Oral Administration Of Fructose Research Articles

Inhibitory effect of Bofutsushosan (Fangfengtongshengsan) extract on the absorption of fructose in rats and mice

Bofutsushosan (BTS; fangfengtongshengsan in Chinese) is a formula in traditional Japanese Kampo and Chinese medicine comprising 18 crude drugs and used to treat obesity and metabolic syndrome. In our previous study, BTS boiling water extract inhibited the uptake of fructose absorbed via glucose transporter 5 into cultured cells. In this study, the inhibitory effect of BTS extract on the absorption of fructose from the intestine was investigated in vivo. The extract of BTS was orally administered to rats at doses equivalent to 25-fold of the daily dose for humans. One minute after sample administration, fructose was orally administered and blood samples were collected from the jugular vein 0.5, 1, 1.5, 2, and 4 h after the administration of fructose. The absorption of fructose from the intestine was significantly reduced by treatment with BTS extract, and this in vivo study reproduced previous in vitro results. Subsequently, the blood samples were collected from the portal vein 30 min after the oral administration of fructose in mice. BTS extract significantly reduced fructose absorption in mice, and compared the effect of modified BTS samples by removing one to several crude drugs from BTS. We found that the dried rhizome of Rheum palmatum (RR) significantly contributed to the inhibitory effect of BTS on fructose absorption. We found sennoside A to be the active ingredient of RR for the inhibition of fructose absorption, and that its effect almost saturated at a dose of 3 mg/kg. These results support the action mechanisms of BTS when used for the treatment of obesity in clinics and drug stores.Graphical abstract

Comparison of oral administration of fructose and glucose on food intake and physiological parameters in broiler chicks

Like glucose, fructose is a monosaccharide, but the mechanisms of its absorption and metabolism in the body are very different between the 2 molecules. In this study, we investigated the effects of oral administration of glucose and fructose on food intake, diencephalic gene expression, and plasma metabolite concentrations in broiler chicks. The animals used in this study were 4-day-old male broiler chicks (Ross 308). They were given glucose, fructose (200 mg/ 0.5 mL/ bird), or a similar volume of distilled water orally after 6 h fasting. After treatment, measurements of food intake (at 0, 30, and 60 min), and blood glucose as well as insulin concentrations were measured over time; however, diencephalic (hypothalamus) gene expression and plasma metabolites were measured at 30 min. The results showed that glucose administration suppressed food intake, but fructose administration did not suppress food intake and it was at the same level as distilled water administration. In addition, fructose administration did not increase plasma glucose and insulin levels as did glucose administration. In the diencephalon, expression levels of genes related to the melanocortin system were unaffected by the treatment, while gene expression levels related to intracellular energy regulation, such as AMP-activated protein kinase were affected by the glucose treatment in the fasted chicks. These results suggest that fructose administration does not suppress feeding behavior as a result of possible reduction in the energy levels in the diencephalon and associated energy metabolism.

Effects of exercise and quercetin on muscle energy charge in metabolic syndrome model of rats

Abstract Objectives This study was performed to investigate whether exercise and quercetin have an effect on muscle energy charge in the metabolic syndrome (MetS) model of rats. Methods Male Sprague-Dawley rats consisting of Control, Fructose, Quercetin, Exercise, Fructose + Exercise, Fructose + Quercetin, Fructose + Quercetin + Exercise groups were randomly divided into seven groups, six rats in each group. Consequently, it was determined that the 20% fructose supplement for 10 weeks with drinking water let to metabolic syndrome in the animals depending on the increase of systolic blood pressure, serum triglyceride, serum insulin and high HOMA-IR scores. MetS criteria were successfully established by oral fructose administration. Results ATP and AMP levels were higher in fructose and exercise groups, and ADP levels were lower. The energy charge increased in quercetin treated groups. We found that regular aerobic exercise and quercetin application might be beneficial in the fructose-mediated MetS in accordance with previous studies. However it was found that quercetin was more effective than exercise in muscle. Conclusions Consequently, it is thought that the regular aerobic exercise alone is a preventive method for the MetS and also it can be used together with quercetin as a beneficial treatment.

Oral administration of fructose improves jejunal villous morphology and nutrient digestion and absorption capabilities in a rat model of total parenteral nutrition

Oral administration of fructose improves jejunal villous morphology and nutrient digestion and absorption capabilities in a rat model of total parenteral nutrition

Effects of fructose-containing sweeteners on fructose intestinal, hepatic, and oral bioavailability in dual-catheterized rats.

