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PubMedDate not supplied

Fructose-enriched diet modifies antioxidant status and lipid metabolism in spontaneously hypertensive rats.

OBJECTIVE: High-fructose consumption in industrial countries has been shown to induce metabolic abnormalities or syndrome X. Changes in antioxidant defense are unknown in hypertension associated with metabolic disorders induced by high-fructose feeding. METHODS: Twenty spontaneously hypertensive rats were assigned to one of two groups; one received a fructose-enriched diet (60% fructose) and the other a starch diet. After a 13-wk diet period, total antioxidant status was assessed in the blood and liver by monitoring the rate of free radical-induced red blood cell hemolysis. Antioxidants (enzymes and vitamins) were determined in blood and liver. Gene expression of antioxidant enzymes (copper/zinc superoxide dismutase and glutathione peroxidase) were also investigated in hepatic tissue. RESULTS: Fructose-fed rats showed blood pressure values similar to that of control rats but had increased glycemia and insulinemia. The antioxidant capacity in the blood of the fructose-fed group represented by copper/zinc superoxide dismutase and glutathione peroxidase activities and ascorbic acid was lower. However, the fructose diet enhanced the total antioxidant capacity of liver correlated with increased antioxidant enzyme activities and retinol concentrations. Gutathione peroxidase mRNA expression was decreased in livers of spontaneously hypertensive rats fed the fructose diet. CONCLUSION: Fructose feeding negatively affects antioxidant capacity in the blood of hypertensive rats but improves this capacity in the liver.

Animals↗
PubMed1999

Effects of oral fructose and glucose on plasma GLP-1 and appetite in normal subjects.

Oral glucose is a potent stimulant of glucagon-like peptide-1 (GLP-1) secretion. The effect of oral fructose on GLP-1 secretion in humans is unknown. The aims of this study were to determine (i) whether oral fructose stimulates GLP-1 secretion and (ii) the comparative effects of oral glucose and fructose on appetite. On 3 separate days, 8 fasting healthy males received, in single-blind randomized order (i) 75 g glucose, (ii) 75 fructose, or (iii) 75 g glucose followed by 75 g fructose I h later. Venous glucose, insulin and GLP-1 were measured. Appetite was assessed by visual analog questionnaires and intake of a buffet meal. Whereas glucose and fructose both increased plasma glucose, insulin and GLP-1 (P < 0.000)] for all), the response to glucose was much greater (P < 0.005 for all). There was no increase in plasma GLP-1 when fructose was given after glucose. There was no difference in food intake after oral glucose or fructose. We conclude that oral fructose (75 g) stimulates GLP-1 (and insulin) secretion, but the response is less than that to 75 g glucose. These observations suggest that neither GLP-1 nor insulin play a major role in the regulation of satiation.

Adult↗
PubMed1997

Effect of ethanol and fructose on liver metabolism: a dynamic 31Phosphorus magnetic resonance spectroscopy study in normal volunteers.

In vivo 31Phosphorus magnetic resonance spectroscopy (31P-MRS) permits evaluation of dynamic changes of individual phosphorus-containing metabolites in the liver parenchyma, such as phosphomonoester (PME), adenosine triphosphate, and inorganic phosphate (Pi). Intravenous fructose load alters phosphorus metabolites and allows assessment of liver function by 31P-MRS. 31P-MRS data obtained in alcoholic liver disease are however inconclusive. To study the hypothesis that fructose load can be used to investigate metabolic effects of ethanol ingestion, the interaction of different metabolites--i.e., fructose and ethanol--were followed in vivo. Using a 1.5 Tesla magnetic resonance system, six healthy volunteers were examined in three sessions each: a session after administration of (a) fructose only (250 mg/kg) was compared with (b) fructose load after ethanol ingestion (0.8 g/kg). A control experiment (c) was done after ethanol only. Spectra were acquired using one-dimensional chemical shift imaging with a temporal resolution of 5 min. Following a fructose load, the concomitant uptake of ethanol showed drastic changes of individual metabolic steps of the hepatic metabolism (averages +/- standard deviation). While the velocity of the net formation of PME (relative increase 0.46 +/- 0.11 without ethanol vs. 0.61 +/- 0.25 with ethanol) and the use of adenosine triphosphate (-0.13 +/- 0.03 vs. -0.16 +/- 0.03) and Pi (-0.022 +/- 0.009 vs. -0.021 +/- 0.004) were not significantly affected by ethanol uptake, a significant (p < 0.01) reduction of PME degradation (31.3 +/- 9.4 vs. 61.9 +/- 16.9 relative total area) and absence of an overshoot for Pi (10.5 +/- 4.9 vs. -7.1 +/- 5.3 relative area 13 min to 43 min) was observed after ethanol administration. Dynamic 31P-MRS allows the observation of individual steps of hepatic metabolism in situ; fructose metabolism in the human liver is slowed down by concomitant ethanol ingestion after the phosphorylation step of fructose. This could be explained by inhibition of aldolase rather than ethanol-induced changes of the hepatic redox state. Fructose load can be used to study effects of alcohol ingestion and might therefore be useful in patients with alcoholic liver disease.

