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Diabetologia. 2017 Feb;60(2):226-236. doi: 10.1007/s00125-016-4181-3. Epub 2016 Dec 16.

Glia: silent partners in energy homeostasis and obesity pathogenesis.

Author information

1
UW Diabetes Institute and Department of Medicine, University of Washington, 850 Republican St, S248, Box 358055, Seattle, WA, 98109, USA.
2
UW Diabetes Institute and Department of Medicine, University of Washington, 850 Republican St, S248, Box 358055, Seattle, WA, 98109, USA. jpthaler@uw.edu.

Abstract

Body weight stability requires homeostatic regulation to balance energy intake and energy expenditure. Research on this system and how it is affected by obesity has largely focused on the role of hypothalamic neurons as integrators of information about long-term fuel storage, short-term nutrient availability and metabolic demand. Recent studies have uncovered glial cells as additional contributors to energy balance regulation and obesity pathogenesis. Beginning with early work on leptin signalling in astrocytes, this area of research rapidly emerged after the discovery of hypothalamic inflammation and gliosis in obese rodents and humans. Current studies have revealed the involvement of a wide variety of glial cell types in the modulation of neuronal activity, regulation of hormone and nutrient availability, and participation in the physiological regulation of feeding behaviour. In addition, one glial type, microglia, has recently been implicated in susceptibility to diet-induced obesity. Together, these exciting new findings deepen our understanding of energy homeostasis regulation and raise the possibility of identifying novel mechanisms that contribute to the pathogenesis of obesity.

KEYWORDS:

Astrocytes; Brain; Central nervous system; Diabetes; Energy homeostasis; Glia; Hypothalamus; Inflammation; Microglia; Obesity; Review

PMID:
27986987
PMCID:
PMC5253392
DOI:
10.1007/s00125-016-4181-3
[Indexed for MEDLINE]
Free PMC Article

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