ArticleHuman molecular genetics2015
The Fragile X proteins Fmrp and Fxr2p cooperate to regulate glucose metabolism in mice.
Article in Human molecular genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 30 citations in OpenAlex.
- Sleep in a mouse model of fragile X syndrome is resistant to metabolic manipulations.Human molecular genetics · 2025Article
- Interaction between neuromuscular junction metabolic requirements in fragile X syndrome and glycogen storage disease models.Disease models & mechanisms · 2025Article
- Review
- Do metabolic deficits contribute to sleep disruption in monogenic intellectual disability syndromes?Trends in neurosciences · 2024Review
- Regulation of endocrine cell alternative splicing revealed by single-cell RNA sequencing in type 2 diabetes pathogenesis.Communications biology · 2024Article
- Deregulation of ER-mitochondria contact formation and mitochondrial calcium homeostasis mediated by VDAC in fragile X syndrome.Developmental cell · 2023Article
- Review
- Integrative omics indicate FMRP sequesters mRNA from translation and deadenylation in human neuronal cells.Molecular cell · 2022Article
- Loss of neurexin-1 in Drosophila melanogaster results in altered energy metabolism and increased seizure susceptibility.Human molecular genetics · 2022Article
- Alteration of Fatty Acid Profile in Fragile X Syndrome.International journal of molecular sciences · 2022Article
- Effects of Soy-Based Infant Formula on Weight Gain and Neurodevelopment in an Autism Mouse Model.Cells · 2022Article
- Intercepting IRE1 kinase-FMRP signaling prevents atherosclerosis progression.EMBO molecular medicine · 2022Article
- Retinoic Acid Supplementation Rescues the Social Deficits inFrontiers in genetics · 2022Article
- Energy metabolism in childhood neurodevelopmental disorders.EBioMedicine · 2021Review
- Depletion of Mitochondrial Components from Extracellular Vesicles Secreted from Astrocytes in a Mouse Model of Fragile X Syndrome.International journal of molecular sciences · 2021Article
- Inefficient thermogenic mitochondrial respiration due to futile proton leak in a mouse model of fragile X syndrome.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Reduced mitochondrial fusion and Huntingtin levels contribute to impaired dendritic maturation and behavioral deficits in Fmr1-mutant mice.Nature neuroscience · 2019Article
- The translational regulator FMRP controls lipid and glucose metabolism in mice and humans.Molecular metabolism · 2019Article
- Comparative Behavioral Phenotypes ofBrain sciences · 2019Article
- Polysomnographic Findings in Fragile X Syndrome Children with EEG Abnormalities.Behavioural neurology · 2019Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Fragile X syndrome results from loss of FMR1 expression. Individuals with the disorder exhibit not only intellectual disability, but also an array of physical and behavioral abnormalities, including sleep difficulties. Studies in mice demonstrated that Fmr1, along with its paralog Fxr2, regulate circadian behavior, and that their absence disrupts expression and cycling of essential clock mRNAs in the liver. Recent reports have identified circadian genes to be essential for normal metabolism. Here we describe the metabolic defects that arise in mice mutated for both Fmr1 and Fxr2. These mice have reduced fat deposits compared with age- and weight-matched controls. Several metabolic markers show either low levels in plasma or abnormal circadian cycling (or both). Insulin levels are consistently low regardless of light exposure and feeding conditions, and the animals are extremely sensitive to injected insulin. Glucose production from introduced pyruvate and glucagon is impaired and the mice quickly clear injected glucose. These mice also have higher food intake and higher VO2 and VCO2 levels. We analyzed liver expression of genes involved in glucose homeostasis and found several that are expressed differentially in the mutant mice. These results point to the involvement of Fmr1 and Fxr2 in maintaining the normal metabolic state in mice.
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