Adenosine Triphosphate↗
PubMed1990

An investigation of fructose utilization in Acanthocheilonema viteae.

The capacity of Acanthocheilonema viteae to metabolize fructose was investigated in vitro. In common with other filarial species A. viteae oxidized fructose to lactate but its rate of consumption was only 40% of the glucose-containing control value. Fructose was not incorporated into glycogen. Release of 14CO2 from [U-14C]fructose was not detected in the presence of glucose and was about 40% of the glucose-containing value under conditions where fructose was the sole hexose substrate. Fructose consumption and lactate excretion increased in proportion to the external concentration of fructose. However, worm viability was not maintained in fructose over a 120 h in vitro incubation. In the presence of fructose, protein synthesis (measured incorporation of [35S]methionine into acid-insoluble material) was reduced compared to the glucose-containing control group; but was significantly greater than the value obtained under glucose-free conditions.

Animals↗
PubMed1967

The activities of fructose 1,6-diphosphatase, phosphofructokinase and phosphoenolpyruvate carboxykinase in white muscle and red muscle.

1. The activities of fructose 1,6-diphosphatase were measured in extracts of muscles of various physiological function, and compared with the activities of other enzymes including phosphofructokinase, phosphoenolpyruvate carboxykinase and the lactate-dehydrogenase isoenzymes. 2. The activity of phosphofructokinase greatly exceeded that of fructose diphosphatase in all muscles tested, and it is concluded that fructose diphosphatase could not play any significant role in the regulation of fructose 6-phosphate phosphorylation in muscle. 3. Fructose-diphosphatase activity was highest in white muscle and low in red muscle. No activity was detected in heart or a deep-red skeletal muscle, rabbit semitendinosus. 4. The lactate-dehydrogenase isoenzyme ratio (activities at high and low substrate concentration) was measured in various muscles because a low ratio is characteristic of muscles that are more dependent on glycolysis for their energy production. As the ratio decreased the activity of fructose diphosphatase increased, which suggests that highest fructose-diphosphatase activity is found in muscles that depend most on glycolysis. 5. There was a good correlation between the activities of fructose diphosphatase and phosphoenolpyruvate carboxykinase in white muscle, where the activities of these enzymes were similar to those of liver and kidney cortex. However, the activities of pyruvate carboxylase and glucose 6-phosphatase were very low in white muscle, thereby excluding the possibility of gluconeogenesis from pyruvate and lactate. 6. It is suggested that the presence of fructose diphosphatase and phosphoenolpyruvate carboxykinase in white muscle may be related to operation of the alpha-glycerophosphate-dihydroxyacetone phosphate and malate-oxaloacetate cycles in this tissue.

Animals↗
PubMed1992

Mechanisms of fructose-induced hypertriglyceridaemia in the rat. Activation of hepatic pyruvate dehydrogenase through inhibition of pyruvate dehydrogenase kinase.

