bims-glecem 2023-03-12 papers

bims-glecem

Biomed News

on Glycogen metabolism in exercise, cancer and energy metabolism

Issue of 2023–03–12
thirteen papers selected by
Dipsikha Biswas, Københavns Universitet

Glycogen Kinetics of Wistar Rats: Different Exercise Intensities and Tissue Analyzed Influence.
Molecular mechanisms of glycogen particle assembly in Escherichia coli.
Valuing Mundane Manifestations of Rare, but Underdiagnosed, Diseases in Portugal: The Example of McArdle Disease.
Role of Astrocytes in the Pathophysiology of Lafora Disease and Other Glycogen Storage Disorders.
Carbohydrate intake before and during high intensity exercise with reduced muscle glycogen availability affects the speed of muscle reoxygenation and performance.
Interior of glycogen probed by pyrene excimer fluorescence.
Persistent acidosis and chronic kidney disease in a patient with type 1 glycogen storage disease.
Exercise Timing Matters for Glycogen Metabolism and Accumulated Fat Oxidation over 24 h.
Effects of enzyme replacement therapy on cardiac function in classic infantile Pompe disease.
Insulin-resistant female rat skeletal muscles display diacylglycerol-mediated PKC activation and inflammation without ceramides accumulation.
Quality of Life with Late-Onset Pompe Disease: Qualitative Interviews and General Public Utility Estimation in the United Kingdom.
Brain Homogenate of a Rat Model of Alzheimer's Disease Modifies the Secretome of 3D Cultured Periodontal Ligament Stem Cells: A Potential Neuroregenerative Therapy.
GBE1 Promotes Glioma Progression by Enhancing Aerobic Glycolysis through Inhibition of FBP1.

Int J Exerc Sci. 2022 ;15(2): 289-299

Glycogen Kinetics of Wistar Rats: Different Exercise Intensities and Tissue Analyzed Influence.

Carlos Dellavechia DE Carvalho, Carlos Augusto Kalva Filho, Alisson Luiz DA Rocha, Adelino Sanchez Ramos Silva, Marcelo Papoti.

The aim of this study is to verify the influence of the intensity on muscle and hepatic glycogen depletion and recovery kinetics of Wistar rats, submitted to three acute training sessions with equalized loads. 81 male Wistar rats performed an incremental test to determine maximal running speed (MRS) and divided into 4 groups: baseline group (Control; n = 9); low intensity training session (GZ1; n = 24; 48 minutes at 50% of MRS); moderate intensity group (GZ2; n = 24; 32 minutes at 75% of MRS) and high intensity group (GZ3; n = 24; 5x5 minutes and 20 seconds at 90% of MRS). Immediately after the sessions and after 6, 12 and 24 hours, 6 animals from each subgroup were euthanized for glycogen quantification in soleus and EDL muscles and liver. A Two-Way ANOVA and the Fisher's Post-hoc test was used (p < 0.05). Glycogen supercompensation occurred between 6 and 12 hours after exercise in muscle tissue and 24 after exercise in the liver. The muscle and hepatic glycogen depletion and recovery kinetics are not modulated by exercise intensity since the load was equalized, but effects were distinct in different tissues. Hepatic glycogenolysis and muscle glycogen synthesis processes seem to run in parallel.

Keywords: Acute exercise; equalized load; recovery; running; supercompensation
Carbohydr Polym. 2023 Jan 01. pii: S0144-8617(22)01105-5. [Epub ahead of print]299 120200

Molecular mechanisms of glycogen particle assembly in Escherichia coli.

Fen Li, Meng-Meng Wang, Qing-Hua Liu, Zhang-Wen Ma, Jun-Jiao Wang, Zi-Yi Wang, Jia-Wei Tang, Jing-Wen Lyu, Zuo-Bin Zhu, Liang Wang.

  It has been reported that glycogen in Escherichia coli has two structural states, that is, fragility and stability, which alters dynamically. However, molecular mechanisms behind the structural alterations are not fully understood. In this study, we focused on the potential roles of two important glycogen degradation enzymes, glycogen phosphorylase (glgP) and glycogen debranching enzyme (glgX), in glycogen structural alterations. The fine molecular structure of glycogen particles in Escherichia coli and three mutants (ΔglgP, ΔglgX and ΔglgP/ΔglgX) were examined, which showed that glycogen in E. coli ΔglgP and E. coli ΔglgP/ΔglgX were consistently fragile while being consistently stable in E. coli ΔglgX, indicating the dominant role of GP in glycogen structural stability control. In sum, our study concludes that glycogen phosphorylase is essential in glycogen structural stability, leading to molecular insights into structural assembly of glycogen particles in E. coli.

