Return to search

Hypothalamic Wnt signalling and its role in energy balance regulation

Yes / Wnt signalling and its downstream effectors are well known for their roles in embryogenesis
and tumourigenesis, including the regulation of cell proliferation, survival and differentiation. In
the nervous system, Wnt signalling has been described mainly during embryonic development,
although accumulating evidence suggests that it also plays a major role in adult brain morphogenesis
and function. Studies have predominantly concentrated on memory formation in the
hippocampus, although recent data indicate that Wnt signalling is also critical for neuroendocrine
control of the developed hypothalamus, a brain centre that is key in energy balance regulation
and whose dysfunction is implicated in metabolic disorders such as type 2 diabetes and
obesity. Based on scattered findings that report the presence of Wnt molecules in the tanycytes
and ependymal cells lining the third ventricle and arcuate nucleus neurones of the hypothalamus,
their potential importance in key regions of food intake and body weight regulation has
been investigated in recent studies. The present review brings together current knowledge on
Wnt signalling in the hypothalamus of adult animals and discusses the evidence suggesting a
key role for members of the Wnt signalling family in glucose and energy balance regulation in
the hypothalamus in diet-induced and genetically obese (leptin deficient) mice. Aspects of Wnt
signalling in seasonal (photoperiod sensitive) rodents are also highlighted, given the recent evidence
indicating that the Wnt pathway in the hypothalamus is not only regulated by diet and
leptin, but also by photoperiod in seasonal animals, which is connected to natural adaptive
changes in food intake and body weight. Thus, Wnt signalling appears to be critical as a modulator
for normal functioning of the physiological state in the healthy adult brain, and is also
crucial for normal glucose and energy homeostasis where its dysregulation can lead to a range
of metabolic disorders.

Identiferoai:union.ndltd.org:BRADFORD/oai:bradscholars.brad.ac.uk:10454/10839
Date14 March 2016
CreatorsHelfer, Gisela, Tups, A.
Source SetsBradford Scholars
LanguageEnglish
Detected LanguageEnglish
TypeArticle, Published version
Rights© 2016 The Authors. Journal of Neuroendocrinology published by John Wiley & Sons Ltd on behalf of British Society for Neuroendocrinology. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited., CC-BY

Page generated in 0.002 seconds