Universität zu Köln

Eifler, Lisa, Hoffmann, Annett, Wagner, Isabel Viola, Kloeting, Nora, Sahlin, Lena, Ebert, Thomas ORCID: 0000-0003-1683-9276, Jessnitzer, Beate, Loessner, Ulrike, Stumvoll, Michael, Soder, Olle, Fasshauer, Mathias and Kralisch, Susan (2018). Leptin restores markers of female fertility in lipodystrophy. Biochim. Biophys. Acta-Mol. Basis Dis., 1864 (10). S. 3292 - 3298. AMSTERDAM: ELSEVIER SCIENCE BV. ISSN 1879-260X

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Abstract

Objectives: Female reproductive dysfunction occurs in patients with pathological loss of adipose tissue, i.e. lipodystrophy (LD). However, mechanisms remain largely unclear and treatment effects of adipocyte-derived leptin have not been assessed in LD animals. Methods: In the current study, C57131/6 LD mice on a low-density lipoprotein receptor knockout background were treated with leptin or saline for 8 weeks and compared to non-LD controls. Results: The number of pups born was 37% lower in breeding pairs consisting of LD female mice x non-LD male mice (n = 3.3) compared to LD male mice x non-LD female mice (n = 5.2) (p < 0.05). Mean uterus weight was significantly lower in the saline-treated LD group (18.8 mg) compared to non-LD controls (52.9 mg; p < 0.0001) and increased significantly upon leptin treatment (46.5 mg; p < 0.001). The mean number of corpora lutea per ovary was significantly lower in saline-treated LD animals compared to non-LD controls (p < 0.01) and was restored to non-LD control levels by leptin (p < 0.05). Mechanistically, mRNA expression of ovarian follicle stimulating hormone receptor (p < 0.01) and estrogen receptor beta (p < 0.05), as well as of pituitary luteinizing hormone beta subunit (p < 0.001) and follicle-stimulating hormone beta subunit (p < 0.05), was significantly up regulated in LD mice compared to non-LD controls. In addition, mean time to vaginal opening as a marker of puberty onset was delayed by 12.5 days in LD mice (50.9 days) compared to non-LD controls (38.4 days; p < 0.001). Conclusions: Female LD animals show impaired fertility which is restored by leptin. Future studies should assess leptin as a subfertility treatment in human leptin-deficiency disorders.

Item Type:	Journal Article
Creators:	Creators Email ORCID ORCID Put Code Eifler, Lisa UNSPECIFIED UNSPECIFIED UNSPECIFIED Hoffmann, Annett UNSPECIFIED UNSPECIFIED UNSPECIFIED Wagner, Isabel Viola UNSPECIFIED UNSPECIFIED UNSPECIFIED Kloeting, Nora UNSPECIFIED UNSPECIFIED UNSPECIFIED Sahlin, Lena UNSPECIFIED UNSPECIFIED UNSPECIFIED Ebert, Thomas UNSPECIFIED orcid.org/0000-0003-1683-9276 UNSPECIFIED Jessnitzer, Beate UNSPECIFIED UNSPECIFIED UNSPECIFIED Loessner, Ulrike UNSPECIFIED UNSPECIFIED UNSPECIFIED Stumvoll, Michael UNSPECIFIED UNSPECIFIED UNSPECIFIED Soder, Olle UNSPECIFIED UNSPECIFIED UNSPECIFIED Fasshauer, Mathias UNSPECIFIED UNSPECIFIED UNSPECIFIED Kralisch, Susan UNSPECIFIED UNSPECIFIED UNSPECIFIED
URN:	urn:nbn:de:hbz:38-171572
DOI:	10.1016/j.bbadis.2018.07.015
Journal or Publication Title:	Biochim. Biophys. Acta-Mol. Basis Dis.
Volume:	1864
Number:	10
Page Range:	S. 3292 - 3298
Date:	2018
Publisher:	ELSEVIER SCIENCE BV
Place of Publication:	AMSTERDAM
ISSN:	1879-260X
Language:	English
Faculty:	Unspecified
Divisions:	Unspecified
Subjects:	no entry
Uncontrolled Keywords:	Keywords Language REPRODUCTIVE FUNCTION; MOUSE; THERAPY; OBESITY; ATHEROSCLEROSIS; WOMEN; MICE Multiple languages Biochemistry & Molecular Biology; Biophysics; Cell Biology Multiple languages
Refereed:	Yes
URI:	http://kups.ub.uni-koeln.de/id/eprint/17157