Keywords:  Escherichia coli; Glycogen debranching enzyme; Glycogen phosphorylase; Glycogen α particle; Structural fragility

DOI:  https://doi.org/10.1016/j.carbpol.2022.120200
Acta Med Port. 2023 Mar 01. 36(3): 220-222

Valuing Mundane Manifestations of Rare, but Underdiagnosed, Diseases in Portugal: The Example of McArdle Disease.

António Mateus-Pinheiro, Tiago Costa, Hélder Esperto, Sónia Moreira.



Keywords:  Glycogen Storage Disease Type V/diagnosis; Glycogen Storage Disease Type V/epidemiology; Portugal

DOI:  https://doi.org/10.20344/amp.19315
Cells. 2023 Feb 24. pii: 722. [Epub ahead of print]12(5):

Role of Astrocytes in the Pathophysiology of Lafora Disease and Other Glycogen Storage Disorders.

Jordi Duran.

  Lafora disease is a rare disorder caused by loss of function mutations in either the EPM2A or NHLRC1 gene. The initial symptoms of this condition are most commonly epileptic seizures, but the disease progresses rapidly with dementia, neuropsychiatric symptoms, and cognitive deterioration and has a fatal outcome within 5-10 years after onset. The hallmark of the disease is the accumulation of poorly branched glycogen in the form of aggregates known as Lafora bodies in the brain and other tissues. Several reports have demonstrated that the accumulation of this abnormal glycogen underlies all the pathologic traits of the disease. For decades, Lafora bodies were thought to accumulate exclusively in neurons. However, it was recently identified that most of these glycogen aggregates are present in astrocytes. Importantly, astrocytic Lafora bodies have been shown to contribute to pathology in Lafora disease. These results identify a primary role of astrocytes in the pathophysiology of Lafora disease and have important implications for other conditions in which glycogen abnormally accumulates in astrocytes, such as Adult Polyglucosan Body disease and the buildup of Corpora amylacea in aged brains.

Keywords:  Lafora disease; aggregation; epilepsy; glycogen; neurodegeneration; neuroinflammation

DOI:  https://doi.org/10.3390/cells12050722
Eur J Appl Physiol. 2023 Mar 10.

Carbohydrate intake before and during high intensity exercise with reduced muscle glycogen availability affects the speed of muscle reoxygenation and performance.

Andrius Ramonas, Paul B Laursen, Micalla Williden, Wee-Leong Chang, Andrew E Kilding.

  Muscle glycogen state and carbohydrate (CHO) supplementation before and during exercise may impact responses to high-intensity interval training (HIIT). This study determined cardiorespiratory, substrate metabolism, muscle oxygenation, and performance when completing HIIT with or without CHO supplementation in a muscle glycogen depleted state. On two occasions, in a cross-over design, eight male cyclists performed a glycogen depletion protocol prior to HIIT during which either a 6% CHO drink (60 g.hr-1) or placebo (%CHO, PLA) was consumed. HIIT consisted of 5 × 2 min at 80% peak power output (PPO), 3 × 10-min bouts of steady-state (SS) cycling (50, 55, 60% PPO), and a time-to-exhaustion (TTE) test. There was no difference in SS [Formula: see text], HR, substrate oxidation and gross efficiency (GE %) between CHO and PLA conditions. A faster rate of muscle reoxygenation (%. s-1) existed in PLA after the 1st (Δ - 0.23 ± 0.22, d = 0.58, P < 0.05) and 3rd HIIT intervals (Δ - 0.34 ± 0.25, d = 1.02, P < 0.05). TTE was greater in CHO (7.1 ± 5.4 min) than PLA (2.5 ± 2.3 min, d = 0.98, P < 0.05). CHO consumption before and during exercise under reduced muscle glycogen conditions did not suppress fat oxidation, suggesting a strong regulatory role of muscle glycogen on substrate metabolism. However, CHO ingestion provided a performance benefit under intense exercise conditions commenced with reduced muscle glycogen. More research is needed to understand the significance of altered muscle oxygenation patterns during exercise.

