Corrigendum to “Low Citrate Synthase Activity Is Associated with Glucose Intolerance and Lipotoxicity”

Alhindi, Yosra; Vaanholt, Lobke M.; Al-Tarrah, Mustafa; Gray, Stuart R.; Speakman, John R.; Hambly, Catherine; Alanazi, Bader S.; Gabriel, Brendan M.; Lionikas, Arimantas; Ratkevičius, Aivaras

doi:10.1155/2019/9153809

Cited by 6 publications

(3 citation statements)

References 1 publication

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“…In the present study, lower concentration of citrate synthase was observed in COVID‐19 patients. Low CS activity is associated with impaired glucose tolerance and abnormalities in lipid metabolism 40 . Malate dehydrogenase catalyzes the reaction involving inter‐conversion of malate and oxaloacetate in TCA cycle, maintaining redox control in mitochondrial matrix 41 .…”

Section: Discussionmentioning

confidence: 99%

“…Low CS activity is associated with impaired glucose tolerance and abnormalities in lipid metabolism. 40 Malate dehydrogenase catalyzes the reaction involving inter-conversion of malate and oxaloacetate in TCA cycle, maintaining redox control in mitochondrial matrix. 41 α-ketoglutarate dehydrogenase (α-KGDH) appears to be more sensitive to disturbed homeostasis than other mitochondrial enzymes.…”

Section: Multivariate Analysis Between the Mutations And Oxidative St...mentioning

confidence: 99%

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“Mitochondrial pathogenic mutations and metabolic alterations associated with COVID‐19 disease severity”

Kumari

Singh

et al. 2023

Journal of Medical Virology

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The severe acute respiratory syndrome coronavirus‐2 (SARS‐CoV‐2) caused global pandemic and drastically affected the humankind. Mitochondrial mutations have been found to be associated with several respiratory diseases. Missense mutation and pathogenic mitochondrial variants might unveil the potential involvement of the mitochondrial genome in coronavirus disease 2019 (COVID‐19) pathogenesis. The present study aims to elucidate the role of mitochondrial DNA (mtDNA) mutations, mitochondrial haplogroup, and energy metabolism in disease severity. The study was performed on 58 subjects comprising COVID‐19‐positive (n = 42) and negative (n = 16) individuals. COVID‐19‐positive subjects were further categorized into severe deceased (SD), severe recovered (SR), moderate (Mo), and mild (Mi) patients, while COVID‐19‐negative subjects were healthy control (HC) for the study. High throughput next‐generation sequencing was done to investigate mtDNA mutations and haplogroups. The computational approach was applied to study the effect of mtDNA mutations on protein secondary structure. Real time polymerase chain reaction was used for mtDNA copy number determination and mitochondrial function parameters were also analyzed. We found 15 mtDNA mutations in MT‐ND5, MT‐ND4, MT‐ND2, and MT‐COI genes uniquely associated with COVID‐19 severity affecting the secondary structure of proteins in COVID‐19‐positive subjects. Haplogroup analysis suggests that mtDNA haplogroups M3d1a and W3a1b might be potentially associated with COVID‐19 pathophysiology. The mitochondrial function parameters were significantly altered in severe patients (SD and SR; p < 0.05). No significant relationship was found between mtDNA mutations and oxidative stress markers (p > 0.05). The study highlights the importance of mitochondrial reprogramming in COVID‐19 patients and may provide a feasible approach toward finding a path for therapeutic interventions to COVID‐19 disease.

