Direct Spectrophotometric Determination of Serum Fructose in Pancreatic Cancer Patients

Hui, Hongxiang; Huang, Danshan; McArthur, David L.; Nissen, Nicholas; Boros, László G.; Heaney, Anthony P.

doi:10.1097/mpa.0b013e3181a7c6e5

Cited by 57 publications

(67 citation statements)

References 21 publications

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“…A previous study indicated that the average level of fasting serum fructose was 5.7 ± 2.5 mM in patients with pancreatic cancer, which was higher than in healthy volunteers (1.9 ± 0.4 mM) [29]. To evaluate whether fructose substitution is beneficial for the growth of subpopulations exhibiting drug resistance and high invasion capability, we transferred PANC-1 cells to medium containing 1g/L of fructose (5.5 mM fructose) and allowed them to grow for 3, 7, 14, or 28 days (Figure 2A).…”

Section: Resultsmentioning

confidence: 99%

Elevation of β-galactoside α2,6-sialyltransferase 1 in a fructose-responsive manner promotes pancreatic cancer metastasis

et al. 2016

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Pancreatic ductal adenocarcinoma (PDAC) is an aggressive type of pancreatic cancer with clinical characteristics of local invasion and early metastasis. Recent cohort studies indicate high fructose intake is associated with an increase in pancreatic cancer risk. However, the mechanisms by which fructose promotes pancreatic tumorigenesis remain unclear. Herein, Kras+/LSLG12D mice were crossed with Elas-CreER transgenic mice to determine whether fructose intake directly contributes to tumor formation. Orthotopic tumor-xenograft experiments were performed to determine whether fructose substitution enhances the metastatic potential of PDAC cells. The mechanisms underlying the effects of fructose were explored by RNAseq analysis in combination with high-performance anion exchange chromatography. Dietary fructose was initially found to promote the development of aggressive pancreatic cancer in mice conditionally expressing KrasG12D in the adult pancreas. We further revealed that fructose substitution enhanced the metastatic potential of human PDAC cell via selective outgrowth of aggressive ABCG2-positive subpopulations and elevating N-acetylmannosamine levels that upregulated β-galactoside α2,6-sialyltransferase 1 (ST6Gal1), thereby promoting distant metastasis. Finally, we observed that PDAC patients expressing higher levels of ST6Gal1 and GLUT5 presented poorer prognosis compared to other groups. In conclusion, our findings have elucidated a crucial role of ST6Gal1 in regulating the invasiveness of PDACs in a fructose-responsive manner.

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Section: Resultsmentioning

confidence: 99%

Elevation of β-galactoside α2,6-sialyltransferase 1 in a fructose-responsive manner promotes pancreatic cancer metastasis

et al. 2016

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“…Gas chromatography/mass spectrometry (GC/MS), high performance liquid chromatography/mass spectrometry (LC/MS), enzymatic assays and colourimetric analysis may be used to quantify carbohydrates in complex matrices [5][6][7][8][9][10], including serum and urine. Serum samples are readily obtained and, by collection of serial samples, can provide a dynamic picture of sucrose absorption kinetics, whereas urine samples are less readily collected and can accumulate in the bladder for a variable time before collection.…”

Section: Introductionmentioning

confidence: 99%

Determination of sucrose in equine serum using liquid chromatography–mass spectrometry (LC/MS)

D'Arcy-Moskwa

Weston

Noble

et al. 2011

Journal of Chromatography B

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“…3) The concentrations of fructose we used are transiently reached within the liver after intake of fructose-sweetened commercially ubiquitous beverages in humans (24,25). This might explain why they were not acutely toxic in any of our experiments, suggesting that we are dealing with non-toxic pharmacological doses of a naturally occurring sugar within a short exposure time toward hepatocytes.…”

Section: Discussionmentioning

confidence: 90%

Fructose Protects Murine Hepatocytes from Tumor Necrosis Factor-induced Apoptosis by Modulating JNK Signaling

Speicher

Köhler

Choukèr³

et al. 2012

Journal of Biological Chemistry

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Background: Fructose-induced ATP depletion selectively protects hepatocytes but not hepatoma cell lines from actinomycin D (ActD)/TNF-induced apoptosis. Results: Fructose induces a cAMP response that via PKA prevents sustained activation of ActD/TNF-induced pro-apoptotic JNK activation, thereby Bid cleavage and apoptosis. Conclusion: These findings explain the hepatocytic mechanism of fructose-mediated cytoprotection against ActD/TNF-induced apoptosis. Significance: These findings explain selective cytoprotection of hepatocytes, potentially enabling selective tumor targeting.

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Direct Spectrophotometric Determination of Serum Fructose in Pancreatic Cancer Patients

Abstract: This spectrophotometric assay for fructose is easy to perform and well suited to determination of serum fructose. Measurement of serum fructose concentration may provide insight into the relationship between refined fructose intake and diseases including pancreatic cancer.

Cited by 57 publications

References 21 publications

Elevation of β-galactoside α2,6-sialyltransferase 1 in a fructose-responsive manner promotes pancreatic cancer metastasis

Elevation of β-galactoside α2,6-sialyltransferase 1 in a fructose-responsive manner promotes pancreatic cancer metastasis

Determination of sucrose in equine serum using liquid chromatography–mass spectrometry (LC/MS)

Fructose Protects Murine Hepatocytes from Tumor Necrosis Factor-induced Apoptosis by Modulating JNK Signaling

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