Atherobesity - DFG KFO 152 "Fett und Gefäß"

Subproject 8: Chronic inflammatory activation in the adipose tissue in obesity: an risk factor for the male infertility?

Principal Investigators:


Prof. Dr. med. Uwe Paasch Prof. Dr. rer. nat. Jürgen Kratzsch
Dermatology, Venereology and Allergology Clinic Institute of Laboratory Medicine, Clinical Chemistry and Molecular Diagnostics
Universität Leipzig Universität Leipzig
Philipp-Rosenthal-Str. 23 Paul-List-Str. 13
04103 Leipzig 04103 Leipzig
Phone: +49 341 97 18600 Phone: +49 341 97 22241
Fax: +49 341 97 18609 Fax: +49 341 97 22249


Summary of the Subproject:

A chronic inflammatory activation in the adipose tissue could be the causal connection between obesity and male infertility. This hypothesis shall be analyzed on patients with obesity and diabetes mellitus in a combined clinical-molecular-biological study.
We aim to answer the question, whether resulting molecular alterations in serum, in seminal plasma and in ejaculated spermatozoa are connected with changes in concentrations of adipokines like adiponectin, leptin, leptin receptor and resistin and in their interaction with conventional parameters of ejaculate (concentration, motility, morphology) and the specific functions of spermatozoa (capacitation, acrosome reaction, apoptosis, NO- und ROS-production and decondensation) on the molecular basis.
The expected results should clarify, if a negative influence of testicular function is attributed to paracrine and / or endocrine dysregulation.
Thereby the effect of adiponectin, leptin and restistin on spermatozoa shall be investigated by measuring appropriate endpoints in a spermatozoa based cell model. Additionally, it should be determined, what the underlying causes for an assumed leptin resistance on spermatozoa of patients with spermatogenesis-dysfunction are. Thereby it will be analyzed, whether an intensified separation of extracellular domain of the leptin-receptor or a changed expression of potential intracellular trigger of a leptin resistance suppressor of cytokine signaling 3 (SOCS-3) or tyrosinphosphatase PTP1B occur in these patients and how the effectiveness of these substances could be blocked. The focus is placed on searching changes in signal transduction of leptin effects in connection with a disrupted spermatogenesis.


  1. Jope T, Lammert A, Kratzsch J, Paasch U, Glander HJ. Leptin and leptinreceptor in human seminal plasma and in human spermatozoa. Int J Androl. 2003;26:335-41.
  2. Kratzsch J, Paasch U, Grunewald S, Mueller MA, Thiery J, Glander HJ. Resistin correlates with elastase and interleukin-6 in human seminal plasma. Reprod BiomedOnline. 2008;16:283-8.
  3. Paasch U, Grunewald S, Kratzsch J, Glander HJ. Obesity and age affect male fertility potential. Fertil Steril. 2010;94:2898-901.
  4. Paasch U, Heidenreich F, Pursche T, Kuhlisch E, Kettner K, Grunewald S, Kratzsch J, Dittmar G, Glander HJ, Hoflack B, Kriegel TM. Identification ofincreased amounts of eppin protein complex components in sperm cells of diabetic and obese individuals by difference gel electrophoresis. Mol Cell Proteomics. 2011;10:M110.007187.
  5. Thomas S, Kratzsch D, Schaab M, Scholz M, Grunewald S, Thiery J, Roessner C, Paasch U, Kratzsch J, Glander HJ, Grunewald S. Sperm apoptosis signalling in diabetic men. Reprod Biomed Online. 2012;25:292-9.
  6. Grunewald S, Glander HJ, Paasch U, Kratzsch J. Age-dependent inhibin B concentration in relation to FSH and semen sample qualities: a study in 2448 men. Reproduction. 2013;145:237-44.
  7. Paasch U, Kratzsch J. Seminal plasma adipokine levels are correlated with functional characteristics of spermatozoa. Fertil Steril. 2013;99:1256-63.e3.
Imprint | Contact | © 2014 Autor: Prof. Dr. M. Blüher