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PubMed2004

Ingestion of guar gum hydrolysate, a soluble and fermentable nondigestible saccharide, improves glucose intolerance and prevents hypertriglyceridemia in rats fed fructose.

Fructose feeding provides a dietary model of insulin resistance accompanied by hypertriglyceridemia. We examined the effects of guar gum hydrolysate (GGH), a soluble and fermentable nondigestible saccharide with low viscosity, on glucose intolerance and hypertriglyceridemia in rats fed high-fructose diets. Rats were fed either a dextrin-based or a fructose-based diet with or without GGH (75 g/kg) for 30 d. Oral glucose tolerance tests (OGTTs) were performed 0, 14, and 28 d after feeding. High-fructose feeding negatively affected glucose tolerance on d 14 and 28. The addition of GGH to the diets improved glucose intolerance on d 28. Fructose feeding induced hyperinsulinemia after an oral glucose load; this was also improved by GGH on d 28. The glycogen concentration in the gastrocnemius muscles of rats was lowered by dietary fructose, and GGH supplementation abolished this decrease. Triglycerides in the plasma and livers of rats fed fructose diets were elevated, and the increases were ameliorated by supplemental GGH. Regardless of the type of carbohydrate, GGH enlarged the cecum and increased the cecal SCFA pools. In conclusion, supplemental feeding of GGH to rats improved the glucose intolerance and hypertriglyceridemia induced by a high-fructose diet. Possible mediators of these beneficial effects of GGH are the SCFAs produced by microbial fermentation of GGH in the large intestine.

Animals↗
PubMed1989

[The sugar substitutes fructose and sorbite: an unnecessary risk in parenteral nutrition].

The glucose substitutes fructose, sorbitol and xylitol are still widely used in parenteral nutrition throughout central Europe. Their main advantage, which has led to their widespread use, is their diminished blood glucose raising effect and the absence of a browning reaction during sterilization with amino acids. During infusions with glucose substitutes in severely ill patients with glucose intolerance it is sometimes possible to avoid insulin therapy since the first steps in the metabolism of these carbohydrates are insulin-independent. These advantages are less relevant today since fat emulsions frequently replace some of the glucose given as energy substrate in parenteral nutrition and glucose intolerance is easier to monitor and to treat. - Specific advantages of xylitol are proposed, but this issue needs further clarification. The major objection to fructose, and therefore also to sorbitol, which is metabolized via fructose, is the life-threatening risk in patients with hereditary fructose intolerance. This congenital disorder affects 1 in 21,000 and there have been more than twelve severe complications due to these solutions, most of which were lethal. All the complications occurred in German-speaking countries where fructose and sorbitol are most widely used in parenteral nutrition. Experience over the years has demonstrated that a history of fructose intolerance cannot be obtained, and warning labels on infusion bottles do not avoid this complication. The central European countries are isolated with regard to their use of fructose and sorbitol containing infusion fluids, which involve doubtful advantages but documented lethal risks. Therefore, fructose and sorbitol containing infusion fluids have no further place in our hospital pharmacies.

Fructose↗
PubMed2000

Coincidental malabsorption of lactose, fructose, and sorbitol ingested at low doses is not common in normal adults.

Normal subjects may incompletely absorb either lactose, fructose, or sorbitol and may therefore have abdominal symptoms. The frequency of coincidental malabsorption of these sugars is not known. This is clinically important, since we often ingest them during the same day and malabsorption may cause abdominal symptoms. To shed light on this issue we studied 32 normal subjects. Volunteers drank in random order the following solutions: 20 g lactulose, 50 g sucrose, 50 and 25 g lactose, 50 and 25 g fructose, 20 and 10 g sorbitol. Semiquantitative carbohydrate malabsorption was estimated with lactulose standards. Frequency of 50-g lactose (69%), 50-g fructose (81%), and 20-g sorbitol (84%) malabsorption was not significantly different (P = 0.3). The estimated median fraction of the ingested high dose malabsorbed was 42, 19, and 68% for lactose, fructose, and sorbitol, respectively. At low challenging doses, 63% of the volunteers absorbed two of three or all three sugars, and 88% were asymptomatic to two or all three sugars. In conclusion, the frequency of coincidental malabsorption of lactose, fructose, and sorbitol and intolerance to these sugars is not common, when normal adults ingest them at low doses.

Adult↗
PubMed1985

Effects of fructose feeding on lipid parameters in obese and lean, diabetic and nondiabetic Zucker rats.