ObjectiveFructose is commonplace in Western diets and is consumed primarily through added sugars as sucrose or high fructose corn syrup. High consumption of fructose has been linked to the development of metabolic disorders, such as cardiovascular diseases. The majority of the harmful effects of fructose can be traced to its uncontrolled and rapid metabolism, primarily within the liver. It has been speculated that the formulation of fructose-containing sweeteners can have varying impacts on its adverse effects. Unfortunately, there is limited data supporting this hypothesis. The objective of this study was to examine the impact of different fructose-containing sweeteners on the intestinal, hepatic, and oral bioavailability of fructose.MethodsPortal and femoral vein catheters were surgically implanted in male Wistar rats. Animals were gavaged with a 1 g/kg carbohydrate solution consisting of fructose, 45% glucose/55% fructose, sucrose, glucose, or water. Blood samples were then collected from the portal and systemic circulation. Fructose levels were measured and pharmacokinetic parameters were calculated.ResultsCompared to animals that were gavaged with 45% glucose/55% fructose or sucrose, fructose-gavaged animals had a 40% greater fructose area under the curve and a 15% greater change in maximum fructose concentration in the portal circulation. In the systemic circulation of fructose-gavaged animals, the fructose area under the curve was 17% and 24% higher and the change in the maximum fructose concentration was 15% and 30% higher than the animals that received 45% glucose/55% fructose or sucrose, respectively. After the oral administration of fructose, 45% glucose/55% fructose, and sucrose, the bioavailability of fructose was as follows: intestinal availability was 0.62, 0.53 and 0.57; hepatic availability was 0.33, 0.45 and 0.45; and oral bioavailability was 0.19, 0.23 and 0.24, respectively.ConclusionsOur studies show that the co-ingestion of glucose did not enhance fructose absorption, rather, it decreased fructose metabolism in the liver. The intestinal, hepatic, and oral bioavailability of fructose was similar between 45% glucose/55% fructose and sucrose.

Oral administration of fructose exacerbates liver fibrosis and hepatocarcinogenesis via increased intestinal permeability in a rat steatohepatitis model.

Recent reports have revealed the impact of a western diet containing large amounts of fructose on the pathogenesis of non-alcoholic steatohepatitis (NASH). Fructose exacerbates hepatic inflammation in NASH by inducing increasing intestinal permeability. However, it is not clear whether fructose contributes to the progression of liver fibrosis and hepatocarcinogenesis in NASH. The aim of this study was to investigate the effect of fructose intake on NASH in a rat model. A choline-deficient/L-amino acid diet was fed to F344 rats to induce NASH. Fructose was administrated to one group in the drinking water. The development of liver fibrosis and hepatocarcinogenesis were evaluated histologically. Oral fructose administration exacerbated liver fibrosis and increased the number of preneoplastic lesions positive for glutathione S-transferase placental form. Fructose-treated rats had significantly higher expression of hepatic genes related to toll-like receptor-signaling, suggesting that fructose consumption increased signaling in this pathway, leading to the progression of NASH. We confirmed that intestinal permeability was significantly higher in fructose-treated rats, as evidenced by a loss of intestinal tight junction proteins. Fructose exacerbated both liver fibrosis and hepatocarcinogenesis by increasing intestinal permeability. This observation strongly supports the role of endotoxin in the progression of NASH.

Acute Effect of Oral Administration of Fructose on Blood Parameters and Hepatic Glycogen in Layer Chicks

Acute Effect of Oral Administration of Fructose on Blood Parameters and Hepatic Glycogen in Layer Chicks

Acute effects of fructose consumption on uric acid and plasma lipids in patients with impaired renal function

ObjectiveMetabolic disturbances are common in patients with renal function impairment and are related to high rates of cardiovascular incidents and mortality. Kidney transplantation leads to improved survival but may lead to additional metabolic alterations caused by immunosuppressive drugs and improved nutrition. Materials and methodsThe short-term effect of oral fructose load on serum uric acid (UA), plasma lipids, and blood pressure (BP) was studied in 85 patients with chronic kidney disease (CKD) and impairment of renal function (glomerular filtration rate 50–65ml/min per 1.73m2), comprising 55 renal transplant recipients (RTR) treated with standard triple immunosuppressive therapy including a calcineurin inhibitor (CNI) cyclosporine A (CsA) or tacrolimus (Tac) and 30 non-transplanted patients with CKD. Both non-transplanted CKD patients and RTR had stable renal function and a comparable degree of kidney dysfunction. All subjects received orally 70g of fructose dissolved in 200ml of water. Serum UA, lipids, and blood pressure were measured at baseline and 60, 120, 180, and 240minutes after fructose administration. ResultsThere was a significant increase of serum UA concentration (p<0.001) in both CKD patients and RTR – CsA- or Tac-treated patients comparable in the latter. Total cholesterol (TC), LDL, and HDL cholesterol significantly decreased and serum triglycerides (TG) markedly increased in RTR, whereas in CKD patients all serum lipid fractions increased. Blood pressure was unaffected by fructose intake. ConclusionBoth non-transplanted and transplanted patients with mild renal function impairment show similar acute purine metabolic disturbances following oral administration of fructose but in the latter dietary fructose may induce a smaller hyperlipidemic response.

