ArticleBMC neuroscience2013
Loss of IP3 receptor function in neuropeptide secreting neurons leads to obesity in adult Drosophila.
Article in BMC neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 26 citations in OpenAlex.
- Lipid Metabolism in Relation to Calcium Homeostasis.Advances in experimental medicine and biology · 2026Review
- Lipid Dyshomeostasis and Inherited Cerebellar Ataxia.Molecular neurobiology · 2022Review
- Predicting novel candidate human obesity genes and their site of action by systematic functional screening in Drosophila.PLoS biology · 2021Article
- Insects as a New Complex Model in Hormonal Basis of Obesity.International journal of molecular sciences · 2021Review
- A Comparative Perspective on Functionally-Related, Intracellular Calcium Channels: The Insect Ryanodine and Inositol 1,4,5-Trisphosphate Receptors.Biomolecules · 2021Review
- What You Eat Matters: Nutrient Inputs Alter the Metabolism and Neuropeptide Expression in Egyptian Cotton Leaf Worm,Frontiers in physiology · 2021Article
- The Role of Peptide Hormones in Insect Lipid Metabolism.Frontiers in physiology · 2020Review
- Calcium Signaling Pathways: Key Pathways in the Regulation of Obesity.International journal of molecular sciences · 2019Review
- ER-Ca2+ sensor STIM regulates neuropeptides required for development under nutrient restriction in Drosophila.PloS one · 2019Article
- Neuronal Calcium Signaling in Metabolic Regulation and Adaptation to Nutrient Stress.Frontiers in neural circuits · 2018Review
- Control of protein translation by IPFly · 2017Article
- IPDevelopment (Cambridge, England) · 2017Article
- THADA Regulates the Organismal Balance between Energy Storage and Heat Production.Developmental cell · 2017Article
- A Gap Junction Protein, Inx2, Modulates Calcium Flux to Specify Border Cell Fate during Drosophila oogenesis.PLoS genetics · 2017Article
- Article
- Absence of intracellular ion channels TPC1 and TPC2 leads to mature-onset obesity in male mice, due to impaired lipid availability for thermogenesis in brown adipose tissue.Endocrinology · 2015Article
- Induction of ER stress-mediated apoptosis by ceramide via disruption of ER Ca(2+) homeostasis in human adenoid cystic carcinoma cells.Cell & bioscience · 2014Article
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4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIntracellular calcium signaling regulates a variety of cellular and physiological processes. The inositol 1,4,5 trisphosphate receptor (IP3R) is a ligand gated calcium channel present on the membranes of endoplasmic reticular stores. In previous work we have shown that Drosophila mutants for the IP3R (itprku) become unnaturally obese as adults with excessive storage of lipids on a normal diet. While the phenotype manifests in cells of the fat body, genetic studies suggest dysregulation of a neurohormonal axis.
resultsWe show that knockdown of the IP3R, either in all neurons or in peptidergic neurons alone, mimics known itpr mutant phenotypes. The peptidergic neuron domain includes, but is not restricted to, the medial neurosecretory cells as well as the stomatogastric nervous system. Conversely, expression of an itpr+ cDNA in the same set of peptidergic neurons rescues metabolic defects of itprku mutants. Transcript levels of a gene encoding a gastric lipase CG5932 (magro), which is known to regulate triacylglyceride storage, can be regulated by itpr knockdown and over-expression in peptidergic neurons. Thus, the focus of observed itpr mutant phenotypes of starvation resistance, increased body weight, elevated lipid storage and hyperphagia derive primarily from peptidergic neurons.
conclusionsThe present study shows that itpr function in peptidergic neurons is not only necessary but also sufficient for maintaining normal lipid metabolism in Drosophila. Our results suggest that intracellular calcium signaling in peptidergic neurons affects lipid metabolism by both cell autonomous and non-autonomous mechanisms.
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