SEARCH · Search PubMed

Results for “fructose”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 505 records · Page 28Linked to original sources

PubMed1976

Comparative effects of fructose and glucose on the lipid and carbohydrate metabolism of perfused rat liver.

1. Livers from rats fed on a standard diet were perfused with whole blood, and infused continuously with glucose and fructose at equimolar rates. 2. Infusion of fructose increased both the secretion of very-low-density-lipoprotein (VLDL)-triglycerides and the incorporation of free fatty acids (FFA) from the perfusate into VLDL-lipids, but neither of these two processes was affected by infusion of glucose. 3. Infusion of fructose decreased the oxidation and increased the esterification of FFA, but glucose infusion had no effect on these processes. When fructose and glucose were infused together was a further decrease in oxidation. 4. When fructose was infused alone or together with glucose, blood concentrations rapidly became stabilized at those found in the hepatic portal vein in vivo, with similar rates of hepatic uptake to those found in the intact animal. Infusion of glucose alone resulted in continuously increasing perfusate glucose concentrations, and rates of uptake which were only 20% of those for fructose. Blood glucose concentrations were reduced, and lactate concentrations were increased by fructose infusion, and when glucose and fructose were infused together there was a greatly increased rate of glucose uptake. 5. Liver glycogen was not affected by the infusion of fructose or glucose alone; however, their combined addition significantly increased its concentration. 6. Uptake of perfusate FFA was not affected by either fructose or glucose infusions. 7. The results are discussed in terms of the differences in nutrition and metabolism between glucose and fructose, with particular reference to the development of hypertriglyceridaemia.

Animals↗

PubMed1987

Effects of fructose, levamisole and vanadate on insulin action in rat adipose tissue.

The effects of dietary fructose, levamisole and vanadate on insulin-stimulated conversion of D-[U-14C]glucose to 14CO2 and to 14C-labeled lipid were examined in rat epididymal adipose tissue. Male weanling rats were fed isoenergetic diets containing either 27% (wt/wt) fructose or glucose for 11 wk. During the final 4 wk, rats in each group were either untreated (control) or treated orally with 20 mg/kg body wt levamisole or 0.5 ppm vanadate via their drinking water. Basal glucose oxidation to CO2 was 45% higher in the fructose-control than in the glucose-control group. Insulin-stimulated glucose oxidation in both control groups was not higher than the basal rate in fructose-fed rats. Basal lipogenesis was 31% lower in the fructose-control than in the glucose-control group. Insulin-stimulated lipogenesis was much higher than basal, but was not different between fructose- and glucose-control groups. Levamisole increased basal lipogenesis in fructose-fed rats. Vanadate acted synergistically with fructose in greatly diminishing insulin-stimulated glucose oxidation. Fasting plasma insulin levels were lower and fasting plasma glucose and triglycerides were higher in fructose- than in glucose-fed rats, irrespective of treatment. Results suggest that adaptation to dietary fructose enhances basal oxidative capacity in an insulin-like fashion and reduces the basal lipogenic capacity of adipose tissue. Treatment with levamisole and vanadate lowers the overall rate of glucose metabolism and alters the effects of fructose.

Adipose Tissue↗

PubMed2005

Fructose selectively modulates c-jun N-terminal kinase activity and insulin signaling in rat primary hepatocytes.

Fructose is a unique nutrient, due in part to its selective metabolism in the liver. Diets enriched in fructose or sucrose induce a hepatic stress response characterized by activation of c-jun N-terminal kinase. The aim of this study was to examine the regulation of c-jun N-terminal kinase by fructose in rat primary hepatocytes. Fructose was provided to rat primary hepatocytes using a fructose regenerating system, consisting of inulin and inulinase. This system provides a more physiologic delivery of fructose and avoids large disturbances in hepatocyte ATP concentrations. Fructose delivery increased c-jun N-terminal kinase activity and serine 307 phosphorylation of insulin receptor substrate-1 and reduced tyrosine phosphorylation of insulin receptor substrate-1. Activation of c-jun N-terminal kinase was maximal at a fructose concentration of 0.6 mmol/L. Fructose delivery did not increase the phosphorylation of p38 mitogen-activated protein kinase, extracellular signal regulated kinase, c-jun, or activating transcription factor-2, the latter 2 downstream nuclear targets of c-jun N-terminal kinase. However, fructose delivery increased the phosphorylation of mitogen-activated protein kinase kinase-7 (MKK7), an upstream activator of c-jun N-terminal kinase, and the association of c-jun N-terminal kinase with c-jun N-terminal kinase-interacting protein-1, a scaffold protein that can sequester protein signaling complexes in the cytosol. These data suggest that fructose may selectively activate c-jun N-terminal kinase via regulation of MKK7 and scaffold proteins.

