• BMB Reports
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• 제51권9호
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• pp.429-436
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• 2018

Fructose in the form of sucrose and high fructose corn syrup is absorbed by the intestinal transporter and mainly metabolized in the small intestine. However, excess intake of fructose overwhelms the absorptive capacity of the small intestine, leading to fructose malabsorption. Carbohydrate response element-binding protein (ChREBP) is a basic helix-loop-helix leucine zipper transcription factor that plays a key role in glycolytic and lipogenic gene expression in response to carbohydrate consumption. While ChREBP was initially identified as a glucose-responsive factor in the liver, recent evidence suggests that ChREBP is essential for fructose-induced lipogenesis and gluconeogenesis in the small intestine as well as in the liver. We recently identified that the loss of ChREBP leads to fructose intolerance via insufficient induction of genes involved in fructose transport and metabolism in the intestine. As fructose consumption is increasing and closely associated with metabolic and gastrointestinal diseases, a comprehensive understanding of cellular fructose sensing and metabolism via ChREBP may uncover new therapeutic opportunities. In this mini review, we briefly summarize recent progress in intestinal fructose metabolism, regulation and function of ChREBP by fructose, and delineate the potential mechanisms by which excessive fructose consumption may lead to irritable bowel syndrome.

• 미생물학회지
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• 제33권3호
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• pp.181-186
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• 1997

유기용매계에서 lipase AK를 사용하여 당 ester화합물을 합성하였다. 유기용매로는 당의 용해도가 높고 반응성이 뛰어난 pyridine을, acyl donor로는 vinyl butyrate을 선택하였다. Transesterification반응에 의해 생성된 monobutyryl fructose와 dibutyryl fructose는 TLC 및 GC 분석으로 확인하였다. Transesterification에 미치는 반응조건은 fructose:vinyl butyrate의 비가 1:10(M/M), 반응온도 40^{\circ}C.$, 교반속도 150rpm, 효소량 10mg/ml의 경우가 적당하였으며 반응시간이 길어질수록 전환율이 높아져, 반응 10일 정도에서 전환율은 90% 이상에 도달하였다. 이때 반응 초기에는 monobutyryl fructose가 주로 합성되었으나 시간이 경과함에 따라 dibutyryl fructose의 함량비가 증가하였다. 반응계에 소량의 수분을 첨가하였을 경우에는 반응속도가 감소함과 동시에 반응산물중 dibutyryl fructose의 양은 줄어들고 monobutyryl fructose의 생성량이 증가하는 경향을 보여주었으며, 수분함량 1%에서는 monobutyryl fructose만이 생성되었다.

• The Korean Journal of Physiology and Pharmacology
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• 제24권4호
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• pp.319-328
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• 2020

High fructose intake induces hyperglycemia and hypertension. However, the mechanism by which fructose induces metabolic syndrome is largely unknown. We hypothesized that high fructose intake induces activation of the renin-angiotensin system (RAS), resulting in hypertension and metabolic syndrome. We provided 11-week-old Sprague-Dawley rats with drinking water, with or without 20% fructose, for two weeks. We measured serum renin, angiotensin II (Ang II), and aldosterone (Aldo) using ELISA kits. The expression of RAS genes was determined by quantitative reverse transcription polymerase chain reaction. High fructose intake increased body weight and water retention, regardless of food intake or urine volume. After two weeks, fructose intake induced glucose intolerance and hypertension. High fructose intake increased serum renin, Ang II, triglyceride, and cholesterol levels, but not Aldo levels. High fructose intake increased the expression of angiotensinogen in the liver; angiotensin-converting enzyme in the lungs; and renin, angiotensin II type 1a receptor (AT1aR), and angiotensin II type 1b receptor (AT1bR) in the kidneys. However, expression of AT1aR and AT1bR in the adrenal glands did not increase in rats given fructose. Taken together, these results indicate that high fructose intake induces activation of RAS, resulting in hypertension and metabolic syndrome.

• Journal of Plant Biology
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• 제30권4호
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• pp.277-285
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• 1987

Undifferentiated suspension cells had the ability to transfer glucose and fructose actively, but the suspension culture cells were unable to transfer saccharide without previously splitting to monosccarides. The uptake of fructose showed the low- and high-affinity system compared to of glucose, which possessed only one saturable uptake system. In this paper, the low affinity system of the uptake of fructose has been studied intensively. Glucose did not inhibit the low affinity system of fructose competitively. The Km value was 47 mM for fructose, 7.4 mM for glucose and Vmax was 69 $\mu$mol/h.g fresh weight for fuctose, 9.8 $\mu$ mol/h.g fresh weight for glucose. Metabolizer inhibitors, both 50 $\mu$M of CCCP and DNP, inhibited 70% of the uptake of the low affinity system of fructose. The proton ions were accompanied by the uptake of fructose. The stoichiometry showed ratio of proton to fructose was 0.17. The mechanism ofthe uptake was fructose-proton-symport. The molecules of fructose accmululated inside 25 times more than outside. Therefore, the low affinity system of fructose was not mere diffusion, but depended on metabolic energy and thus transported actively. The importance of this system was discussed.

