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Publication
Disruption of Lipid Uptake in Astroglia Exacerbates Diet-Induced Obesity.
Authors Gao Y, Layritz C, Legutko B, Eichmann TO, Laperrousaz E, Moullé VS,
Cruciani-Guglielmacci C, Magnan C, Luquet S, Woods SC, Eckel RH, Yi CX,
Garcia-Caceres C, Tschöp MH
Submitted By Robert Eckel on 8/8/2018
Status Published
Journal Diabetes
Year 2017
Date Published 10/1/2017
Volume : Pages 66 : 2555 - 2563
PubMed Reference 28710138
Abstract Neuronal circuits in the brain help to control feeding behavior and systemic
metabolism in response to afferent nutrient and hormonal signals. Although
astrocytes have historically been assumed to have little relevance for such
neuroendocrine control, we investigated whether lipid uptake via lipoprotein
lipase (LPL) in astrocytes is required to centrally regulate energy homeostasis.
Ex vivo studies with hypothalamus-derived astrocytes showed that LPL expression
is upregulated by oleic acid, whereas it is decreased in response to palmitic
acid or triglycerides. Likewise, astrocytic LPL deletion reduced the
accumulation of lipid droplets in those glial cells. Consecutive in vivo studies
showed that postnatal ablation of LPL in glial fibrillary acidic
protein-expressing astrocytes induced exaggerated body weight gain and glucose
intolerance in mice exposed to a high-fat diet. Intriguingly, astrocytic LPL
deficiency also triggered increased ceramide content in the hypothalamus, which
may contribute to hypothalamic insulin resistance. We conclude that hypothalamic
LPL functions in astrocytes to ensure appropriately balanced nutrient sensing,
ceramide distribution, body weight regulation, and glucose metabolism.






Genes
SymbolDescription
Lpllipoprotein lipase

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