Modeling the Effect of Cigarette Smoke on Hexose Utilization in Spermatocytes

Omurtag, Kenan; Esakky, Prabagaran; DeBosch, Brian J.; Schoeller, Erica L.; Maggie, M.; Moley, Kelle H.

doi:10.1177/1933719114533727

Cited by 7 publications

(6 citation statements)

References 62 publications

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“…The Washington University Mass Spectrometry Core Facility measured mouse serum uric acid levels as previously described 51 . Serum glucose (%CV = 2.1) and fructose (%CV = 1.3 levels) in mice were determined as previously described 46 52 .…”

Section: Methodsmentioning

confidence: 99%

“…Analysis was performed as previously described 51 at the Washington University Mass Spectrometry Core Facility. ATP levels in mouse placentas were measured as previously described 52 . To determine XO and AMPD activity in mouse placentas, each fresh placenta was homogenized in ice-cold 100 mM Tris HCl, 1 mM EDTA, pH7.5, and centrifuged at 9,300xg for 10 minutes.…”

Section: Methodsmentioning

confidence: 99%

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Maternal fructose drives placental uric acid production leading to adverse fetal outcomes

Asghar

Thompson

Chi

et al. 2016

Sci Rep

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Maternal metabolic diseases increase offspring risk for low birth weight and cardiometabolic diseases in adulthood. Excess fructose consumption may confer metabolic risks for both women and their offspring. However, the direct consequences of fructose intake per se are unknown. We assessed the impact of a maternal high-fructose diet on the fetal-placental unit in mice in the absence of metabolic syndrome and determined the association between maternal serum fructose and placental uric acid levels in humans. In mice, maternal fructose consumption led to placental inefficiency, fetal growth restriction, elevated fetal serum glucose and triglyceride levels. In the placenta, fructose induced de novo uric acid synthesis by activating the activities of the enzymes AMP deaminase and xanthine oxidase. Moreover, the placentas had increased lipids and altered expression of genes that control oxidative stress. Treatment of mothers with the xanthine oxidase inhibitor allopurinol reduced placental uric acid levels, prevented placental inefficiency, and improved fetal weights and serum triglycerides. Finally, in 18 women delivering at term, maternal serum fructose levels significantly correlated with placental uric acid levels. These findings suggest that in mice, excess maternal fructose consumption impairs placental function via a xanthine oxidase/uric acid-dependent mechanism, and similar effects may occur in humans.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Maternal fructose drives placental uric acid production leading to adverse fetal outcomes

Asghar

Thompson

Chi

et al. 2016

Sci Rep

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“…Preventing glucose uptake into hepatocytes is predicted to induce a starvationlike state and activate cellular autophagy. We therefore determined whether trehalose depleted hepatocyte intracellular ATP by incubating primary hepatocyte cultures with or without trehalose for 30 min before lysis and then performing an enzymatic-fluorimetric ATP concentration assay (17,18). ATP concentration in trehalose-treated hepatocyte cultures was 20% lower when compared with untreated cultures (Fig.…”

Section: Trehalose Rapidly Induces Ampk and Ulk1 Activation In Cultur...mentioning

confidence: 99%

Trehalose inhibits solute carrier 2A (SLC2A) proteins to induce autophagy and prevent hepatic steatosis

et al. 2016

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Trehalose is a naturally occurring disaccharide that has gained attention for its ability to induce cellular autophagy and mitigate diseases related to pathological protein aggregation. Despite decades of ubiquitous use as a nutraceutical, preservative, and humectant, its mechanism of action remains elusive. Here, we showed that trehalose inhibited members of the SLC2A (also known as GLUT) family of glucose transporters. Trehalose-mediated inhibition of glucose transport induced AMPK (adenosine 5′-monophosphate-activated protein kinase)-dependent autophagy regression of hepatic steatosis in vivo, and a reduction in the accumulation of lipid droplets in primary murine hepatocyte cultures. Our data indicated that, by inhibiting glucose transport, trehalose triggers beneficial cellular autophagy.

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“…Last, AhR-knockout mice were more sensitive to LPS-induced septic shock, indicating that AhR has a role in antagonising lipopolysaccharide LPS-induced inflammation (10) . Interestingly, as of February 2019, when using the combination of keywords 'fructose' and 'ahr', only one relevant study was retrieved from the PubMed database in which researchers examined the effects of antagonist AhR on glucose and fructose utilisation in spermatocytes (26) .…”

Section: Discussionmentioning

confidence: 99%

Hepatic transcriptomics analysis reveals that fructose intervention down-regulated xenobiotics-metabolising enzymes through aryl hydrocarbon receptor signalling suppression in C57BL/6N mice

et al. 2019

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For decades, fructose intake has been recognised as an environmental risk for metabolic syndromes and diseases. Here we comprehensively examined the effects of fructose intake on mice liver transcriptomes. Fructose-supplemented water (34 %; w/v) was fed to both male and female C57BL/6N mice at their free will for 6 weeks, followed by hepatic transcriptomics analysis. Based on our criteria, differentially expressed genes (DEG) were selected and subjected to further computational analyses to predict key pathways and upstream regulator(s). Subsequently, predicted genes and pathways from the transcriptomics dataset were validated via quantitative RT-PCR analyses. As a result, we identified eighty-nine down-regulated and eighty-eight up-regulated mRNA in fructose-fed mice livers. These DEG were subjected to bioinformatics analysis tools in which DEG were mainly enriched in xenobiotic metabolic processes; further, in the Ingenuity Pathway Analysis software, it was suggested that the aryl hydrocarbon receptor (AhR) is an upstream regulator governing overall changes, while fructose suppresses the AhR signalling pathway. In our quantitative RT-PCR validation, we confirmed that fructose suppressed AhR signalling through modulating expressions of transcription factor (AhR nuclear translocator; Arnt) and upstream regulators (Ncor2, and Rb1). Altogether, we demonstrated that ad libitum fructose intake suppresses the canonical AhR signalling pathway in C57BL/6N mice liver. Based on our current observations, further studies are warranted, especially with regard to the effects of co-exposure to fructose on (1) other types of carcinogens and (2) inflammation-inducing agents (or even diets such as a high-fat diet), to find implications of fructose-induced AhR suppression.

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Modeling the Effect of Cigarette Smoke on Hexose Utilization in Spermatocytes

Cited by 7 publications

References 62 publications

Maternal fructose drives placental uric acid production leading to adverse fetal outcomes

Maternal fructose drives placental uric acid production leading to adverse fetal outcomes

Trehalose inhibits solute carrier 2A (SLC2A) proteins to induce autophagy and prevent hepatic steatosis

Hepatic transcriptomics analysis reveals that fructose intervention down-regulated xenobiotics-metabolising enzymes through aryl hydrocarbon receptor signalling suppression in C57BL/6N mice

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