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Adipose tissue uncoupling protein 1 levels and function are increased in a mouse model of developmental obesity induced by maternal exposure to high-fat diet

Published online by Cambridge University Press:  17 May 2018

E. Bytautiene Prewit*
Affiliation:
Department of Obstetrics & Gynecology, The University of Texas Medical Branch at Galveston, Galveston, TX, USA
C. Porter
Affiliation:
Department of Surgery, The University of Texas Medical Branch at Galveston, Shriners Hospitals for Children, Galveston, TX, USA
M. La Rosa
Affiliation:
Department of Obstetrics & Gynecology, The University of Texas Medical Branch at Galveston, Galveston, TX, USA
N. Bhattarai
Affiliation:
Department of Surgery, The University of Texas Medical Branch at Galveston, Shriners Hospitals for Children, Galveston, TX, USA
H. Yin
Affiliation:
Department of Obstetrics & Gynecology, The University of Texas Medical Branch at Galveston, Galveston, TX, USA
P. Gamble
Affiliation:
Department of Obstetrics & Gynecology, The University of Texas Medical Branch at Galveston, Galveston, TX, USA
T. Kechichian
Affiliation:
Department of Obstetrics & Gynecology, The University of Texas Medical Branch at Galveston, Galveston, TX, USA
L. S. Sidossis
Affiliation:
Department of Surgery, The University of Texas Medical Branch at Galveston, Shriners Hospitals for Children, Galveston, TX, USA Department of Kinesiology and Health Department of Medicine, Rutgers University, New Brunswick, NJ, USA
*
*Address for correspondence: E. Bytautiene Prewit, Department of Obstetrics & Gynecology, The University of Texas Medical Branch at Galveston, 301 University Blvd, Galveston, TX 77555-1062, USA. E-mail: [email protected]

Abstract

With brown adipose tissue (BAT) becoming a possible therapeutic target to counteract obesity, the prenatal environment could represent a critical window to modify BAT function and browning of white AT. We investigated if levels of uncoupling protein 1 (UCP1) and UCP1-mediated thermogenesis are altered in offspring exposed to prenatal obesity. Female CD-1 mice were fed a high-fat (HF) or standard-fat (SF) diet for 3 months before breeding. After weaning, all pups were placed on SF. UCP1 mRNA and protein levels were quantified using quantitative real-time PCR and Western blot analysis, respectively, in brown (BAT), subcutaneous (SAT) and visceral (VAT) adipose tissues at 6 months of age. Total and UCP1-dependent mitochondrial respiration were determined by high-resolution respirometry. A Student’s t-test and Mann–Whitney test were used (significance: P<0.05). UCP1 mRNA levels were not different between the HF and SF offspring. UCP1 protein levels, total mitochondrial respiration and UCP1-dependent respiration were significantly higher in BAT from HF males (P=0.02, P=0.04, P=0.005, respectively) and females (P=0.01, P=0.04, P=0.02, respectively). In SAT, the UCP1 protein was significantly lower in HF females (P=0.03), and the UCP1-dependent thermogenesis was significantly lower from HF males (P=0.04). In VAT, UCP1 protein levels and UCP1-dependent respiration were significantly lower only in HF females (P=0.03, P=0.04, respectively). There were no differences in total respiration in SAT and VAT. Prenatal exposure to maternal obesity leads to significant increases in UCP1 levels and function in BAT in offspring with little impact on UCP1 levels and function in SAT and VAT.

Type
Original Article
Copyright
© Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2018 

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