1. The effects of purified diets containing 70% glucose or 70% fructose on the activation state of hepatic pyruvate dehydrogenase (PDHa), activity of mitochondrial PDH kinase, plasma triacylglycerols (TG) and hepatic lipogenesis de novo in rats were measured. 2. Plasma TG were significantly increased in the fructose-fed compared with the glucose-fed group (125 +/- 45 mg/dl versus 57 +/- 19 mg/dl; P less than 0.002) after 3-5 weeks on the diet despite less daily food intake. 3. Hepatic PDHa in fructose-fed rats was 144% of the value in glucose-fed rats (15.4 +/- 1.2% versus 10.7 +/- 0.5%; P less than 0.002), whereas cardiac muscle PDHa was not different (45.5 +/- 6.6% versus 41.0 +/- 7.8%). 4. Intrinsic hepatic PDH kinase activity was decreased to 34% of glucose-fed values by fructose feeding (-k = 3.56 +/- 0.39 versus 10.41 +/- 1.85 min-1; P less than 0.005). 5. The fractional contribution to very-low-density-lipoprotein palmitate from hepatic lipogenesis de novo, measured by a stable-isotope mass-spectrometric method, was 10.49 +/- 2.42% (n = 8) in fructose-fed rats versus 5.55 +/- 1.38% (n = 9) in glucose-fed rats (P less than 0.05), and 2.66 +/- 2.39% (n = 3) in chow-fed rats (P less than 0.05 versus fructose-fed group). The absolute contribution to circulating TG from lipogenesis de novo was also significantly higher in the fructose-fed than in the glucose-fed group (14.9 +/- 5.1 mg/dl versus 2.9 +/- 0.6 mg/dl; P less than 0.05) 6. Portal insulin concentrations were significantly higher in the fructose-fed rats (206 +/- 49 mu-units/ml versus 81 +/- 15 mu-units/ml; P less than 0.05). 7. In conclusion, dietary fructose appears to have a specific activating effect on hepatic PDH, mediated at least in part by inhibition of PDH kinase. These results are consistent with increased flux through hepatic PDH and synthesis of new fat, not just increased re-esterification of non-esterified fatty acids.

Animals↗
PubMed1997

Investigation on the mechanism by which fructose, hexitols and other compounds regulate the translocation of glucokinase in rat hepatocytes.

In isolated hepatocytes in suspension, the effect of sorbitol but not that of fructose to increase the concentration of fructose 1-phosphate and to stimulate glucokinase was abolished by 2-hydroxymethyl-4-(4-N,N-dimethylamino-1-piperazino)-pyrimidine (SDI 158), an inhibitor of sorbitol dehydrogenase. In hepatocytes in primary culture, fructose was metabolized at approximately one-quarter of the rate of sorbitol, and was therefore much less potent than the polyol in increasing the concentration of fructose 1-phosphate and the translocation of glucokinase. In cultures, sorbitol, commercial mannitol, fructose, D-glyceraldehyde or high concentrations of glucose caused fructose 1-phosphate formation and glucokinase translocation in parallel. Commercial mannitol was contaminated by approx. 1% sorbitol, which accounted for its effects. The effects of sorbitol, fructose and elevated concentrations of glucose were partly inhibited by ethanol, glycerol and glucosamine. Mannoheptulose increased translocation without affecting fructose 1-phosphate concentration. Kinetic studies performed with recombinant human beta-cell glucokinase indicated that this sugar, in contrast with N-acetylglucosamine, binds to glucokinase competitively with the regulatory protein. All these observations indicate that translocation is promoted by agents that favour the dissociation of the glucokinase-regulatory-protein complex either by binding to the regulatory protein (fructose I-phosphate) or to glucokinase (glucose, mannoheptulose). They support the hypothesis that the regulatory protein of glucokinase acts as an anchor for this enzyme that slows down its release from digitonin-permeabilized cells.

Acetylglucosamine↗
PubMed2000

D-tagatose, a stereoisomer of D-fructose, increases blood uric acid concentration.