Effects of fructose feeding in moderate amounts on lipid metabolism of obese versus lean, and diabetic versus nondiabetic Zucker rats, were studied. Forty pairs of male lean and obese animals were assigned to two dietary groups, fructose and glucose. For each diet, one-half of lean and obese animals were injected with streptozotocin intraperitoneally (i.p.) to induce diabetes, and the other half were injected with buffer i.p. as a nondiabetic control group. After 9 wk of feeding, animals were fasted overnight, decapitated and exsanguinated. Organs were removed and weighed. Blood glucose, insulin, lactic acid, triglycerides, cholesterol, total liver lipids and urinary glucose were determined. Hyperphagia was observed in obese, non-diabetic and lean-diabetic animals. Streptozotocin injection drastically reduced insulin levels, and produced an impairment of growth, hyperglycemia, glucosuria, polydipsia and polyuria. Fructose feeding increased organ weights in kidney, liver and retroperitoneal adipose tissue, regardless of diabetic state. However, lactic acid levels were lower in fructose-fed groups than glucose-fed groups. In obese rats serum triglyceride levels were also lower in fructose-fed groups than in glucose-fed groups. Serum cholesterol was not affected by fructose feeding. The results indicated that fructose feeding did not produce hyperlipemia and lactic acidosis in the blood circulation in Zucker rats. However, fructose feeding did not improve glucose intolerance in diabetic animals, rather fructose feeding produced hyperinsulinemia in nondiabetic, obese animals.

Animals↗
PubMed1989

[Parenteral nutrition--peripheral venous feeding].

Generally, the terms peripheral-venous nutrition and hypocaloric parenteral nutrition are synonymous. Both supply the patients with roughly 2 g carbohydrates and 1.0 g-1.5 g amino acids/kg BW/day. In Germany there are so-called 'complete' or 'combination' solutions on the market, which contain these amounts of nutrients in 3-liter-concepts. For peripheral-venous application the osmolality of the solutions is important. Generally, only solutions with an osmolality of twice the concentrations of plasma will be tolerated by peripheral veins. Since osmolality is widely a function of electrolyte concentrations, solutions with a low mineral content are preferable for peripheral-venous use. The main advantage of hypocaloric parenteral nutrition is its easy handling in the early postoperative period. In clinical practice, due to the hazard of intolerance reactions to fructose and sorbit, the use of glucose or xylitol as carbohydrates in hypocaloric parenteral solutions is recommended.

Amino Acids↗
PubMed2001

Gene therapy attenuates the elevated blood pressure and glucose intolerance in an insulin-resistant model of hypertension.

OBJECTIVE: Fructose feeding in male Sprague-Dawley (SD) rats results in a mild hypertension and glucose intolerance. Although the mechanism of this glucose intolerance and hypertension is not completely understood, a role for the renin-angiotensin system (RAS) has been proposed. In the current study our aim was to test the hypothesis that intervention of the RAS with a gene therapy approach would be effective in preventing the development of hypertension and glucose intolerance in this animal model. DESIGN AND METHODS: Five-day-old SD rats were administered either an empty retroviral vector (LNSV) or retroviral vector containing AT1 receptor antisense DNA (AT1R-AS). The virus (25 microl, 8 x 10(9) CFU/ml) was injected into the heart and the animals were returned to their mothers. After weaning, half the animals from each group were placed on breeder's chow or a 60% fructose diet. Indirect blood pressures (BP) were determined and an oral glucose tolerance test (OGTT) was performed when the animals had been on the respective diets for 2 months. RESULTS: Fructose-fed animals developed mild hypertension (145 +/- 3 versus 132 +/- 4 mmHg) by 6 weeks of dietary intervention. This increase in BP was prevented by AT1R-AS treatment (125 +/- 3 mmHg). At 2 months of age, fasting blood glucose was comparable among the four groups; however, the glucose excursion during the OGTT was significantly greater and more prolonged in the LNSV-treated, fructose-fed group than the other three groups. AT1R-AS treatment significantly prevented glucose intolerance in the fructose rat to levels observed in the controls. CONCLUSIONS: Early fructose dietary treatment results in moderate hypertension and glucose intolerance, which is prevented by a single neonatal treatment with AT1R-AS. These results suggest that the RAS is involved in the glucose intolerance associated with fructose feeding and that genetic intervention is effective in this rat model.

Animals↗
PubMed2006

Effect of anthocyanin-rich extract from black rice (Oryza sativa L. indica) on hyperlipidemia and insulin resistance in fructose-fed rats.

