ArticleThe Journal of biological chemistry2015
Muscle glycogen remodeling and glycogen phosphate metabolism following exhaustive exercise of wild type and laforin knockout mice.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- Solving the Insoluble: Regulation of α-Polyglucan Solubility and Functionality in Nature.Molecules (Basel, Switzerland) · 2026Review
- Covalently linked phosphate monoesters on alpha-polyglucans reduce substrate affinity of branching enzymes.Carbohydrate polymers · 2025Article
- Clinicopathologic Dissociation: Robust Lafora Body Accumulation in Malin KO Mice Without Observable Changes in Home-Cage Behavior.The Journal of comparative neurology · 2024Article
- GDE5/Gpcpd1 activity determines phosphatidylcholine composition in skeletal muscle and regulates contractile force in mice.Communications biology · 2024Article
- In situ mass spectrometry imaging reveals heterogeneous glycogen stores in human normal and cancerous tissues.EMBO molecular medicine · 2022Article
- Skeletal Muscle Metabolic Alternation Develops Sarcopenia.Aging and disease · 2022Review
- Mice with Whole-Body Disruption of AMPK-Glycogen Binding Have Increased Adiposity, Reduced Fat Oxidation and Altered Tissue Glycogen Dynamics.International journal of molecular sciences · 2021Article
- Brain glycogen serves as a critical glucosamine cache required for protein glycosylation.Cell metabolism · 2021Article
- Sensitive quantification of α-glucans in mouse tissues, cell cultures, and human cerebrospinal fluid.The Journal of biological chemistry · 2020Article
- Polyglucosan body structure in Lafora disease.Carbohydrate polymers · 2020Article
- Effects of Nutrient Intake Timing on Post-Exercise Glycogen Accumulation and its Related Signaling Pathways in Mouse Skeletal Muscle.Nutrients · 2019Article
- Skeletal Muscle Glycogen Chain Length Correlates with Insolubility in Mouse Models of Polyglucosan-Associated Neurodegenerative Diseases.Cell reports · 2019Article
- Brain Glycogen Structure and Its Associated Proteins: Past, Present and Future.Advances in neurobiology · 2019Review
- Lafora disease - from pathogenesis to treatment strategies.Nature reviews. Neurology · 2018Review
- Lafora disease: from genotype to phenotype.Journal of genetics · 2018Review
- Lafora disease offers a unique window into neuronal glycogen metabolism.The Journal of biological chemistry · 2018Review
- Pathogenesis of Lafora Disease: Transition of Soluble Glycogen to Insoluble Polyglucosan.International journal of molecular sciences · 2017Review
- Abnormal glycogen chain length pattern, not hyperphosphorylation, is critical in Lafora disease.EMBO molecular medicine · 2017Article
- Lafora disease.Epileptic disorders : international epilepsy journal with videotape · 2016Review
- Mechanisms for greater insulin-stimulated glucose uptake in normal and insulin-resistant skeletal muscle after acute exercise.American journal of physiology. Endocrinology and metabolism · 2015Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Glycogen, the repository of glucose in many cell types, contains small amounts of covalent phosphate, of uncertain function and poorly understood metabolism. Loss-of-function mutations in the laforin gene cause the fatal neurodegenerative disorder, Lafora disease, characterized by increased glycogen phosphorylation and the formation of abnormal deposits of glycogen-like material called Lafora bodies. It is generally accepted that the phosphate is removed by the laforin phosphatase. To study the dynamics of skeletal muscle glycogen phosphorylation in vivo under physiological conditions, mice were subjected to glycogen-depleting exercise and then monitored while they resynthesized glycogen. Depletion of glycogen by exercise was associated with a substantial reduction in total glycogen phosphate and the newly resynthesized glycogen was less branched and less phosphorylated. Branching returned to normal on a time frame of days, whereas phosphorylation remained suppressed over a longer period of time. We observed no change in markers of autophagy. Exercise of 3-month-old laforin knock-out mice caused a similar depletion of glycogen but no loss of glycogen phosphate. Furthermore, remodeling of glycogen to restore the basal branching pattern was delayed in the knock-out animals. From these results, we infer that 1) laforin is responsible for glycogen dephosphorylation during exercise and acts during the cytosolic degradation of glycogen, 2) excess glycogen phosphorylation in the absence of laforin delays the normal remodeling of the branching structure, and 3) the accumulation of glycogen phosphate is a relatively slow process involving multiple cycles of glycogen synthesis-degradation, consistent with the slow onset of the symptoms of Lafora disease.
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