Selenium protects against nesfatin‐1 modulation of the hypothalamic‐pituitary‐testicular axis during hypothyroidism in male rats

Author:

El‐Shaer Rehab Ahmed Ahmed1ORCID,Ibrahim Sarah2ORCID,Hewady Passant Medhat1ORCID,Atef Marwa Mohamed3ORCID,El‐Deeb Omnia Safwat3ORCID,Hafez Yasser Mostafa4ORCID,Amer Rania Saed5ORCID,El‐Sharnoby Jehan Abd El‐Hameed5,AbuoHashish Norhan Ahmed6ORCID,Awad Marwa Mahmoud1ORCID

Affiliation:

1. Medical Physiology Department, Faculty of Medicine Tanta University Tanta Egypt

2. Human Anatomy and Embryology Department, Faculty of Medicine Tanta University Tanta Egypt

3. Biochemistry Department, Faculty of Medicine Tanta University Tanta Egypt

4. Internal Medicine Department, Faculty of Medicine Tanta University Tanta Egypt

5. Clinical Pathology Department, Faculty of Medicine Tanta University Tanta Egypt

6. Pharmacology Department, Faculty of Medicine Tanta University Tanta Egypt

Abstract

AbstractNormal gonadal function can be disrupted by hypothyroidism. Hypothyroidism disturbs testicular function directly and centrally by affecting the hypothalamic‐pituitary‐testicular axis with unclear mechanism. As nesfatin‐1 neurons co‐localized with TRH and GnRH neurons in the hypothalamus, it could play a role in centrally hypothyroidism induced testicular dysfunction. Selenium (Se), by affecting thyroid iodide supply, could relieve these disturbances. So, we aim to identify the role of nesfatin‐1 as a link between testicular dysfunction and hypothyroidism through modulating the MAPK/ERK pathway while discussing the possible role of Se in alleviating hypothyroidism and associated testicular damage. Forty male rats were divided equally into: Control: distilled water, Se: Se orally, Propylthiouracil (PTU): PTU orally, PTU + Se: Se with PTU orally. Serum thyroid function, gonadal hormones, nesfatin‐1, testicular redox status, sperm analysis, brain tissue GnRH, nucleobindin 2‐derived polypeptide, pMAPK/ERK gene expression, histological changes and immunohistochemical expression of testicular proliferating cell antigen (PCNA) were done. PTU induced hypothyroidism and reduction of gonadal hormones which both were correlated with reduced nesfatin‐1. There was testicular stress with reduced GnRH, NUCB2, pMAPK/ERK gene expression, and PCNA immunopositive cells. These parameters were reversed by Se. Nesfatin‐1 could be the central link between hypothyroidism and disturbances of the hypothalamic pituitary testicular axis.

Publisher

Wiley

Subject

Physiology (medical),Physiology

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