A single oral dose of fructose induces some features of metabolic syndrome in rats: Role of oxidative stress

Background and aimsTo determine if a single oral dose of fructose to rats reproduces some features of metabolic syndrome observed after chronic administration and if so, to investigate its mechanisms. Methods and resultsSystolic blood pressure was measured in rats before and after oral administration of fructose, and in animals pretreated with lipoic acid, methyldopa, losartan or streptozotocin. In other rats, glucose, insulin, uric acid, and insulin sensitivity index, were determined before and after fructose or lipoic acid plus fructose. Glutathione was measured in liver before and after fructose administration. In aortic rings from other rats, incubation with mannitol, fructose, or fructose plus lipoic acid was evaluated on the relaxation by acetylcholine. Fructose produced a moderate increase in blood pressure, which was prevented by lipoic acid or streptozotocin. Methyldopa and losartan decreased the pressor response minimally. Fructose increased oxidized glutathione, plasma glucose, insulin and uric acid, and diminished the insulin sensitivity index, and the reduced glutathione. Lipoic acid prevented hyperglycemia and hyperuricemia, and improved the insulin sensitivity index. Finally, endothelial dysfunction was prevented by lipoic acid. ConclusionA single dose of fructose reproduces some of the features of metabolic syndrome, most changes were caused by oxidative stress and insulin resistance.

Effect of Oral Fructose Load on Serum Uric Acid and Lipids in Kidney Transplant Recipients Treated With Cyclosporine or Tacrolimus

Hyperuricemia, frequently observed following kidney transplantation, may adversely affect graft survival. Although hyperuricemia is a well-known adverse effect of cyclosporine (CsA), a similar effect of tacrolimus (Tac) remains debatable. Hyperuricemia is also seen after oral fructose intake in beverages and processed foods. This sugar is blamed for the epidemic of obesity and metabolic syndrome. The aim of our study was to compare the effects of CsA and Tac on an acute oral fructose load in terms of plasma uric acid, serum lipids, and blood pressure in kidney transplant patients. Thirty-two kidney transplant recipients treated with CsA- or Tac-based triple (calcineurin inhibitor + mycophenolate mofetil + prednisone) immunosuppressive therapy displaying stable allograft function (mean glomerular filtration rate = 53 mL/min/1.73m 2) received an oral challenge with 70 g of fructose. Serum uric acid, lipids, and blood pressure were measured before as well as 60, 120, 180, and 240 minutes after fructose administration. A significant increase in serum uric acid was observed in both groups after oral fructose administration ( P < .001). A peak increase in serum uric acid was recorded at 120 minutes after fructose intake. Serum total, LDL, and HDL cholesterol also significantly decreased and serum triglycerides increased to a similar extent in both CsA and Tac groups. No significant changes in blood pressure were observed after fructose consumption. Oral fructose intake induced an acute rise in serum uric acid and triglycerides and decrease in serum cholesterol among kidney transplant recipients. Those changes were similar among patients treated with CsA or Tac.

Effect of oral fructose administration on alchohol-induced increase in plasma urate

ABSTRACT: Oral fructose administration has been demonstrated to stimulate the oxidation of alcohol. However, its influence on alcohol-induced hyperuricemia is yet to be documented. This study therefore, reports the effect of fructose on alcohol- induced increase in plasma urate in adult albino rabbits. Twelve male adult albino rabbits, divided into A, B and C experimental groups were purchased from Yoha Farms, Warri, Delta State. Group A, the control animals (n=4) were given normal saline, while Group B animals (n=4) orally received 1.5 g (40%) ethanol/kg body weight as single daily dose for a routine period of fifteen weeks. Group C rabbits (n=4) were treated in a similar manner but 0.25 g fructose/kg body weight was usually given after about 10 min of administering the ethanol dose. The results obtained show that ethanol administration significantly increased (P

Mechanism of Stimulation of Liver Glycogen Synthesis by Fructose in Alloxan Diabetic Rats