D-Fructose has been found to increase uric acid production by accelerating the degradation of purine nucleotides, probably due to hepatocellular depletion of inorganic phosphate (Pi) by an accumulation of ketohexose-1-phosphate. The hyperuricemic effect of D-tagatose, a stereoisomer of D-fructose, may be greater than that of D-fructose, as the subsequent degradation of D-tagatose-1-phosphate is slower than the degradation of D-fructose-1-phosphate. We tested the effect of 30 g oral D-tagatose versus D-fructose on plasma uric acid and other metabolic parameters in 8 male subjects by a double-blind crossover design. Both the peak concentration and 4-hour area under the curve (AUC) of serum uric acid were significantly higher after D-tagatose compared with either 30 g D-fructose or plain water. The decline in serum Pi concentration was greater at 50 minutes after D-tagatose versus D-fructose. The thermogenic and lactacidemic responses to D-tagatose were blunted compared with D-fructose. D-Tagatose attenuated the glycemic and insulinemic responses to a meal that was consumed 255 minutes after its administration. Moreover, both fructose and D-tagatose increased plasma concentrations of cholecystokinin (CCK) and glucagon-like peptide-1 (GLP-1). The metabolic effects of D-tagatose occurred despite its putative poor absorption.

Administration, Oral↗
PubMed2002

Acceleration by fructose of the ATP-sensitive K(+) channel-independent pathway of glucose-induced insulin secretion.

The mechanism with which fructose augments glucose-induced insulin secretion is still unclear. The present study was aimed at examining whether the ketohexose potentiates the ATP-sensitive K(+) channel-independent pathway of glucose-induced insulin secretion and, if so, how this happens. When isolated rat islets were depolarized by incubating them with 50 mM KCl in the presence of 150 microM diazoxide (an opener of ATP-sensitive K(+) channels), 10 mM glucose plus 20 mM fructose elicited significantly higher insulin secretion than 10 mM glucose alone, whereas 20 mM fructose alone did not stimulate insulin secretion. The fructose 1,6-bisphosphate and inositol trisphosphate contents were markedly higher in islets incubated with glucose plus fructose than in islets incubated with glucose alone. The results demonstrate that fructose has the ability to potentiate the ATP-sensitive K(+) channel-independent pathway of glucose-induced insulin secretion. The increase in fructose 1,6-bisphosphate content induced by the co-presence of fructose with glucose, resulting in the rise in inositol trisphosphate content, is likely to be one of the signals involved in the fructose potentiation of glucose-induced insulin secretion.

ATP-Binding Cassette Transporters↗
PubMed1981

Fructose-bisphosphatase as a substrate of cyclic AMP-dependent protein kinase.

We have tested rat liver fructose-bisphosphatase (D-fructose-1,6-bisphosphate 1-phosphohydrolase, EC 3.1.3.11) and three other gluconeogenic fructose-bisphosphatases as substrates for the catalytic subunit of cyclic AMP-dependent protein kinase. In contrast to the rat liver enzyme, homogeneous preparations of mouse liver, rabbit liver, and pig kidney fructose-bisphosphatase could not be phosphorylated by the kinase. Comparative sodium dodecyl sulfate/polyacrylamide gel electrophoresis of the four above fructose-bisphosphatases revealed that the subunit molecular weight of the isolated rat liver enzyme (ca. 40,000-42,000) was greater than that of mouse liver, rabbit liver, and pig kidney fructose-bisphosphatases (ca. 36,000-37,000). Treatment of 32P-labeled rat liver fructose-bisphosphatase with trypsin resulted in the conversion of the rat liver enzyme to an active species with a subunit molecular weight identical to that of the three other enzymes, with complete loss of the 32P-labeled site. Identical trypsin treatment of pig kidney fructose-bisphosphatase caused no change in the molecular weight of the enzyme. The results suggest that the purified mouse liver, rabbit liver, and pig kidney fructose-bisphosphatases are not substrates for the cyclic AMP-dependent protein kinase in vitro because they lack the phosphorylation-site peptide.

Animals↗
PubMed1983

Involvement of kinases in glucose and fructose uptake by Saccharomyces cerevisiae.

