ArticleInternational journal of obesity (2005)2020
Ganglioside deficiency in hypothalamic POMC neurons promotes body weight gain.
Article in International journal of obesity (2005), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- Hypothalamic ceramide metabolism in obesity and dysregulation of glucose homeostasis.Reviews in endocrine & metabolic disorders · 2026Review
- CerS6-dependent ceramide synthesis in hypothalamic neurons promotes ER/mitochondrial stress and impairs glucose homeostasis in obese mice.Nature communications · 2023Article
- Allosteric modulation of ghrelin receptor signaling by lipids.Nature communications · 2021Article
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Authors and funding
5 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundGlucosylceramide synthase (GCS; gene: UDP-glucose:ceramide glucosyltransferase (Ugcg))-derived gangliosides comprise a specific class of lipids in the plasma membrane that modulate the activity of transmembrane receptors. GCS deletion in hypothalamic arcuate nucleus (Arc) neurons leads to prominent obesity. However, it has not yet been studied how ganglioside depletion affects individual Arc neuronal subpopulations. The current study investigates the effects of GCS deletion specifically in anorexigenic pro-opiomelanocortin (POMC) neurons. Additionally, we investigate insulin receptor (IR) signaling and phosphatidylinositol-(3,4,5)-trisphosphate (PIP MATERIALS AND
methodsWe generated Ugcgf/f-Pomc-Cre mice with ganglioside deficiency in POMC neurons. Moreover, the CRISPR (clustered regulatory interspaced short palindromic repeats)/Cas9 technology was used to inhibit GCS-dependent ganglioside biosynthesis in cultured mouse POMC neurons, yielding Ugcg
resultsChow-fed Ugcgf/f-Pomc-Cre mice showed a moderate but significant increase in body weight gain and they failed to display an increase of anorexigenic neuropeptide expression during the fasting-to-re-feeding transition. IR, IRS-2, p85, and overall insulin-evoked IR and IRS-2 phosphorylation were elevated in ganglioside-depleted Ugcg
conclusionOur work suggests that GCS deletion in POMC neurons promotes body weight gain. Gangliosides are required for an appropriate adaptation of anorexigenic neuropeptide expression in the Arc during the fasting-to-re-feeding transition. Moreover, gangliosides might modulate K
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