Animals↗

PubMed1990

Metabolic effects of dietary fructose.

Fructose, a naturally occurring hexose, is a component of many fruits, vegetables, and sweeteners. Because of the introduction of high fructose corn sweeteners in 1967, the amount of free fructose in the diet of Americans has increased substantially in the last 20 years. Fructose is sweeter, more soluble, and less glucogenic than glucose or sucrose, so it has been recommended as a replacement for these sugars in the diets of diabetic and obese people. Although an acute dose of fructose causes smaller increases in glucose and insulin than a comparable dose of glucose, there are a number of changes after dietary adaptation that may reduce its desirability as a sugar replacement in certain segments of the population. Fructose is absorbed primarily in the jejunum and metabolized in the liver. When consumed in excess of dietary glucose, it may be malabsorbed. Fructose is more lipogenic than glucose or starches, and usually causes greater elevations in triglycerides and sometimes in cholesterol than other carbohydrates. Dietary fructose has resulted in increases in blood pressure, uric acid, and lactic acid. People who are hypertensive, hyperinsulinemic, hypertriglyceridemic, non-insulin-dependent diabetic, or postmenopausal are more susceptible to these adverse effects of dietary fructose than healthy young subjects. Although consumption of fructose as a component of fruits and vegetables is an unavoidable consequence of eating a healthy diet, added fructose seems to provide little advantage over other caloric sweetners and compares unfavorably to complex carbohydrates in susceptible segments of the population.

Animals↗

PubMed1993

Conversion of fructose to glucose in the rabbit small intestine. A reappraisal of the direct pathway.

Gopher et al [Gopher, A., Vaisman, N., Mandel, H. & Lapidot, A. (1990) Proc. Natl Acad. Sci. USA 87, 5449-5453] recently reported that about 50% of the glucose formed from [U-13C]fructose infused nasogastrically in children contained 13C3 adjacent to 13C4. Assuming a high isotopic dilution of the triosephosphate pool, the authors concluded that about 50% of the fructose converted to glucose in liver and intestine bypassed the classical aldolase pathway, utilizing a hypothetical direct pathway that would involve the phosphorylation of fructose 1-phosphate to fructose 1,6-bisphosphate. The present work was undertaken in order to establish to what extent the conversion of fructose to glucose in the intestine could account for this unexpected isotopic distribution. The technique of everted sleeves was used to define the rate of conversion of [U-14C]glucose and [U-14C]fructose in the small intestine of 24-h-fasted rabbits. It appeared that, at the low concentration of fructose used by Gopher et al., almost as much fructose was converted to glucose as remained unmodified in the tissue. Fructose uptake was not inhibited by glucose, and the presence of all the necessary enzymes in the tissue indicated that the fructose to glucose conversion occurred by the aldolase pathway. Remarkably, this conversion operated with an isotopic dilution not exceeding 25%, due to the low rate of glucose metabolism and the near absence of gluconeogenesis from lactate. It can, therefore, be postulated that, in the presence of pure [U13C]fructose, the triosephosphate pool is highly enriched in 13C with little dilution by 12C, essentially giving rise to [U-13C]glucose, as reported by Gopher et al. There is, therefore, no need to postulate the participation of a direct pathway.

Animals↗

PubMed2004

The effect of high-fat and high-fructose diets on glucose tolerance and plasma lipid and leptin levels in rats.