Keywords:  Endurance exercise; Fat oxidation; Low glycogen availability; Muscle glycogen; Muscle oxygenation

DOI:  https://doi.org/10.1007/s00421-023-05162-y
Carbohydr Polym. 2023 Jan 01. pii: S0144-8617(22)01110-9. [Epub ahead of print]299 120205

Interior of glycogen probed by pyrene excimer fluorescence.

Damin Kim, Jean Duhamel.

  A glycogen sample from oyster (O) and another from corn (C) were fluorescently labeled with 1-pyrenebutyric acid to yield two series of pyrene-labeled glycogen samples (Py-Glycogen(O/C)). Analysis of the time-resolved fluorescence (TRF) measurements of the Py-Glycogen(O/C) dispersions in dimethyl sulfoxide yielded the maximum number (<Nblobexp>) of anhydroglucose units (AGUs), that could separate two pyrene-labeled AGUs and still allow efficient pyrene excimer formation (PEF) between an excited and a ground-state pyrene. Molecular mechanics optimizations (MMOs) were conducted on a lattice of hexagonally close packed oligosaccharide helices to determine how the theoretical Nblobtheo varied as a function of the lattice density. Comparing <Nblobexp> and <Nblobtheo>, obtained after integrating Nblobtheo along the local density profile ρ(r) across the glycogen particles, led to the conclusion that ρ(r) took a maximum value at the center of the glycogen particles contrary to expectations based on the Tier Model.

Keywords:  Glycogen; Polysaccharides; Pyrene excimer formation

DOI:  https://doi.org/10.1016/j.carbpol.2022.120205
Clin Nephrol. 2023 Mar 05.

Persistent acidosis and chronic kidney disease in a patient with type 1 glycogen storage disease.

Kai Xiong Lim, Yan Mee Law, Weiwen Guo.

Type 1 glycogen storage disease (GSDI) is a rare autosomal recessive disorder caused by glucose-6-phosphatase (G6Pase) deficiency. We discuss a case of a 29-year-old gentleman who had GSDI with metabolic complications of hypoglycemia, hypertriglyceridemia, hyperuricemia, and short stature. He also suffered from advanced chronic kidney disease, nephrotic range proteinuria, and hepatic adenomas. He presented with acute pneumonia and refractory metabolic acidosis despite treatment with isotonic bicarbonate infusion, reversal of hypoglycemia, and lactic acidosis. He eventually required kidney replacement therapy. The case report highlights the multiple contributing mechanisms and challenges to managing refractory metabolic acidosis in a patient with GSDI. Important considerations for dialysis initiation, decision for long-term dialysis modality and kidney transplantation for patients with GSDI are also discussed in this case report.

DOI: https://doi.org/10.5414/CN111005
Nutrients. 2023 Feb 23. pii: 1109. [Epub ahead of print]15(5):

Exercise Timing Matters for Glycogen Metabolism and Accumulated Fat Oxidation over 24 h.

Kaito Iwayama, Jaehoon Seol, Kumpei Tokuyama.

  Due to increasingly diverse lifestyles, exercise timings vary between individuals: before breakfast, in the afternoon, or in the evening. The endocrine and autonomic nervous systems, which are associated with metabolic responses to exercise, show diurnal variations. Moreover, physiological responses to exercise differ depending on the timing of the exercise. The postabsorptive state is associated with greater fat oxidation during exercise compared to the postprandial state. The increase in energy expenditure persists during the post-exercise period, known as "Excess Post-exercise Oxygen Consumption". A 24 h evaluation of accumulated energy expenditure and substrate oxidation is required to discuss the role of exercise in weight control. Using a whole-room indirect calorimeter, researchers revealed that exercise performed during the postabsorptive state, but not during the postprandial state, increased accumulated fat oxidation over 24 h. The time course of the carbohydrate pool, as estimated by indirect calorimetry, suggests that glycogen depletion after postabsorptive exercise underlies an increase in accumulated fat oxidation over 24 h. Subsequent studies using 13C magnetic resonance spectroscopy confirmed that the variations in muscle and liver glycogen caused by postabsorptive or postprandial exercise were consistent with indirect calorimetry data. These findings suggest that postabsorptive exercise alone effectively increases 24 h fat oxidation.

