Fructose-1,6-bisphosphate preserves glucose metabolism integrity and reduces reactive oxygen species in the brain during experimental sepsis

Catarina, Anderson Velasque; Luft, Carolina; Greggio, Samuel; Venturin, Gianina Teribele; Ferreira, Fernanda Silva; Marques, Eduardo; Rodrigues, Letícia; Wartchow, Krista Minéia; Leite, Marina Concli; Gonçalves, Carlos Alberto; Wyse, Ângela T. S.; Costa, Jaderson Costa da; Oliveira, Jarbas Rodrigues de; Branchini, Gisele; Nunes, Fernanda Bordignon

doi:10.1016/j.brainres.2018.06.024

Cited by 13 publications

(10 citation statements)

References 76 publications

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“…Moreover, fructose-1,6-bisphosphate is another glycolytic intermediate that shows neuroprotective effect against various harmful conditions in many brain injury models [ 30 ]. Particularly, fructose-1,6-bisphosphate could improve cerebral metabolic outcomes via ameliorating inflammation and oxidative stress and preserving glucose metabolism integrity in sepsis [ 31 ]. Unfortunately, the effect of fructose-1,6-bisphosphate on AD is rarely covered.…”

Section: The Potential Association Between Redox Signaling and Metabomentioning

confidence: 99%

Redox signaling and Alzheimer’s disease: from pathomechanism insights to biomarker discovery and therapy strategy

Chen

Wang²,

Wang

et al. 2020

Biomark Res

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Aging and average life expectancy have been increasing at a rapid rate, while there is an exponential risk to suffer from brain-related frailties and neurodegenerative diseases as the population ages. Alzheimer’s disease (AD) is the most common neurodegenerative disease worldwide with a projected expectation to blossom into the major challenge in elders and the cases are forecasted to increase about 3-fold in the next 40 years. Considering the etiological factors of AD are too complex to be completely understood, there is almost no effective cure to date, suggesting deeper pathomechanism insights are urgently needed. Metabolites are able to reflect the dynamic processes that are in progress or have happened, and metabolomic may therefore provide a more cost-effective and productive route to disease intervention, especially in the arena for pathomechanism exploration and new biomarker identification. In this review, we primarily focused on how redox signaling was involved in AD-related pathologies and the association between redox signaling and altered metabolic pathways. Moreover, we also expatiated the main redox signaling-associated mechanisms and their cross-talk that may be amenable to mechanism-based therapies. Five natural products with promising efficacy on AD inhibition and the benefit of AD intervention on its complications were highlighted as well. Graphical Abstract

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Section: The Potential Association Between Redox Signaling and Metabomentioning

confidence: 99%

Redox signaling and Alzheimer’s disease: from pathomechanism insights to biomarker discovery and therapy strategy

Chen

Wang²,

Wang

et al. 2020

Biomark Res

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“…Metabolic and hemodynamic changes also precede cognitive impairment and structural changes in the brain, such as atrophy of white and gray matter [31][32][33]. Changes in brain metabolism may represent a key component to trigger encephalopathy during the pathological process of sepsis [16,17,34]. Once SAE's cause remains unknown, its treatment is limited, and one of the therapeutic strategies, such as patient sedation, is clearly unsatisfactory as treatment of such complex condition [19].…”

Section: Introductionmentioning

confidence: 99%

Sepsis-Associated Encephalopathy: from Pathophysiology to Progress in Experimental Studies