AIM: High-fat and high-fructose diets are usually used to induce animal model diabetes mellitus. The purposes of this research were to compare the abnormalities of glucose metabolism caused by high-fructose diet and a high-fat diet and the effects of the high-fructose diet and high-fat diet on plasma leptin. METHODS: In this research, 24 Sprague-Dawley rats were used as the experimental animals, which were divided into three groups: chow diet (control group), high-fructose diet (60% fructose w/w) and high-fat diet (20% lard w/w). They were fed for a period of 8 weeks, during which an oral glucose tolerance test was conducted in the seventh week, and after completion of the eighth week, the abdominal adipose tissue and liver of the rats were excised and weighed, and the plasma cholesterol, triglyceride, insulin and leptin concentrations were assayed. RESULTS: The high-fat diet group presented a fasting blood glucose concentration that was higher than that of the control group. Furthermore, after 2 h of glucose challenge, the rats in the high-fat and high-fructose diet groups all presented higher plasma glucose concentrations than did the control group. The high-fat diet group showed higher body weight, higher relative liver weight, a higher plasma cholesterol concentration and higher amylase activity than did the other groups, whereas the high-fructose diet group showed higher fasting insulin and triglyceride concentrations. As for adipose tissue, the high-fat diet group presented an amount that was higher than that of the high-fructose and control groups, but the plasma leptin concentration of the high-fructose group was higher than that of the control group. CONCLUSIONS: It can be concluded from the above-mentioned experimental results that a high-fructose diet can cause hyperinsulinaemia, while a high-fat diet can result in impaired pancreatic function of insulin secretion and glucose intolerance, indicating that high-fructose diet and a high-fat diet may exert divergent effects on glucose metabolism in rats.

3-Hydroxybutyric Acid↗

PubMed2006

Oral treatment and in vitro incubation with fructose modify vascular prostanoid production in the rat.

1.-- In the rat, a fructose-enriched diet induces hyperglycaemia, hypertriglyceridaemia, insulin resistance and hypertension; a model which resembles the human metabolic syndrome. 2.-- Prostanoids, metabolites of arachidonic acid, include vasoactive substances synthesized and released from the vascular wall that have been implicated in the increase of peripheral resistance, one of the mechanisms involved in the fructose-induced hypertension. 3.-- The aim of the present study was to: (i) analyse the effects of the in vitro incubation with fructose on the production and release of prostanoids in rat thoracic aorta and in rat mesenteric bed and (ii) compare the effects of incubation with those of the in vivo acute and chronic treatment of rats with fructose and with the combination of both in vivo and in vitro procedures. 4.-- Blood pressure, glycaemia and triglyceridaemia were significantly elevated in both 4- and 22-week fructose-treated groups. Meanwhile, body and heart weight as well as insulinaemia were similar between experimental animals and controls. 5.-- In aortae, 4 weeks of Fructose treatment did not modify the prostanoid pattern release, but in vitro incubation decreased prostacyclin (PGI(2)) production. However, after 22 weeks, fructose treatment and incubation exerted the same effect. 6.-- In mesenteric bed, after 4 weeks, the incubation and the combination of both procedures reduced the release of the vasodilators PGI(2) and PGE(2), while fructose treatment only diminished the PGE(2) release. On the contrary, the production of the vasoconstrictor thromboxane A(2) (TXA(2)) was enhanced by incubation and both the procedures. After 22 weeks, fructose treatment increased PGI(2) release, while it was reduced by incubation. The combination of both did not modify this peripheral resistance when compared with controls. Finally, incubation of tissues from treated rats increased the release of the vasoconstrictors, PGF(2alpha) and TXA(2). 7.-- In conclusion, the mesenteric bed, a resistance vascular bed, seems to be more sensitive than the aorta, a conductance vessel, to the effects of fructose on prostanoid production. This difference could be related to a more relevant role of resistance vessels in the regulation of peripheral resistance and consequently of blood pressure. The observed effects should contribute to a shift in the balance of the release of prostanoid in favour of vasoconstrictor metabolites. This phenomenon could be related to an increase in the peripheral resistance and the mild hypertension observed in the fructose-treated rats.

6-Ketoprostaglandin F1 alpha↗

PubMed1974

Metabolic consequences of a block in the synthesis of 5-keto-D-fructose in a mutant of Gluconobacter cerinus.