• Nutrition Research and Practice
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• 제2권4호
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• pp.252-258
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• 2008

This study was designed to determine whether acute fructose or sucrose administration at different levels (0.05 g/kg, 0.1 g/kg or 0.4 g/kg body weight) might affect oral glucose tolerance test (OGTT) in normal and type 2 diabetic rats. In OGTT, there were no significant differences in glucose responses between acute fructose- and sucrose-administered groups. However, in normal rats, the AUCs of the blood glucose response for the fructose-administered groups tended to be lower than those of the control and sucrose-administered groups. The AUCs of the lower levels fructose- or sucrose-administered groups tended to be smaller than those of higher levels fructose- or sucrose-administered groups. In type 2 diabetic rats, only the AUC of the lowest level of fructose-administered (0.05 g/kg body weight) group was slightly smaller than that of the control group. The AUCs of fructose-administered groups tended to be smaller than those of the sucrose-administered groups, and the AUCs of lower levels fructose-administered groups tended to be smaller than those fed higher levels of fructose. We concluded from this experiment that fructose has tendency to be more effective in blood glucose regulation than sucrose, and moreover, that smaller amount of fructose is preferred to larger amount. Specifically, our experiments indicated that the fructose level of 0.05 g/kg body weight as dietary supplement was the most effective amount for blood glucose regulation from the pool of 0.05 g/kg, 0.1 g/kg and 0.4 g/kg body weights. Therefore, our results suggest the use of fructose as the substitute sweetener for sucrose, which may be beneficial for blood glucose regulation.

• Biotechnology and Bioprocess Engineering:BBE
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• 제7권4호
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• pp.254-254
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• 2002

A process for the production of mannitol from fructose (5% to 25%) using Leuconosyoc mesenteroides NRRL B-1149 was investigated. Fermentations were carried out in bat도 of fed-batch fermentations without aeration at 28℃, pH 5.0. When 5% fructose was used in batch culture fermentation, the yield of mannitol was 78% of that expected theoretically. When the fructose concentration was increased to 10%, the yield dropped to 59.6% of the theoretical value. However, in the fed-batch culture, using 10% fructose, the yield was 81.9% of the theoretical value. In a 15% fructose fed-bat도 culture, with 5% fructose being added initially and the other 10% fructose being added as a continuous supply, the final yield was 83.7% of the theoretical yield. When 20% fructose was used in the same manner, the yield was 89.5% of theoretical yield.

• 운동영양학회지
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• 제16권2호
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• pp.101-111
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• 2012

The purpose of this thesis is to investigate whether taurine supplementation in combination with fructose improves both energy metabolism and exercise capacity. Eight collegiate female subjects were recruited for the study. Each subject went through threecross-over designs: control(fluid), fructose, and taurine plus fructose supplementation trials. Subjects received taurine supplementation 100 mg/kg a day for two weeks. After the supplementation, all subjects take 10% fructose at 15 min prior to exercise, immediately before exercise, and every 15 min during exercise. Subjects received 150 ml fluid as placebo during the same procedure. The subjects performed submaximal exercise at the exercise intensity of 60% for 45 min and then 80% of maximal oxygen uptake (VO_2max) until exhaustion time. A 10ml blood sample was taken for measuring the level of glucose, ammonia, lactate, free fatty acids, and insulin every 15 min during exercise at 60% of VO_2max. The blood glucose levels was significantly higher at 45 min and 50 min exercise after supplementation of fructose, and immediately before exercise and 50 min exercise after taurine plus fructose compared to the placebo trial. However, the values tended to be lower in taurine plus fructose supplementation compared to the fructose trial. The levels of both lactate and ammonia were significantly lower compared to the placebo, while the exhaustion time was significantly increased. The level of free-fatty acids was significantly lower at 30, 45, and 50 min after fructoseand fructose plus taurine supplementation compared to the placebo trial. The level of glucagon was significantly lower at 15, 30, 45, and 50 min after fructose and fructose plus taurine supplementation compared to the placebo trial. There was no differences in insulin concentration among three treatments. This thesis concludes that combined taurine and fructose supplementation prior to exercise may improve exercise tolerance time and energy metabolism, lowering the muscle fatigue factors such as lactate and ammonia.

