Increase in cardiac muscle fructose content in streptozotocin-induced diabetic rats

Kashiwagi, Atsunori; Obata, Toshiyuki; Suzaki, M; Takagi, Yoshifumi; Kida, Yasuo; Ogawa, Takasuke; Tanaka, Yasushi; Asahina, Takayuki; Ikebuchi, Motoyoshi; Saeki, Yukikazu; Kikkawa, Ryuichi; Shigeta, Yukio

doi:10.1016/0026-0495(92)90283-g

Cited by 42 publications

(21 citation statements)

References 32 publications

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“…Thus, the shift in myocardial substrate and energy metabolism may contribute to increased levels of CML and decreased levels of CEL. The diabetic heart is also characterized by increased levels of fructose, leading to the accumulation of fructose-3-phosphate and its decomposition product 3-DG [24,25]. In accordance, also in our study, we found increased levels of 3DG in the diabetic heart.…”

Section: Discussionsupporting

confidence: 91%

Mild Oxidative Damage in the Diabetic Rat Heart Is Attenuated by Glyoxalase-1 Overexpression

Brouwers

Vos-Houben

Niessen

et al. 2013

IJMS

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Diabetes significantly increases the risk of heart failure. The increase in advanced glycation endproducts (AGEs) and oxidative stress have been associated with diabetic cardiomyopathy. We recently demonstrated that there is a direct link between AGEs and oxidative stress. Therefore, the aim of the current study was to investigate if a reduction of AGEs by overexpression of the glycation precursor detoxifying enzyme glyoxalase-I (GLO-I) can prevent diabetes-induced oxidative damage, inflammation and fibrosis in the heart. Diabetes was induced in wild-type and GLO-I transgenic rats by streptozotocin. After 24-weeks of diabetes, cardiac function was monitored with ultrasound under isoflurane anesthesia. Blood was drawn and heart tissue was collected for further analysis. Analysis with UPLC-MSMS showed that the AGE Nɛ-(1-carboxymethyl)lysine and its precursor 3-deoxyglucosone were significantly elevated in the diabetic hearts. Markers of oxidative damage, inflammation, and fibrosis were mildly up-regulated in the heart of the diabetic rats and were attenuated by GLO-I overexpression. In this model of diabetes, these processes were not accompanied by significant changes in systolic heart function, i.e., stroke volume, fractional shortening and ejection fraction. This study shows that 24-weeks of diabetes in rats induce early signs of mild cardiac alterations as indicated by an increase of oxidative stress, inflammation and fibrosis which are mediated, at least partially, by glycation.

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Section: Discussionsupporting

confidence: 91%

Mild Oxidative Damage in the Diabetic Rat Heart Is Attenuated by Glyoxalase-1 Overexpression

Brouwers

Vos-Houben

Niessen

et al. 2013

IJMS

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“…Compared to glucose, its ketose isomer fructose is more reactive in Maillard reaction [12], because fructose has higher concentration of acyclic forms in aqueous solutions [40]. Moreover, glucose to fructose shunt via polyol pathway becomes more active in diabetic condition [13], causing increased fructose concentration. Considering these facts, it seems worthwhile to study the fructation of Mb.…”

Section: Resultsmentioning

confidence: 99%

“…Fructose is more potent in glycation and AGE formation than glucose [12]. Moreover, glucose to fructose shunt via polyol pathway becomes more active in diabetic condition resulting in increased concentration of fructose [13]. Fructose-induced Maillard reactions may thus play a significant role in the pathogenesis of diabetic complications.…”

Section: Introductionmentioning

confidence: 99%

Fructose-induced modifications of myoglobin: Change of structure from met (Fe3+) to oxy (Fe2+) form

Bhattacherjee

Chakraborti

2011

International Journal of Biological Macromolecules

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“…2 Under diabetic conditions, fructose serum concentration increases, most probably because glucose is converted into fructose via the polyol pathway. 3, 4 Moreover, the splanchnic territory is physiologically exposed to high concentrations of glucose and fructose during the postprandial period. 5 Therefore, β -cells can face hyperglycemia or hyperfructosemia in type 2 diabetes or when pancreatic islets are transplanted into the splanchnic territory.…”

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confidence: 99%

Protection of pancreatic INS-1 β-cells from glucose- and fructose-induced cell death by inhibiting mitochondrial permeability transition with cyclosporin A or metformin

et al. 2011

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Hyperglycemia is detrimental to β-cell viability, playing a major role in the progression of β-cell loss in diabetes mellitus. The permeability transition pore (PTP) is a mitochondrial channel involved in cell death. Recent evidence suggests that PTP inhibitors prevent hyperglycemia-induced cell death in human endothelial cells. In this work, we have examined the involvement of PTP opening in INS-1 cell death induced by high levels of glucose or fructose. PTP regulation was studied by measuring the calcium retention capacity in permeabilized INS-1 cells and by confocal microscopy in intact INS-1 cells. Cell death was analyzed by flow cytometry. We first reported that metformin and cyclosporin A (CsA) prevented Ca2+-induced PTP opening in permeabilized and intact INS-1 cells. We then showed that incubation of INS-1 cells in the presence of 30 mM glucose or 2.5 mM fructose induced PTP opening and led to cell death. As both metformin and CsA prevented glucose- and fructose- induced PTP opening, and hampered glucose- and fructose- induced cell death, we conclude that PTP opening is involved in high glucose- and high fructose- induced INS-1 cell death. We therefore suggest that preventing PTP opening might be a new approach to preserve β-cell viability.

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Increase in cardiac muscle fructose content in streptozotocin-induced diabetic rats

Cited by 42 publications

References 32 publications

Mild Oxidative Damage in the Diabetic Rat Heart Is Attenuated by Glyoxalase-1 Overexpression

Mild Oxidative Damage in the Diabetic Rat Heart Is Attenuated by Glyoxalase-1 Overexpression

Fructose-induced modifications of myoglobin: Change of structure from met (Fe3+) to oxy (Fe2+) form

Protection of pancreatic INS-1 β-cells from glucose- and fructose-induced cell death by inhibiting mitochondrial permeability transition with cyclosporin A or metformin

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