Keywords:  glycogen; postabsorptive state; postprandial state; whole-room indirect calorimeter

DOI:  https://doi.org/10.3390/nu15051109
Int J Cardiol. 2023 Mar 07. pii: S0167-5273(23)00338-8. [Epub ahead of print]

Effects of enzyme replacement therapy on cardiac function in classic infantile Pompe disease.

L E Scheffers, R Kok, L E van den Berg, Hout Jmp, E Boersma, C I van Capelle, W A Helbing, A T Ploeg, L P Koopman.

   OBJECTIVE: Patients with classic infantile Pompe disease are born with a hypertrophic cardiomyopathy, which resolves after treatment with Enzyme replacement therapy (ERT). We aimed to assess potential deterioration of cardiac function over time using myocardial deformation analysis.
METHODS: Twenty-seven patients treated with ERT were included. Cardiac function was assessed at regular time intervals (before and after start with ERT) using conventional echocardiography and myocardial deformation analysis. Separate linear mixed effect models were used to asses temporal changes within the first year and the long-term follow-up period. Echocardiograms of 103 healthy children served as controls.
RESULTS: A total of 192 echocardiograms were analyzed. Median follow-up was 9.9 years (IQR: 7.5-16.3). Mean LVMI before start of ERT was increased 292.3 g/m2 (95% CI: 202.8-381.8, mean Z-score + 7.6) and normalized after 1 year of ERT 87.3 g/m2 (CI: 67.5-107.1, mean Z-score + 0.8, p < 0.001). Mean shortening fraction was within normal limits before start of ERT, up to 22 years of follow-up. Cardiac function measured by RV/LV longitudinal, and circumferential strain was diminished before start of ERT, but normalized (<-16%) within 1 year after start of ERT, and all remained within normal limits during follow-up. Only LV circumferential strain gradually worsened in Pompe patients (+0.24%/year) during follow-up compared to controls. LV longitudinal strain was diminished in Pompe patients, but did not change significantly over time compared to controls.
CONCLUSION: Cardiac function, measured using myocardial deformation analysis, normalizes after start of ERT, and seems to remain stable over a median follow-up period of 9.9 years.

Keywords:  Cardiac deformation analyses; Cardiac imaging techniques; Cardiomyopathies; Echocardiography; Glycogen storage disease type II; Metabolic disease

DOI:  https://doi.org/10.1016/j.ijcard.2023.03.010
J Physiol. 2023 Mar 11.

Insulin-resistant female rat skeletal muscles display diacylglycerol-mediated PKC activation and inflammation without ceramides accumulation.

Shailee Jani, Daniel Da Eira, Rolando B Ceddia.

  This study investigated the role of diacylglycerol (DAG)-mediated protein kinase C (PKC) activation, ceramides accumulation, and inflammation in insulin-resistant female oxidative and glycolytic skeletal muscles induced by an obesogenic high-fat sucrose-enriched (HFS) diet. The HFS diet impaired insulin-stimulated AKTThr308 phosphorylation and glycogen synthesis, whereas rates of fatty acid oxidation and basal lactate production were significantly elevated in soleus (Sol), extensor digitorum longus (EDL), and epitrochlearis (Epit) muscles. Insulin resistance was accompanied by increases in triacylglycerol (TAG), and DAG contents in Sol and EDL, whereas in Epit muscles only TAG content and markers of inflammation were associated with HFS diet-induced insulin resistance. Analysis of membrane-bound/cytoplasm PKC fractions revealed that the HFS diet promoted activation/translocation of PKCδ and θ isoforms in Sol, EDL, and Epit muscles. However, none of these muscles displayed alterations in ceramides contents in response to HFS feeding. This could be explained by a significant increase in Dgat2 mRNA expression in Sol, EDL, and Epit muscles, which likely diverted most of the intramyocellular acyl-CoAs toward TAG synthesis instead of ceramides. Overall, this study helps elucidate the molecular mechanisms underlying insulin resistance caused by diet-induced obesity in female skeletal muscles with distinct fiber type compositions. KEY POINTS: Feeding female Wistar rats a high-fat sucrose-enriched diet (HFS) led to diacylglycerol (DAG)-induced PKC activation and insulin resistance in oxidative and glycolytic skeletal muscles. HFS diet-induced toll-like receptor 4 (Tlr4) expression did not lead to increased ceramide content in female skeletal muscles. In highly glycolytic female muscles, elevated TAG content and markers of inflammation underlied HFS diet-induced insulin resistance. The HFS diet suppressed glucose oxidation and increased lactate production in oxidative and glycolytic female muscles. Increased Dgat2 mRNA expression likely diverted most of the intramyocellular acyl-CoAs toward TAG synthesis and prevented ceramides formation in skeletal muscles of HFS-fed female rats. Abstract figure legend Feeding female Wistar rats for 8 weeks an obesogenic high-fat sucrose-enriched (HFS) caused insulin resistance in Soleus (Sol), Extensor Digitorum Longus (EDL), and Epitrochlearis (Epit) muscles. In all muscles studied, the HFS diet increased diacylglycerol (DAG) content and Dgat2 mRNA expression, but did not affect ceramide levels. PKCθ and PKCδ activities and the expression of inflammatory markers were altered in a fiber type-specific manner by HFS feeding. In Sol and EDL muscles, PKCθ activity was increased, whereas in Epit it remained unaltered by the HFS diet. PKCδ activity was only elevated in Sol muscles by HFS feeding and the mRNA expression of inflammatory markers increased in EDL and Epit, but not in Sol muscles. ↑ = increase; ↔ = no change This article is protected by copyright. All rights reserved.

