All articles tagged with #glycogen
WEHI researchers report that ubiquitin can directly regulate glycogen, revealing a second on-demand pathway for stored sugar and a potential new route to treat diabetes, liver/heart diseases, and rare glycogen storage disorders using a novel NoPro-clipping technique.
A Case Western Reserve University–led study links a gut bacteria–produced inflammatory glycogen to ALS and FTD. In mouse models, certain gut bacteria produce glycogen that provokes brain inflammation and blood-brain barrier breakdown, with the C9ORF72 gene variant acting as a brake on glycogen’s harmful effects. Introducing bacteria like Parabacteroides merdae worsened inflammation, while the enzyme alpha-amylase reduced inflammation and extended lifespan in mice. Human stool samples showed elevated inflammatory glycogen in most ALS patients and in one FTD patient, suggesting a potential gut-targeted avenue for therapy, pending larger human studies and early clinical trials.
A new method, NoPro-clipping, reveals widespread ubiquitination of non-protein biomolecules in mammalian cells and tissues, notably glycogen (highest in liver and skeletal muscle) and endogenous glycerol and spermine. Glycogen ubiquitination can route glycogen to lysosomes and lower its levels, is altered in glycogen storage diseases, and increases in fasting liver, suggesting ubiquitin participates in physiological glycogen breakdown. The study broadens ubiquitin’s role from a protein modifier to a general modifier of biomolecules, with implications for metabolism and disease.
New research shows harmful sugars produced by gut bacteria trigger immune responses that damage brain cells in ALS and frontotemporal dementia; elevated levels were found in a majority of patients studied, and experiments reducing these sugars improved brain health and lifespan, pointing to gut-targeted therapies and biomarkers to slow disease progression—especially in carriers of the C9orf72 mutation.
A new study suggests that abnormal glycogen buildup in neurons may contribute to Alzheimer's disease by disrupting energy management and increasing oxidative stress, and that breaking down glycogen could offer a new therapeutic approach.
New research shows neurons store their own glycogen, acting as backup energy reserves during metabolic stress, which could lead to new treatments for neurological diseases involving energy failure.
A new study reveals that glycogen stored in the brain interacts with tau proteins involved in Alzheimer's disease, suggesting that boosting glycogen breakdown through enzymes like GlyP or dietary interventions could offer new therapeutic strategies for neurodegeneration. The research highlights the importance of brain sugar management in preventing or slowing Alzheimer's progression and opens avenues for potential treatments involving metabolic regulation.
New research suggests that breaking down excess glycogen in neurons can protect against dementia by reducing oxidative stress, with dietary restriction and drugs that activate glycogen phosphorylase showing potential as therapies for conditions like Alzheimer's.
Research on fruit flies reveals that the neurotransmitter octopamine determines whether food memories are stored long-term or short-term based on energy reserves, influencing future eating behavior. High glycogen levels lead to stable food memories and increased food intake, suggesting similar mechanisms may contribute to overeating and obesity in humans.
Bonking, or hitting the wall, occurs when the body runs out of glycogen, the stored form of glucose and the major fuel source for exercise. Once glycogen stores are depleted, the body must rely on fat for fuel, which is released much more slowly and requires more oxygen to break down compared to glycogen. Bonking can be prevented by ensuring glycogen stores are filled up before setting off, taking in some carbohydrate during the ride, and training the gut to absorb more carbohydrate during exercise. Training too often in a carb-depleted state may even slow you down.