A mutant of Gluconobacter cerinus var. ammoniacus, IFO 3267, has been isolated which is deficient with respect to fructose 5-dehydrogenase, the enzyme catalyzing the oxidation of d-fructose to 5-keto-d-fructose (5 KF). Growth of this mutant on fructose as the sole carbon source was impaired unless the culture medium was supplemented with 5 KF. Significant randomization of the 1 and 6 positions of fructose has been reported previously for the wild-type organism during growth on this ketohexose. The pattern of (3)H incorporation into the C5 position of ribonucleic acid-ribose when the mutant was grown on [1-(3)H]fructose and [6-(3)H]fructose in the presence of 5 KF indicated that such randomization did not occur in this variant. The randomization observed in the wild type is, therefore, a consequence of the partial oxidation of fructose to the symmetrical 5 KF intermediate prior to its conversion to pentose. When the mutant was grown on [1-(3)H]fructose in the presence of unlabeled 5 KF, [5-(3)H]fructose appeared in the culture medium. Thus, 5 KF served as the oxidant for the nicotinamide adenine dinucleotide phosphate, reduced form, generated during growth on fructose.

Alcohol Oxidoreductases↗

PubMed1987

Regulation of fructose uptake and catabolism by succinate in Azospirillum brasilense.

Fructose uptake and catabolism in Azospirillum brasilense is dependent on three fructose-inducible enzymes (fru-enzymes): (i) enzyme I and (ii) enzyme II of the phosphoenolpyruvate:fructose phosphotransferase system and (iii) 1-phosphofructokinase. In minimal medium containing 3.7 mM succinate and 22 mM fructose as sources of carbon, growth of A. brasilense was diauxic, succinate being utilized in the first phase of growth and fructose in the second phase with a lag period between the two growth phases. None of the fru-enzymes could be detected in cells grown with succinate as the sole source of carbon, but they were detectable toward the end of the first phase of diauxie. All the fru-enzymes were coinduced by fructose and coordinately repressed by succinate. Studies on the effect of succinate on differential rates of syntheses of the fru-enzymes revealed that their induced syntheses in fructose minimal medium were subject to transient as well as permanent (catabolite) repression by succinate. Succinate also caused a similar pattern of transient and permanent repression of the fructose transport system in A. brasilense. However, no inducer (fructose) exclusionlike effect was observed as there was no inhibition of fructose uptake in the presence of succinate with fructose-grown cells even when they were fully induced for succinate uptake activity.

Culture Media↗

PubMed1986

Absorption capacity of fructose in healthy adults. Comparison with sucrose and its constituent monosaccharides.

The capacity to absorb fructose in 10 healthy adults was investigated by means of hydrogen breath analysis. Fructose absorption was quantified with lactulose standards. Significant hydrogen production (greater than or equal to 20 ppm rise of breath hydrogen) was found after challenge with 10% solutions of 50, 37.5, 25, 20, and 15 g fructose in eight, seven, five, four and one subjects, respectively. One subject showed malabsorption after a 10 g dose and possibly also 5 g fructose. In contrast, no malabsorption could be detected in any of the 10 subjects after ingestion of 100 g, 75 g, or 50 g sucrose or a mixture of 50 g glucose and 50 g fructose. After ingestion of mixtures of 50 g fructose +25 g glucose and 50 g fructose +12.5 g glucose malabsorption was present in three and seven subjects, respectively. Symptoms during all challenges were mild, or absent. It is concluded that in the healthy state the absorption capacity of fructose given alone ranges from less than 5 g to more than 50 g. The absorption capacity of fructose given as sucrose is much higher. Glucose stimulates fructose uptake in a dose dependent fashion. The possible existence of more than one intestinal transport system for fructose is considered. The elucidation of the clinical relevance of the findings is important.

Adult↗

PubMed1984

Metabolic effects of oral fructose in the liver of fasted rats.

