • Béla NAGY (Veterinary Medical Research Institute, Budapest, Hungary)
  • Tibor NÉMETH (University of Veterinary Medicine, Budapest, Hungary)
  • Zsuzsanna NEOGRÁDY (University of Veterinary Medicine, Budapest, Hungary)
  • Dušan PALIĆ (Ludwig Maximilian University, Munich, Germany)
  • Alessandra PELAGALLI (University of Naples Federico II, Naples, Italy)
  • Kurt PFISTER (Ludwig-Maximilians-University of Munich, Munich, Germany)
  • László SOLTI (University of Veterinary Medicine, Budapest, Hungary)
  • József SZABÓ (University of Veterinary Medicine, Budapest, Hungary)
  • Péter VAJDOVICH (University of Veterinary Medicine, Budapest, Hungary)
  • János VARGA (University of Veterinary Medicine, Budapest, Hungary)
  • Štefan VILČEK (University of Veterinary Medicine in Kosice, Kosice, Slovak Republic)
  • Károly VÖRÖS (University of Veterinary Medicine, Budapest, Hungary)
  • Herbert WEISSENBÖCK (University of Veterinary Medicine, Vienna, Austria)
  • Attila ZSARNOVSZKY (Szent István University, Gödöllő, Hungary)

ACTA VETERINARIA HUNGARICA

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H-1078 Budapest, István utca 2., Hungary

Phone: (36 20) 560 4183 (ed.-in-chief) or (36 1) 478 4100/8430 (editor)

E-mail: acta.veterinaria@univet.hu (ed.-in-chief)

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2023  
Web of Science  
Journal Impact Factor 0.7
Rank by Impact Factor Q3 (Veterinary Sciences)
Journal Citation Indicator 0.4
Scopus  
CiteScore 1.8
CiteScore rank Q2 (General Veterinary)
SNIP 0.39
Scimago  
SJR index 0.258
SJR Q rank Q3

Acta Veterinaria Hungarica
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Acta Veterinaria Hungarica
Language English
Size A4
Year of
Foundation
1951
Volumes
per Year
1
Issues
per Year
4
Founder Magyar Tudományos Akadémia
Founder's
Address
H-1051 Budapest, Hungary, Széchenyi István tér 9.
Publisher Akadémiai Kiadó
Publisher's
Address
H-1117 Budapest, Hungary 1516 Budapest, PO Box 245.
Responsible
Publisher
Chief Executive Officer, Akadémiai Kiadó
ISSN 0236-6290 (Print)
ISSN 1588-2705 (Online)

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