Seasonal plasticity of the brain: the use of sheep model to study leptin resistance and obesity

• Autorzy: Zieba D.A. , Szczesna M. , Kirsz K. , Molik E.
• Języki publikacji: EN

Abstrakty

EN

The core of the leptin resistance hypothesis promulgated several years ago to explain obesity as a result of environmental causes consists of two tenets: the extinction of leptin-induced intracellular signaling downstream of leptin binding to the long form of the neuronal receptor LTRb in the hypothalamus and the impedance to leptin entry imposed at the blood-brain barrier (BBB). A recent comprehensive investigation concluded that a central leptin insufficiency associated with obesity can be attributed to a decreased efficiency of BBB leptin transport and not to leptin insensitivity within the hypothalamus. Interestingly, anorectic leptin’s effects are counteracted in some individuals by a natural resistance associated with hyperleptinemia, which is related to changes in hypothalamic sensitivity to leptin associated with, for example, seasonal reproduction, malnutrition or obesity. In sheep, it was observed that the hypothalamus is resistant to leptin in some periods, and this phenomenon is related to the adaptation of these animals to annual changes in energy supply and demand. However, a broad range of ambiguities exists regarding the implications that the intracellular signaling of signal transducer and activator of transcription-2/ suppressor of cytokine signaling 3 (STAT2/SOCS3) imparts central leptin resistance. Furthermore, several plausible alternative possibilities have been proposed, such as compensatory functional and anatomical reorganizations in the appetite regulating network (ARN), rearrangements in the afferent hormonal feedback signaling involved in weight homeostasis and modifications in leptin transport to the hypothalamus across the BBB. Taken together, these observations suggest that the contention that impaired intracellular signaling downstream of leptin entry into the ARN expedites environmentally induced obesity remains unsubstantiated and requires further evidence. FINANCIAL SUPPORT: Supported by NCN grants No. 2013/09 /B/NZ4/01532 and No. 2015/19/B/NZ9/01314.

• Wydawca: -
• Czasopismo: Acta Neurobiologiae Experimentalis
• Rocznik: 2017
• Tom: 77
• Numer: Suppl.1
• Opis fizyczny: p.43

Twórcy

autor

Zieba D.A.

• Agricultural University of Cracow, Department of Animal Biotechnology, Laboratory of Biotechnology and Genomics, Cracow, Poland

autor

Szczesna M.

• Agricultural University of Cracow, Department of Animal Biotechnology, Laboratory of Biotechnology and Genomics, Cracow, Poland

autor

Kirsz K.

• Agricultural University of Cracow, Department of Animal Biotechnology, Laboratory of Biotechnology and Genomics, Cracow, Poland

autor

Molik E.

• Agricultural University of Cracow, Department of Animal Biotechnology, Laboratory of Biotechnology and Genomics, Cracow, Poland