Uptake of glucose, fructose, and the nonmetabolizable analog 6-deoxyglucose was measured in wild-type Saccharomyces cerevisiae and two mutant strains, one (hxk1 hxk2) lacking both hexokinase A(P-I) and B(P-II) but containing glucokinase (and hence able to grow on glucose but not fructose) and the other (hxk1 hxk2 glk) also lacking glucokinase (and not able to grow on glucose either). Uptake of the nonmetabolized substances (i.e., 6-deoxyglucose in all three strains, fructose in the two mutants, and glucose in the triple mutant) reached a plateau at or below the external concentration. The kinetic characteristics of uptake were determined from 5-sec incubations by plotting velocity (V) vs. velocity/substrate concentration (V/S) curves. According to such plots, in the wild-type strain uptake had two components, "high affinity uptake" with Km values of ca. 1 mM for glucose and 6 mM for fructose and "low affinity uptake" with Km values of ca. 20 and 50 mM, respectively. The double kinase mutant showed both components for glucose but only the high Km component for fructose, while the triple kinase mutant showed only high Km uptake for both glucose and fructose. Genetic analysis showed that only in strains lacking both hexokinases (hxk1 hxk2) was the low Km system for fructose absent. Low Km uptake was restored to the triple mutant by introduction of the cloned wild-type genes: HXK1 or HXK2, for fructose uptake, and HXK1, HXK2, or GLK1, for glucose uptake. A phosphoglucose isomerase mutant had both low and high Km uptake for glucose. These results indicate the presence of two types of uptake mechanism for glucose and fructose in yeast, the functioning of one of which, the low Km system, is influenced by the cognate kinases.

Biological Transport↗
PubMed1990

The effect of various levels of fructose in a copper-deficient diet on Cu deficiency in male rats.

The present study was designed to examine the effects of various levels of fructose in a copper-deficient diet on some of the signs of Cu deficiency in the rat. Weanling male rats were randomly assigned to one of five diets which contained 0.6 micrograms Cu/g diet and 627 g carbohydrate/kg which was (g/kg): 627 fructose (diet 100); 470 fructose, 157 starch (diet 75); 313.5 fructose, 313.5 starch (diet 50); 157 fructose, 470 starch (diet 25); or 627 starch (diet 0). Rats ate their respective diets for either 2 or 5 weeks. There was a significant linear inverse response of body-weight (P less than 0.0001), packed cell volume (P less than 0.0001) and erythrocyte superoxide dismutase (EC 1.15.1.1) activity (P less than 0.008) to increasing levels of dietary fructose and a direct linear response of plasma cholesterol (P less than 0.05) and blood urea nitrogen concentrations (P less than 0.001) to increasing levels of dietary fructose. Liver, kidney and pancreatic Cu concentrations decreased in a dose-response manner as the level of dietary fructose increased. In general, if fructose was included in the diet the signs of Cu deficiency were exacerbated in a dose-response manner.

Animals↗
PubMedDate not supplied

Chromatographic separation of fructose from date syrup.

The objective of this study is to provide a process for separating fructose from a mixture of sugars containing essentially fructose and glucose, obtained from date palm fruits. The extraction procedure of date syrup from fresh dates gave a yield of 86.5% solids after vacuum drying. A process for separating fructose from an aqueous solution of date syrup involved adding the date syrup solutions (20, 30 and 40% by weight) to a chromatographic column filled with Dowex polystyrene strong cation exchange gel matrix resin Ca2 + and divinylbenzene, a functional group, sulfonic acid, particle size 320 microm, with a flow rate of 0.025 and 0.05 bed volume/min, under 30 and 70 degrees C column temperature. After the date sugar solution batch, a calculated quantity of water was added to the column. Glucose was retained by the resin more weakly than fructose and proceeded faster into the water batch flowing ahead. Three fractions were collected: a glucose-rich fraction, a return fraction, and a fructose-rich fraction. The return fraction is based on when the peaks of fructose and glucose were reached, which could be determined by means of an analyzer (polarimeter) based on the property of glucose and fructose solutions to turn the polarization level of polarized light. A high yield of fructose is obtained at 70 degrees C column temperature with a flow rate of 0.025 bed volume/min and date syrup solution containing 40% sugar concentration. The low recovery by weight obtained using date syrup solutions having a sugar concentration of 20 and 30%, encourages the use of a concentration of 40%. However, with the 40% date syrup supply the average concentrations of glucose and fructose in the return fractions were more than 40%, which can be used for diluting the thick date syrup solution extracted from dates.

Chromatography, Ion Exchange↗
PubMed1987

An insulinogenic effect of oral fructose in humans during postprandial hyperglycemia.