et al. 2021

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Sepsis is an organ dysfunction caused by an uncontrolled inflammatory response from the host to an infection. Sepsis is the main cause of morbidity and mortality in intensive care units (ICU) worldwide. One of the first organs to suffer from injuries resulting from sepsis is the brain. The central nervous system (CNS) is particularly vulnerable to damage, mediated by inflammatory and oxidative processes, which can cause the sepsis-associated encephalopathy (SAE), being reported in up to 70% of septic patients. This review aims to bring a summary of the main pathophysiological changes and dysfunctions in SAE, and the main focuses of current experimental studies for new treatments and therapies. The pathophysiology of SAE is complex and multifactorial, combining intertwined processes, and is promoted by countless alterations and dysfunctions resulting from sepsis, such as inflammation, neuroinflammation, oxidative stress, reduced brain metabolism, and injuries to the integrity of the blood-brain barrier (BBB). The treatment is limited once its cause is not completely understood. The patient's sedation is far to provide an adequate treatment to this complex condition. Studies and experimental advances are important for a better understanding of its pathophysiology and for the development of new treatments, medicines, and therapies for the treatment of SAE and to reduce its effects during and after sepsis. Keywords Sepsis . Encephalopathy . Experimental studies . Brain Abbreviations SAE Sepsis-associated encephalopathy ICU Intensive care units CNS Central nervous system BBB Blood-brain barrier TNF-α Necrosis factor alpha IL Interleukins CSF Cerebrospinal fluid ROS Reactive oxygen species NO Nitric oxide RNS Reactive nitrogen species H 2 O 2 Hydrogen peroxide O 2 .

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“…Fructose‐1,6‐bisphosphate (F1,6 BP ), an endogenous intermediate of the glycolytic pathway, is produced through phosphorylation of fructose 6‐phosphate by the phosphofructokinase‐1 activity (Kirtley & McKay, 1977). Its therapeutic effects have been documented in a wide range of pathological situations, including sepsis (Catarina et al, 2018), hepatic diseases (De Mesquita et al, 2013), and nephrotoxicity (Azambuja et al, 2011). Also, it was demonstrated that F1,6 BP has antiproliferative effects against hepatocellular carcinoma (Lima et al, 2018; Lu, Yu, & Zhu, 2014) and papillary carcinoma (Li, Wei, Shen, & Hu, 2014).…”

Section: Introductionmentioning

confidence: 99%

Fructose‐1,6‐bisphosphate induces generation of reactive oxygen species and activation of p53‐dependent cell death in human endometrial cancer cells

Costa

Nassr

Diz

et al. 2020

J of Applied Toxicology

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Fructose‐1,6‐bisphosphate (F1,6BP), an intermediate of the glycolytic pathway, has been found to play a promising anticancer effect; nevertheless, the mechanisms involved remain poorly understood. The present study aimed to evaluate the effect and mechanisms of F1,6BP in a human endometrial cancer cell line (Ishikawa). F1,6BP showed an antiproliferative and non‐cytotoxic effect on endometrial cancer cells. These effects are related to the increase in reactive oxygen species (ROS) levels and mitochondrial membrane potential (ΔΨm). These harmful stimuli trigger the upregulation of the expression of pro‐apoptotic genes (p53 and Bax), leading to the reduction of cell proliferation through inducing programmed cell death by apoptosis. Furthermore, F1,6BP‐treated cells had the formation of autophagosomes induced, as well as a decrease in their proliferative capacity after withdrawing the treatment. Our results demonstrate that F1,6BP acts as an anticancer agent through the generation of mitochondrial instability, loss of cell function, and p53‐dependent cell death. Thus, F1,6BP proves to be a potential molecule for use in the treatment against endometrial cancer.

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Fructose-1,6-bisphosphate preserves glucose metabolism integrity and reduces reactive oxygen species in the brain during experimental sepsis

Cited by 13 publications

References 76 publications

Redox signaling and Alzheimer’s disease: from pathomechanism insights to biomarker discovery and therapy strategy

Redox signaling and Alzheimer’s disease: from pathomechanism insights to biomarker discovery and therapy strategy

Sepsis-Associated Encephalopathy: from Pathophysiology to Progress in Experimental Studies

Fructose‐1,6‐bisphosphate induces generation of reactive oxygen species and activation of p53‐dependent cell death in human endometrial cancer cells

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