Twenty-four-hour-fasted rats were given fructose (4 g/kg) by gavage. Fructose absorption and the portal vein, aorta, and hepatic vein plasma fructose, glucose, lactate, and insulin concentrations as well as liver fructose and fructose 1-P, glucose, glucose 6-P, UDPglucose, lactate, pyruvate, ATP, ADP, AMP, inorganic phosphate (Pi), cAMP, and Mg2+, and glycogen synthase I and phosphorylase alpha were measured at 10, 20, 30, 40, 60 and 120 min after gavage. Liver and muscle glycogen and serum uric acid and triglycerides also were measured. Fifty-nine percent of the fructose was absorbed in 2 h. There were modest increases in plasma and hepatic fructose, glucose, and lactate and in plasma insulin. Concentrations in the portal vein, aorta, and hepatic vein plasma indicate rapid removal of fructose and lactate by the liver and a modest increase in production of glucose. The source of the increase in plasma lactate is uncertain. Hepatic glucose 6-P increased twofold; UDPglucose rose transiently and then decreased below the control level. Fructose 1-P increased linearly to a concentration of 3.3 mumol/g wet wt by 120 min. There was no change in ATP, ADP, AMP, cAMP, Pi, or Mg2+. Serum triglycerides and uric acid were unchanged. Glycogen synthase was activated by 20 min without a change in phosphorylase alpha. This occurred with a fructose dose that did not significantly increase either the liver glucose or fructose concentrations. Liver glycogen increased linearly after 20 min, and glycogen storage was equal in liver (38.4%) and muscle (36.5%).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

PubMed1993

Whole body and splanchnic oxygen consumption and blood flow after oral ingestion of fructose or glucose.

The contribution of the splanchnic tissues to the initial 2-h rise in whole body energy expenditure after ingestion of glucose or fructose was examined in healthy subjects. Indirect calorimetry and catheter techniques were employed to determine pulmonary gas exchange, cardiac output, splanchnic blood flow, splanchnic oxygen uptake, and blood temperatures before and for 2 h after ingestion of 75 g of either fructose or glucose in water solution or of water only. Fructose ingestion was found to increase total oxygen uptake by an average of 9.5% above basal levels; the corresponding increase for glucose was 8.8% and for water only 2.5%. The respiratory exchange ratio increased from 0.84 in the basal state to 0.97 at 45 min after fructose ingestion and rose gradually after glucose to 0.86 after 120 min. The average 2-h thermic effect, expressed as percent of ingested energy, was 5.0% for fructose and 3.7% for glucose (not significant). Splanchnic oxygen consumption did not increase measurably after ingestion of either fructose or glucose. The arterial concentration of lactate rose, arterial pH fell, and PCO2 remained essentially unchanged after fructose ingestion. Glucose, but not fructose, elicited increases in cardiac output (28%) and splanchnic blood flow (56%). Fructose, but not glucose, increased arterial blood temperature significantly. It is concluded that both fructose and glucose-induced thermogenesis occurs exclusively in extrasplanchnic tissues. Compared with glucose, fructose ingestion is accompanied by a more marked rise in CO2 production, possibly reflecting an increased extrasplanchnic oxidation of lactate and an accumulation of heat in the body.

Adult↗

PubMed2004

Dietary lipids modify the age-associated changes in intestinal uptake of fructose in rats.

Because reduced nutrient absorption may contribute to malnourishment in the elderly, age and diet modulate fructose uptake in mice, and alterations in fructose uptake may be paralleled by changes in the abundance of fructose transporters, the objectives of this study were to determine 1) the effects of aging on fructose absorption in rats, 2) the effect of feeding diets enriched with saturated fatty acids (SFA) vs. polyunsaturated fatty acids (PUFA), and 3) the mechanisms of these age-and diet-associated changes. Male Fischer 344 rats aged 1, 9, and 24 mo received isocaloric diets enriched with SFA or PUFA. The uptake of (14)C-labeled D-fructose was determined in vitro using the intestinal sheet method. Northern and Western blot analyses and immunohistochemistry were used to determine the abundance of sodium-independent glucose and fructose transporters (GLUT)2 and GLUT5. When expressed on the basis of mucosal surface area, jejunal fructose uptake was increased in 9 and 24 mo compared with 1-mo-old animals fed SFA. PUFA-fed animals demonstrated increased fructose uptake at 24 mo compared with younger animals. Ileal fructose uptake was increased with SFA vs. PUFA in 9-mo-old rats but was reduced with SFA in 1- and 24-mo-old rats. Variations in GLUT2 and GLUT5 abundance did not parallel changes in uptake. These results indicate that 1) age increases fructose uptake when expressed on the basis of mucosal surface area, 2) age influences the adaptive response to dietary lipid modifications, and 3) alterations in fructose uptake are not explained by variations in GLUT2 or GLUT5.

Absorption↗

PubMed2004

Effect of imidapril, an angiotensin-converting enzyme inhibitor, on fructose-induced insulin resistance in rats.