This study proposed to determine whether the stimulation of insulin secretion observed in humans infused with fructose when glucose levels were elevated could be observed when fructose was consumed during postprandial hyperglycemia. At 2-wk intervals, healthy volunteers consumed drinks containing glucose, starch, glucose followed 20 min later by fructose, starch followed 20 min later by fructose, and water followed 20 min later by fructose. Fructose consumption following glucose or starch drinks produced significantly higher levels of plasma insulin, but not plasma glucose, as compared to corresponding drinks consumed without fructose. Ten subjects whose blood glucose response levels were above 155 mg% after a glucose-containing drink appeared to be particularly responsive to the effects of fructose with increases in insulin levels of 60-288%. Results indicate that oral fructose can be insulinogenic in humans when blood glucose levels are elevated.

Administration, Oral↗
PubMed2006

A 4-wk high-fructose diet alters lipid metabolism without affecting insulin sensitivity or ectopic lipids in healthy humans.

BACKGROUND: High fructose consumption is suspected to be causally linked to the epidemics of obesity and metabolic disorders. In rodents, fructose leads to insulin resistance and ectopic lipid deposition. In humans, the effects of fructose on insulin sensitivity remain debated, whereas its effect on ectopic lipids has never been investigated. OBJECTIVE: We assessed the effect of moderate fructose supplementation on insulin sensitivity (IS) and ectopic lipids in healthy male volunteers (n = 7). DESIGN: IS, intrahepatocellular lipids (IHCL), and intramyocellular lipids (IMCL) were measured before and after 1 and 4 wk of a high-fructose diet containing 1.5 g fructose . kg body wt(-1) . d(-1). Adipose tissue IS was evaluated from nonesterified fatty acid suppression, hepatic IS from suppression of hepatic glucose output (6,6-2H2-glucose), and muscle IS from the whole-body glucose disposal rate during a 2-step hyperinsulinemic euglycemic clamp. IHCL and IMCL were measured by 1H magnetic resonance spectroscopy. RESULTS: Fructose caused significant (P < 0.05) increases in fasting plasma concentrations of triacylglycerol (36%), VLDL-triacylglycerol (72%), lactate (49%), glucose (5.5%), and leptin (48%) without any significant changes in body weight, IHCL, IMCL, or IS. IHCL were negatively correlated with triacylglycerol after 4 wk of the high-fructose diet (r = -0.78, P < 0.05). CONCLUSION: Moderate fructose supplementation over 4 wk increases plasma triacylglycerol and glucose concentrations without causing ectopic lipid deposition or insulin resistance in healthy humans.

Adult↗
PubMed1984

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 significantly 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.

Administration, Oral↗
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↗
PubMed1998

Long-term fructose consumption accelerates glycation and several age-related variables in male rats.

Fructose intake has increased steadily during the past two decades. Fructose, like other reducing sugars, can react with proteins through the Maillard reaction (glycation), which may account for several complications of diabetes mellitus and accelerating aging. In this study, we evaluated the effect of fructose intake on some age-related variables. Rats were fed for 1 y a commercial nonpurified diet, and had free access to water or 250 g/L solutions of fructose, glucose or sucrose. Early glycation products were evaluated by blood glycated hemoglobin and fructosamine concentrations. Lipid peroxidation was estimated by urine thiobarbituric reactive substances. Skin collagen crosslinking was evaluated by solubilization in natural salt or diluted acetic acid solutions, and by the ratio between beta- and alpha-collagen chains. Advanced glycation end products were evaluated by collagen-linked fluorescence in bones. The ratio between type-III and type-I collagens served as an aging variable and was measured in denatured skin collagen. The tested sugars had no effect on plasma glucose concentrations. Blood fructose, cholesterol, fructosamine and glycated hemoglobin levels, and urine lipid peroxidation products were significantly higher in fructose-fed rats compared with the other sugar-fed and control rats. Acid-soluble collagen and the type-III to type-I ratio were significantly lower, whereas insoluble collagen, the beta to alpha ratio and collagen-bound fluorescence at 335/385 nm (excitation/emission) were significantly higher in fructose-fed rats than in the other groups. The data suggest that long-term fructose consumption induces adverse effects on aging; further studies are required to clarify the precise role of fructose in the aging process.

Aging↗