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2015 | 75 | Supl. |

Tytuł artykułu

Effects of gonadectomy and testosterone replacement on NKB-ir cell number in the arcute nucleus of the hypothalamus in obese and diabet male rats

Warianty tytułu

Języki publikacji

EN

Abstrakty

EN
BACKGROUND AND AIMS: Reproduction is governed by the hypothalamus-pituitary-gonadal (HPG) axis, with the gonadotropin releasing hormone being on the top of the axis. In the arcute nucleus (ARC) of hypothalamus, population of neurons expressing kisspeptin, neurokinin B (NKB) and dynorphin (KNDy neurons) is present. Those neurons are important in regulation of GnRH secretion. Beside metabolic problems obesity and diabetes are a major risk factors for reproductive dysfunctions (e.g. steroid imbalance and hypogonadism). Moreover, in hypogonadotropic hypogonadism patients mutation in NKB gene (TAC3) and its receptor – TAC3R was reported. In animals data on the role of gonadectomy (GDX) and sex steroids replacement in regulation of NKB expression is spare. We hypothesized that: (1) diet-induced obese (DIO), and/or streptozotocin (STZ)-induced diabetic (type 1 and 2) male rats would have altered number of NKB-ir neurons in the ARC; (2) gonadectomy and testosterone (T) replacement would differentially altered number of NKB-ir neurons. METHODS: Rats were fed with high fat diet (HFD) or control (C) diet for 5 weeks. Injections of STZ were performed to induce diabetes type 1 (C/STZ) or diabetes type 2 (HFD/STZ). The following groups were obtain: C, C/STZ, HFD, HFD/STZ. Next, animals were divided into 3 groups: gonadectomy (GDX); gonadectomy and T replacement (GDX+T) and  (Sham). Immunocytochemistry for the NKB was performed. RESULTS: We found that in C group there was no difference in number of NKB-ir neurons in the ARC between Sham and GDX. In contrast, in all experimental groups a decrease in NKB-ir cell number after GDX was shown. T replacement caused a decrease in NKB-ir cell number in C, HFD and HFD/STZ groups compare to Sham, respectively. CONCLUSION: Obesity and diabetes type 1 and type 2 leads to alter response of NKB-ir cells in response to GDX. Supported by NCN grant 2011/01/B/NZ4/04992.

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Wydawca

-

Rocznik

Tom

75

Numer

Opis fizyczny

p.S57

Twórcy

autor
  • Laboratory of Neurobiology, Institute of Zoology, Poznan University of Life Sciences, Poznan, Poland
  • Department of Animal Physiology and Biochemistry, Poznan University of Life Sciences, Poznan, Poland
  • Department of Animal Physiology and Biochemistry, Poznan University of Life Sciences, Poznan, Poland
autor
  • Laboratory of Neurobiology, Institute of Zoology, Poznan University of Life Sciences, Poznan, Poland
autor
  • Laboratory of Neurobiology, Institute of Zoology, Poznan University of Life Sciences, Poznan, Poland
autor
  • Department of Animal Physiology and Biochemistry, Poznan University of Life Sciences, Poznan, Poland
  • Laboratory of Neurobiology, Institute of Zoology, Poznan University of Life Sciences, Poznan, Poland

Bibliografia

Typ dokumentu

Bibliografia

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