• 대한약리학회지
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• 제22권1호
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• pp.51-59
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• 1986

Lidocaine의 심근수축력 억제 작용에 관한 기전연구 일환으로 lidocaine에 의해 수축력이 감소된 흰쥐 적출심방에 대한 fructose의 효과를 검토하였다. Fructose는 기질제거에 의해 감소된 적출심방의 수축력을 현저히 증가시켰으며, 30mM에서 최대 증가효과를 나타냈다. Krebs-Ringer glucose용액에 현수한 적출심방의 수축력은 0.1mM lidocaine에 의해 약 50%의 감소를 나타냈으며, 30mM fructose의 투여는 이 감소된 수축력을 현저히 증가 시켰다. Lidocaine 억제심방에 대한 fructose의 실험 성적은 pyruvate나 acetate에서 얻은 실험성적과 유사하였다. 그러나 같은 농도의 fructose는 저 calcium(1/2)농도의 Krebs-Ringer glucose medium에서 감소(약 50% 감소)된 적출심방의 수축력을 증가시키지 못하였다. 이상의 결과에서 lidocaine은 심근내 포도당 대사를 해당과정에서 억제한다는 가능성을 재확인하고 있으며, 나아가서 lidocaine은 해당과정의 phosphofructokinase step 이전의 초기단계에서 억제하고 있을 가능성을 시사하고 있다.

• Molecules and Cells
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• 제46권8호
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• pp.496-512
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• 2023

A fructose-enriched diet is thought to contribute to hepatic injury in developing non-alcoholic steatohepatitis (NASH). However, the cellular mechanism of fructose-induced hepatic damage remains poorly understood. This study aimed to determine whether fructose induces cell death in primary hepatocytes, and if so, to establish the underlying cellular mechanisms. Our results revealed that treatment with high fructose concentrations for 48 h induced mitochondria-mediated apoptotic death in mouse primary hepatocytes (MPHs). Endoplasmic reticulum stress responses were involved in fructose-induced death as the levels of phosho-eIF2α, phospho-C-Jun-N-terminal kinase (JNK), and C/EBP homologous protein (CHOP) increased, and a chemical chaperone tauroursodeoxycholic acid (TUDCA) prevented cell death. The impaired oxidation metabolism of fatty acids was also possibly involved in the fructose-induced toxicity as treatment with an AMP-activated kinase (AMPK) activator and a PPAR-α agonist significantly protected against fructose-induced death, while carnitine palmitoyl transferase I inhibitor exacerbated the toxicity. However, uric acid-mediated toxicity was not involved in fructose-induced death as uric acid was not toxic to MPHs, and the inhibition of xanthine oxidase (a key enzyme in uric acid synthesis) did not affect cell death. On the other hand, treatment with inhibitors of the nicotinamide adenine dinucleotide (NAD)⁺-consuming enzyme CD38 or CD38 gene knockdown significantly protected against fructose-induced toxicity in MPHs, and fructose treatment increased CD38 levels. These data suggest that CD38 upregulation plays a role in hepatic injury in the fructose-enriched diet-mediated NASH. Thus, CD38 inhibition may be a promising therapeutic strategy to prevent fructose-enriched diet-mediated NASH.

• 대한물리치료과학회지
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• 제9권4호
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• pp.45-52
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• 2002

Rats that are fed a fructose-rich diet develop hypertension, insulin resistance, and hypertriglyceridemia. To elucidate whether altered expression levels of endothelin-1 and nitric oxide synthase are related to the development of insulin-resistant hypertension, we examined the present study. Male Sprague-Dawley rats were fed a fructose-rich diet for 5 weeks. Systolic blood pressure significantly increased in fructose-fed rats. While serum free fatty acid and plasma nitrite/nitrate levels did not significantly differ between the fructose-fed and control groups, plasma insulin and serum triglyceride concentrations significantly increased in the former. Endothelin-1 mRNA expression in the aorta increased in fructose-fed rats. Neither the protein expression of constitutive nitric oxide synthase nor that of inducible nitric oxide synthase were significantly affected by fructose feeding. However, nitrite/nitrate levels in the aorta were significantly increased. These results suggest that an increase in vascular endothelin-1 is an important contributing factor to the development of hypertension in fructose-fed rats. However, the vascular nitric oxide pathway may not be causally related to the development of fructose-induced hypertension.