This study was designed to evaluate the effect of an anthocyanin-rich extract from black rice on hyperlipidemia and insulin resistance in fructose-fed rats. Rats fed fructose diet for 4 weeks exhibited significantly higher plasma insulin levels and lower insulin sensitivity than the control rats fed AIN-93G diet. Dietary supplementation with the anthocyanin-rich extract (5 g/kg of high-fructose diet) prevented the development of fructose-induced insulin resistance. After fructose-induced insulin resistance had been established, 4-week treatment with the anthocyanin-rich extract (5 g/kg of high-fructose diet) or pioglitazone (270 mg/kg of high-fructose diet) ameliorated the glucose intolerance and hyperlipidemia, but the extract failed to reverse the fructose-induced hyperinsulinemia as pioglitazone did. In addition, rats supplemented by the extract exhibited lower oxidative stress than the fructose-fed controls, as indicated by the lower concentrations of plasma thiobarbituric acid reactive substances and blood oxidized glutathione. Overall, these results suggest that the anthocyanin-rich extract from black rice improves certain metabolic abnormalities associated with diets high in fructose.

Animals↗
PubMed2006

Nocturnal hypertension in mice consuming a high fructose diet.

OBJECTIVE: To investigate the effect of fructose consumption on the light/dark pattern of blood pressure, heart rate and autonomic neural function in mice. BACKGROUND: Insulin resistant diabetes is associated with hypertension and autonomic dysfunction. There is evidence that the increasing incidence of diabetes may be related to dietary changes, including consumption of high levels of fructose. DESIGN/METHODS: C57/BL mice, instrumented with radiotelemetric arterial catheters, were fed a control or high fructose diet (60%). Cardiovascular parameters measured were light/dark pattern of mean arterial pressure (MAP), heart rate (HR) and variability (time and frequency domain). We also measured plasma insulin, glucose, lipids and angiotensin II (Ang II) as well as glucose tolerance. In situ hybridization was used to measure brainstem expression of tyrosine hydroxylase (TH) and Ang AT1a mRNA. RESULTS: Fructose diet (8 weeks) produced an increase in MAP, variance and low frequency domain (14+/-3 vs. 33+/-4 mm Hg(2), variance and 10+/-2 vs. 26+/-4 mm Hg(2), LF, control vs. fructose, P<0.01). The changes occurred only at night, a period of activity for mice. Glucose tolerance was attenuated in the fructose group. Fructose also increased plasma cholesterol (80+/-1 vs. 126+/-2 mg/dl, control vs. fructose, P<0.05) and plasma Ang II (18+/-5 vs.65+/-12 pg/ml, control vs. fructose, P<0.05). Depressor responses to alpha(1)-adrenergic blockade with prasozin were augmented in fructose-fed mice. Using quantitative in situ hybridization, we found that Ang AT1a receptor and TH mRNA expression were significantly increased in the brainstem locus coeruleus. CONCLUSION: A high fructose diet in mice produced nocturnal hypertension and autonomic imbalance which may be related to activation of sympathetic and angiotensin systems.

Adrenergic alpha-Antagonists↗
PubMed2005

Improvement of insulin resistance by panax ginseng in fructose-rich chow-fed rats.

In an attempt to probe a new target for handling insulin resistance, we used Panax ginseng root to screen the effect on insulin resistance induced by fructose-rich chow in rats. Insulin action on glucose disposal rate was measured using the glucose-insulin index, which is the product of the areas under the curve of glucose and insulin during the intraperitoneal glucose tolerance test. Oral administration of Panax ginseng root (125.0 mg/kg) into rats three times daily for three days after receiving fructose-rich chow for four weeks reversed the increased glucose-insulin index, indicating that Panax ginseng root has the ability to improve insulin sensitivity. In addition, the plasma glucose concentrations in rats repeatedly treated with Panax ginseng root were not elevated as markedly as those of the vehicle-treated group during the fructose-rich chow-feeding period. Also, the time in which the plasma glucose-lowering response to tolbutamide (10.0 mg/kg, i. p.) receded in fructose-rich chow fed rats was markedly delayed by repeated Panax ginseng root treatment compared to the vehicle-treated group. The plasma glucose-lowering activity of tolbutamide is believed to depend on the secretion of endogenous insulin, which is widely used as an indicator of insulin resistance development. Thus, it provided supportive data that oral administration of Panax ginseng root could delay the development of insulin resistance in rats. In conclusion, our results suggest that oral administration of Panax ginseng root improves insulin sensitivity and may be used as an adjuvant therapy for treating diabetic patients with insulin resistance.

Animals↗