Keywords:  AKT; DGAT; TLR4; glucose oxidation; glycogen synthesis; inflammation; intramuscular lipids; obesity

DOI:  https://doi.org/10.1113/JP284324
J Health Econ Outcomes Res. 2023 ;10(1): 41-50

Quality of Life with Late-Onset Pompe Disease: Qualitative Interviews and General Public Utility Estimation in the United Kingdom.

Lena Hubig, Anna-Katrine Sussex, Alasdair MacCulloch, Derralynn Hughes, Ryan Graham, Liz Morris, Syed Raza, Andrew J Lloyd, Amanda Sowinski, Katy Gallop.

  Background: Late-onset Pompe disease (LOPD) is a rare, progressive neuromuscular condition typically characterized by weakness of skeletal muscles, including those involved in respiration and diaphragmatic dysfunction. Individuals with LOPD typically eventually require mobility and/or ventilatory support. Objectives: This study aimed to develop health state vignettes and estimate health state utility values for LOPD in the United Kingdom. Methods: Vignettes were developed for 7 health states of LOPD with states defined in terms of mobility and/or ventilatory support. Vignettes were drafted based on patient-reported outcome data from the Phase 3 PROPEL trial (NCT03729362) and supplemented by a literature review. Qualitative interviews with individuals living with LOPD and clinical experts were conducted to explore the health-related quality-of-life (HRQoL) impact of LOPD and to review the draft vignettes. Vignettes were finalized following a second round of interviews with individuals living with LOPD and used in health state valuation exercises with people of the UK population. Participants rated the health states using the EQ-5D-5L, visual analogue scale, and time trade-off interviews. Results: Twelve individuals living with LOPD and 2 clinical experts were interviewed. Following the interviews, 4 new statements were added regarding dependence on others, bladder control problems, balance issues/fear of falling, and frustration. One hundred interviews with a representative UK population sample were completed. Mean time trade-off utilities ranged from 0.754 (SD = 0.31) (no support) to 0.132 (SD = 0.50) (invasive ventilatory and mobility support-dependent). Similarly, EQ-5D-5L utilities ranged from 0.608 (SD = 0.12) to -0.078 (SD = 0.22). Discussion: The utilities obtained in the study are consistent with utilities reported in the literature (0.670-0.853 for nonsupport state). The vignette content was based on robust quantitative and qualitative evidence and captured the main HRQoL impacts of LOPD. The general public rated the health states consistently lower with increasing disease progression. There was greater uncertainty around utility estimates for the severe states, suggesting that participants found it harder to rate them. Conclusion: This study provides utility estimates for LOPD that can be used in economic modeling of treatments for LOPD. Our findings highlight the high disease burden of LOPD and reinforce the societal value of slowing disease progression.

Keywords:  EQ-5D-5L; Pompe disease; glycogen storage disease type II; health-related quality of life; time trade-off; utility

DOI:  https://doi.org/10.36469/001c.68157
Iran J Pharm Res. 2022 Dec;21(1): e133668

Brain Homogenate of a Rat Model of Alzheimer's Disease Modifies the Secretome of 3D Cultured Periodontal Ligament Stem Cells: A Potential Neuroregenerative Therapy.