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Section: Discussionmentioning

confidence: 99%

Section: Multivariate Analysis Between the Mutations And Oxidative St...mentioning

confidence: 99%

“Mitochondrial pathogenic mutations and metabolic alterations associated with COVID‐19 disease severity”

Kumari

Singh

et al. 2023

Journal of Medical Virology

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“…CS is a key mitochondrial enzyme involved in energyproducing metabolic pathways, and decreased CS activity is associated with insulin resistance and impaired lipid metabolism in skeletal muscles (Ørtenblad et al, 2005;Alhindi et al, 2019). Our study indicates that HIIT increased protein and gene expression levels of CS compared to untrained diabetic rats are supported by other findings that show decreases in CS protein levels in diabetic rats are reversed by 4 weeks of exercise training (Irrcher et al, 2008), and that CS mRNA levels are increased by interval walking training in individuals with type 2 diabetes (Karstoft et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Effects of two workload-matched high intensity interval training protocols on regulatory factors associated with mitochondrial biogenesis in the soleus muscle of diabetic rats

et al. 2022

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Aims: High intensity interval training (HIIT) improves mitochondrial characteristics. This study compared the impact of two workload-matched high intensity interval training (HIIT) protocols with different work:recovery ratios on regulatory factors related to mitochondrial biogenesis in the soleus muscle of diabetic rats.Materials and methods: Twenty-four Wistar rats were randomly divided into four equal-sized groups: non-diabetic control, diabetic control (DC), diabetic with long recovery exercise [4–5 × 2-min running at 80%–90% of the maximum speed reached with 2-min of recovery at 40% of the maximum speed reached (DHIIT1:1)], and diabetic with short recovery exercise (5–6 × 2-min running at 80%–90% of the maximum speed reached with 1-min of recovery at 30% of the maximum speed reached [DHIIT2:1]). Both HIIT protocols were completed five times/week for 4 weeks while maintaining equal running distances in each session.Results: Gene and protein expressions of PGC-1α, p53, and citrate synthase of the muscles increased significantly following DHIIT1:1 and DHIIT2:1 compared to DC (p ˂ 0.05). Most parameters, except for PGC-1α protein (p = 0.597), were significantly higher in DHIIT2:1 than in DHIIT1:1 (p ˂ 0.05). Both DHIIT groups showed significant increases in maximum speed with larger increases in DHIIT2:1 compared with DHIIT1:1.Conclusion: Our findings indicate that both HIIT protocols can potently up-regulate gene and protein expression of PGC-1α, p53, and CS. However, DHIIT2:1 has superior effects compared with DHIIT1:1 in improving mitochondrial adaptive responses in diabetic rats.

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De Novo Lipogenesis as a Source of Second Messengers in Adipocytes

Hsiao

Guertin

2019

Curr Diab Rep

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Purpose of review: Obesity is a major risk factor for Type 2 Diabetes. Although adipose tissue allows storage of excess calories in periods of overnutrition, in obesity, adipose tissue metabolism becomes dysregulated and can promote metabolic diseases. This review discusses recent advances in understandings how adipocyte metabolism impacts metabolic homeostasis. Recent findings: The ability of adipocytes to synthesize lipids from glucose is a marker of metabolic fitness, e.g. low de novo lipogenesis (DNL) in adipocytes correlates with insulin resistance in obesity. Adipocyte DNL may promote synthesis of special "insulin sensitizing" signaling lipids that act hormonally. However, each metabolic intermediate in the DNL pathway (i.e. citrate, acetyl-CoA, malonyl-CoA, and palmitate) also has second messenger functions. Mounting evidence suggests these signaling functions may also be important for maintaining healthy adipocytes. Summary: While adipocyte DNL contributes to lipid storage, lipid precursors may have additional second messenger functions critical for maintaining adipocyte health, and thus systemic metabolic homeostasis.

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Corrigendum to “Low Citrate Synthase Activity Is Associated with Glucose Intolerance and Lipotoxicity”

Cited by 6 publications

References 1 publication

“Mitochondrial pathogenic mutations and metabolic alterations associated with COVID‐19 disease severity”

“Mitochondrial pathogenic mutations and metabolic alterations associated with COVID‐19 disease severity”

Effects of two workload-matched high intensity interval training protocols on regulatory factors associated with mitochondrial biogenesis in the soleus muscle of diabetic rats

De Novo Lipogenesis as a Source of Second Messengers in Adipocytes

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