The effect of imidapril, an angiotensin-converting enzyme (ACE) inhibitor, on insulin resistance was studied in high-fructose-fed rats. A sequential hyperinsulinemic euglycemic clamp procedure (insulin infusion rates: 3 and 30 mU/kg BW/min) was employed in 15 high-fructose-fed rats and 10 normal chow-fed rats under the awake condition. Five of the high-fructose-fed and five of the normal chow-fed rats, respectively, were continuously given imidapril (5 mg/kg BW/min) or saline during the two-step euglycemic clamp study. Furthermore, both imidapril and L-NMMA were infused in another 5 high-fructose-fed rats during the low-dose insulin clamp. Glucose infusion rate (GIR) was regarded as an index of the whole-body insulin action. In the low-dose insulin infusion, the high-fructose feeding resulted in a marked decrease in GIR (p<0.05). Imidapril infusion significantly raised the GIRs in the high-fructose-fed rats (p<0.05). There was no significant difference in GIRs between the chow-fed rats and the imidapril-infused rats with high-fructose diet. In the high-fructose-fed rats, L-NMMA abolished the increase in GIR induced by imidapril (p<0.05). Imidapril did not significantly change the GIRs in the chow-fed rats. In the high-dose insulin infusion, no significant difference in GIR was found among the chow-fed rats, the chow-fed rats given imidapril, the high-fructose-fed rats, and the high-fructose-fed rats given imidapril. These results suggest that, in insulin-resistant rats induced by the high-fructose feeding, an ACE inhibitor, such as imidapril, can improve the whole-body insulin-mediated glucose disposal and that this effect of imidapril is essentially linked to increased activation of NO-pathway.

Administration, Oral↗

PubMed2002

Fructose amplifies counterregulatory responses to hypoglycemia in humans.

Glucokinase (GK) is required for cellular glucose sensing, although there is a paucity of data regarding its role in the counterregulatory response to hypoglycemia in humans. Because fructose has been shown to modulate GK activity, we examined the effects of an acute infusion of fructose on hypoglycemia counterregulation in seven lean nondiabetic subjects. Using stepped hypoglycemia clamp studies (5.0, 4.4, 3.9, and 3.3 mmol/l target plasma glucose steps, 50 min each), subjects were studied on two separate occasions, without (control) or with co-infusion of fructose (1.2 mg.kg(-1).min(-1)). Fructose induced a resetting of the glycemic thresholds for secretion of epinephrine (3.8 +/- 0.1 mmol/l) and glucagon (3.9 +/- 0.2 mmol/l) to higher plasma glucose concentrations (4.0 +/- 0.1 mmol/l [P = 0.006] and 4.1 +/- 0.1 mmol/l [P = 0.03], respectively). In addition, the magnitude of increase in epinephrine and glucagon concentrations was higher after administration of fructose (48 and 39%, respectively, P < 0.05 for both). The amplification of these hormonal responses was specific because plasma norepinephrine, growth hormone, and cortisol were comparable in both sets of studies. Endogenous glucose production, measured with [3-(3)H]glucose, increased by 47% (P < 0.05) in the fructose infusion studies compared with 14% (P = NS) in the control studies. In addition, glucose uptake was more suppressed with fructose infusion (by 33%, P < 0.05). In concert with these effects of fructose on glucose kinetics, average glucose infusion rate was markedly reduced in the fructose infusion studies during the 3.9-mmol/l glucose step (4.6 +/- 0.9 vs. 7.4 +/- 1.1 micromol.kg(-1).min(-1), respectively, P = 0.03) and during the 3.3-mmol/l glucose step (0.5 +/- 0.1 vs. 5.2 +/- 1.2 micromol.kg(-1).min(-1), respectively, P < 0.001), suggesting more potent glucose counterregulation and improved recovery from hypoglycemia with fructose infusion. We conclude that infusion of a catalytic dose of fructose amplifies the counterregulatory response to hypoglycemia by both increases in hormonal activation and augmentation of glucose counterregulation in humans.

Adult↗

PubMed1989

Metabolic effects of fructose supplementation in diabetic individuals.