In diabetic animals and humans, stimulation of liver glycogen synthesis has been reported after administration of a large parenteral fructose load. The effects of an oral fructose load have not been examined previously. In the diabetic state, glycogen synthase phosphatase activity is reduced, and synthase D (the inactive form) is a poor substrate for the phosphatase. Thus, activation of synthase to the synthase R and synthase I (R + I) (active) forms by fructose would not be expected. We have determined that oral fructose administration does stimulate glycogen synthesis and have examined the mechanism by which this is accomplished. In 24-h-fasted alloxan diabetic rats, basal liver glycogen was higher than in normal rats (8.3 +/- 1.8 vs. 3.0 +/- 0.5 mg/g wet wt). After fructose (4 g/kg) was given, the initial rate of glycogen synthesis was normal in diabetic rats, but total glycogen synthesis was reduced. By 240 min, liver glycogen increased to 18 +/- 4.0 mg/g wet wt in diabetic rats versus 30.5 +/- 1.5 mg/g wet wt in normal rats. Synthase R + I was low and did not increase significantly (0.063 +/- 0.006 to 0.064 +/- 0.010 U/g wet wt) after fructose administration to the diabetic animals. Phosphorylase a did not decrease significantly during the period of active glycogen synthesis. In the diabetic rats, glucose-6-phosphate increased by 84% (0.103 +/- 0.010 to 0.184 +/- 0.020 mumol/g wet wt) within 10 min and remained elevated above the control level. UDPglucose decreased from 0.336 +/- 0.013 to 0.271 +/- 0.011 mumol/g wet wt at 10 min and remained below the control level.(ABSTRACT TRUNCATED AT 250 WORDS)

Metabolic effects of dietary versus parenteral fructose.

Fructose has been considered as an alternative sweetener to sucrose because it results in less glycemia when given to normal subjects or to those with mild noninsulin-dependent diabetes mellitus. Oral fructose also results in efficient glycogen synthesis. However, multiple hepatotoxic effects have been reported following parenteral fructose administration. We have examined the effects of large oral fructose and glucose loads (4 g/kg) and of graded intravenous fructose doses (50-500 mg/kg) on hepatic metabolism and glycogen synthesis in normal, fasted rats. Fructose was absorbed more slowly than glucose when given by gavage (59% vs 91% absorbed in 120 min). Oral fructose administration resulted in greater liver and muscle glycogen synthesis, despite smaller increases in plasma glucose and insulin concentrations, than was found after oral glucose administration. Increases in percent glycogen synthase I (active form) occurred after both oral fructose and glucose loads (67% vs 115% increase). There was no evidence of hepatotoxicity even after a very large oral fructose load. When small (less than or equal to 125 mg/kg) iv doses of fructose were given, the portal vein fructose concentration remained less than or equal to that found after oral fructose administration (1.1 mM). The percent synthase I increased up to threefold, and there was no evidence of hepatotoxicity. Larger iv doses resulted in a fall in percent synthase I, an increase in percent phosphorylase a, and inorganic phosphate and nucleotide depletion. We conclude that the slow absorption of an oral fructose load prevents hepatotoxic effects and permits efficient glycogen synthesis.

Intestinal Metabolism of Orally Administered Glucose and Fructose in Yucatan Miniature Swine

Absorption rates and metabolism of orally administered glucose and fructose were quantitated in conscious, overnight-fasted, Yucatan miniature swine. The pigs were surgically prepared, with catheters in the portal vein and a carotid artery. A continuous wave Doppler flow cuff was placed around the portal vein. Four to 7 days after surgery, arterial and portal venous blood samples were obtained in the basal state and at 15-minute intervals for 4 hours following oral administration of glucose or fructose (1.5 g/kg body weight). Absorption rates and intestinal metabolism were calculated from portal blood flow and arterio-venous concentration differences for glucose, fructose and lactate. Oral fructose administration was accompanied by a rise in intestinal lactate production, which correlated significanly with the fructose absorption rate. Intestinal lactate output during fructose absorption could account for 12% of the fructose absorbed or metabolized. A small rise in glucose output from the gut was also observed. In contrast, after oral glucose administration, only a modest rise in intestinal lactate output was noted. It could account for only 2% of the glucose absorbed or metabolized. No correlation between glucose absorption rate and intestinal lactate output was observed. These studies indicate that a significant portion of oral fructose is converted to lactate during absorption but that the major part enters the portal vein as fructose. Only minimal intestinal metabolism of ingested glucose occurs.

Effect of oral administration of fructose on purine nucleotide metabolism in rats

1. 1. Oral administration of fructose (4 g/kg body wt) accelerated the production of uric acid and allantoin in rat liver. 2. 2. Changes in the concentrations of various metabolites in the liver after the administration of fructose suggested that this was due to the acceleration of AMP degradation induced by the rapid fall in adenylate energy charge resulted from rapid phosphorylation of fructose with ATP.

The effect of fructose on purine metabolism in the lung

Oral administration of fructose to rats resulted in a transient depression of pulmonary adenosine triphosphate and a marked increase in serum uric acid and allantoin. Accompanying this increase were elavations in activity of 5′ nucleotidase, adenylate deaminase and adenosine deaminase in the lung. Increased enzyme activity resulted from enhanced protein synthesis as demonstrated by an increased incorporation of (4-5-3H) leucine and a partial inhibition by inhibitors of protein synthesis. These data confirm the presence of an active purine nucleotide cycle in lung and that the enzymes involved in purine catabolism can be stimulated in a manner similar to those in the liver.