Fariba Mohebichamkhorami, Zahra Niknam, Mona Khoramjouy, Elmira Heidarli, Rasoul Ghasemi, Simzar Hosseinzadeh, Seyedeh Sarvenaz Mohseni, Arman Hajikarim-Hamedani, Amirhossein Heidari, Yekta Ghane, Matin Mahmoudifard, Hakimeh Zali, Mehrdad Faizi.

   Background: Alzheimer's disease (AD) is a progressive neurodegenerative disease leading to neuronal cell death and manifested by cognitive disorders and behavioral impairment. Mesenchymal stem cells (MSCs) are one of the most promising candidates to stimulate neuroregeneration and prevent disease progression. Optimization of MSC culturing protocols is a key strategy to increase the therapeutic potential of the secretome.
Objectives: Here, we investigated the effect of brain homogenate of a rat model of AD (BH-AD) on the enhancement of protein secretion in the secretome of periodontal ligament stem cells (PDLSCs) when cultured in a 3D environment. Moreover, the effect of this modified secretome was examined on neural cells to study the impact of the conditioned medium (CM) on stimulation of regeneration or immunomodulation in AD.
Methods: PDLSCs were isolated and characterized. Then, the spheroids of PDLSCs were generated in a modified 3D culture plate. PDLSCs-derived CM was prepared in the presence of BH-AD (PDLSCs-HCM) and the absence of it (PDLSCs-CM). The viability of C6 glioma cells was assessed after exposure to different concentrations of both CMs. Then, a proteomic analysis was performed on the CMs.
Results: Differentiation into adipocytes and high expression of MSCs markers verified the precise isolation of PDLSCs. The PDLSC spheroids were formed after 7 days of 3D culturing, and their viability was confirmed. The effect of CMs on C6 glioma cell viability showed that both CMs at low concentrations (> 20 mg/mL) had no cytotoxic effect on C6 neural cells. The results showed that PDLSCs-HCM contains higher concentrations of proteins compared to PDLSCs-CM, including Src-homology 2 domain (SH2)-containing PTPs (SHP-1) and muscle glycogen phosphorylase (PYGM) proteins. SHP-1 has a role in nerve regeneration, and PYGM is involved in glycogen metabolism.
Conclusions: The modified secretome derived from 3D cultured spheroids of PDLSCs treated by BH-AD as a reservoir of regenerating neural factors can serve as a potential source for AD treatment.

Keywords:  Alzheimer's Disease; Nerve Regeneration; Periodontal Ligament Stem Cells; Secretome; Spheroid

DOI:  https://doi.org/10.5812/ijpr-133668
Cancers (Basel). 2023 Mar 03. pii: 1594. [Epub ahead of print]15(5):

GBE1 Promotes Glioma Progression by Enhancing Aerobic Glycolysis through Inhibition of FBP1.

Zhen Chen, Han Bao, Jingfang Long, Peiqi Zhao, Xiaowei Hu, Hao Wang, Ying Zhang, Jianjing Yang, Qichuan Zhuge, Lei Xia.

  Tumor metabolism characterized by aerobic glycolysis makes the Warburg effect a unique target for tumor therapy. Recent studies have found that glycogen branching enzyme 1 (GBE1) is involved in cancer progression. However, the study of GBE1 in gliomas is limited. We determined by bioinformatics analysis that GBE1 expression is elevated in gliomas and correlates with poor prognoses. In vitro experiments showed that GBE1 knockdown slows glioma cell proliferation, inhibits multiple biological behaviors, and alters glioma cell glycolytic capacity. Furthermore, GBE1 knockdown resulted in the inhibition of the NF-κB pathway as well as elevated expression of fructose-bisphosphatase 1 (FBP1). Further knockdown of elevated FBP1 reversed the inhibitory effect of GBE1 knockdown, restoring glycolytic reserve capacity. Furthermore, GBE1 knockdown suppressed xenograft tumor formation in vivo and conferred a significant survival benefit. Collectively, GBE1 reduces FBP1 expression through the NF-κB pathway, shifting the glucose metabolism pattern of glioma cells to glycolysis and enhancing the Warburg effect to drive glioma progression. These results suggest that GBE1 can be a novel target for glioma in metabolic therapy.

Keywords:  NF-κB; Warburg effect; fructose-bisphosphatase 1; glucan branching enzyme 1; glucose metabolism

DOI:  https://doi.org/10.3390/cancers15051594