With new diabetes diet guidelines recommending high carbohydrate intake, questions arise regarding acceptable intake of simple sugars. Whereas several short-term studies report flattened glycemic and insulin response to fructose consumption, some also report increased serum triglyceride levels. Few studies examine the effects of long-term fructose consumption. We evaluated the long-term safety of fructose consumption in 14 middle-aged men with diabetes. Subjects followed an ambulatory high-fiber high-carbohydrate control diet at home for 8 wk, entered the hospital for 5 days on this diet, and spent the next 7 days on a similar diet supplemented with 50-60 g fructose. They continued the fructose diet at home for 23 wk, then resumed a postcontrol diet for an additional 16 wk. In the hospital, glycemic control improved significantly on the fructose-supplemented diet compared with the hospital control diet. In the ambulatory setting, no significant differences in plasma glucose, glycohemoglobin, serum cholesterol, triglycerides, lactate, or urate occurred between precontrol, fructose, or postcontrol periods. Fasting serum lactate was higher by 0.5 meq/L during the ambulatory fructose period than during the precontrol period. Body weight also increased during the ambulatory fructose period due to higher calorie intake. Adherence to fructose consumption was excellent and improved adherence to carbohydrate and fat recommendations. If total calorie intake is controlled to promote desirable body weight, crystalline fructose used with a high-carbohydrate high-fiber low-fat diet appears to be safe and acceptable for diabetic individuals.

Blood Glucose↗

PubMed2002

Increased fructose concentrations in blood and urine in patients with diabetes.

OBJECTIVE: To investigate fructose metabolic changes in patients with diabetes. RESEARCH DESIGN AND METHODS: Serum and urinary fructose concentrations were determined in healthy subjects (n = 23) and in nondiabetic (n = 23) and diabetic patients (n = 26). Fructose was measured using our newly developed method, and (13)C(6)-fructose was used as the internal standard. After adding sample to a fixed amount of internal standard, ion-exchange resins and high-performance liquid chromatography pretreatments were performed. Then, the amount of fructose in the sample was measured by gas chromatography-mass spectrometry. RESULTS: Serum fructose concentrations in patients with diabetes (12.0 +/- 3.8 micromol/l) were significantly higher than those in healthy subjects (8.1 +/- 1.0 micromol/l, P < 0.001) and nondiabetic patients (7.7 +/- 1.6 micromol/l, P < 0.001), and daily urinary fructose excretion was significantly greater in patients with diabetes (127.8 +/- 106.7 micromol/day) than in nondiabetic patients (37.7 +/- 23.0 micromol/day, P < 0.001). In patients with diabetes (n = 20), serum fructose concentrations (8.6 +/- 1.8 micromol/l, P < 0.001) and daily urinary fructose excretion (63.4 +/- 63.8 micromol/day, P < 0.01) significantly decreased by week 2 after admission. CONCLUSIONS: The present results differed from those of previous studies in that we found that the serum and urinary fructose concentrations decreased rapidly, concomitant with an improvement in glycemia. Therefore, hyperglycemia was associated with increased serum and urinary fructose concentrations in patients with diabetes.

Adult↗

PubMed2004

Metabolism of 13C-enriched D-fructose in hepatocytes from Goto-Kakizaki rats.

This study aims at assessing the conversion of exogenous D-[1-13C]fructose, D-[2-13C]fructose or D-[6-13C]-fructose (10 mM) to 13C-enriched and either hydrogenated or deuterated D-glucose, L-lactate and L-alanine released by rat liver cells prepared from Goto-Kakizaki rats and incubated for 120 min in the presence of unlabelled D-glucose (also 10 mM) and D2O. The results of this study are relevant to the relative contribution of fructokinase and hexokinase isoenzyme to the phosphorylation of D-fructose, the capacity of D-glucose to confer to glucokinase positive cooperativity towards D-fructose, the circulation of D-fructose 6-phosphate in the pentose phosphate pathway, the regulation of the cytosolic NADD/NADH ratio, the respective fate of D-fructose-derived D-glyceraldehyde and dihydroxyacetone phosphate, the deuteration of fructose-derived glycolytic intermediates at the phosphoglucoisomerase, phosphomannoisomerase, enolase, pyruvate kinase and glutamate-alanine transaminase levels, and the unequal generation of L-[1-13C]lactate by cells exposed to D-[1-13C]fructose or D-[6-13C]fructose versus D-[2-13C]-fructose.

Alanine↗