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PubMed1988

Incomplete absorption of pure fructose in healthy subjects and the facilitating effect of glucose.

Small-intestinal absorption of fructose was investigated in healthy human subjects by sequential breath-hydrogen measurements. Fifty-eight percent of 103 subjects produced greater than 20 microL H2/L after consuming 50 g pure fructose in water. About half of those who absorbed fructose incompletely (incomplete absorbers) had abdominal symptoms. Malabsorption of medium doses of pure fructose may therefore be common in man. When 25 g pure fructose was consumed, only 19% of 21 poor absorbers (of 50 g fructose) still produced excess breath H2. When glucose was taken with fructose, the frequency and amount of excessive breath H2 was substantially reduced. This facilitating phenomenon is not generally known but is important because in natural foods fructose occurs in association or in combination (as sucrose) with glucose. Plasma fructose responses were not lower in poor absorbers presumably because these responses depend more on how much fructose passes through the liver than on how much is absorbed.

Adult↗
PubMed2000

Effects of dietary fructose on plasma lipids in healthy subjects.

BACKGROUND: About 9% of average dietary energy intake in the United States comes from fructose. Such a high consumption raises concern about the metabolic effects of this sugar. OBJECTIVE: The objective of this study was to determine the effect of dietary fructose on plasma lipids. DESIGN: The study was conducted in the General Clinical Research Center at Fairview-University of Minnesota Medical Center. The participants were 24 healthy adult volunteers (12 men and 12 women; 6 of each sex were aged <40 y and 6 of each sex were aged >/=40 y). All subjects received 2 isoenergetic study diets assigned by using a randomized, balanced crossover design. One diet provided 17% of energy as fructose. The other diet was sweetened with glucose and was nearly devoid of fructose. Each diet was fed for 6 wk. Both diets were composed of common foods and contained nearly identical amounts of carbohydrate, protein, fat, fiber, cholesterol, and saturated, monounsaturated, and polyunsaturated fatty acids. All meals were prepared in the metabolic kitchen of the General Clinical Research Center. RESULTS: The responses to the study diets differed by sex. In men, the fructose diet produced significantly higher fasting, postprandial, and daylong plasma triacylglycerol concentrations than did the glucose diet. The daylong plasma triacylglycerol concentration after 6 wk of the fructose diet was 32% greater in men than the corresponding concentration during the glucose diet (P: < 0.001). The fructose diet had no significant effect on fasting or postprandial plasma triacylglycerol concentrations in women. The fructose diet also had no persistent effect on fasting plasma cholesterol, HDL cholesterol, or LDL cholesterol in either men or women. CONCLUSIONS: Dietary fructose was associated with increased fasting and postprandial plasma triacylglycerol concentrations in men. Diets high in added fructose may be undesirable, particularly for men. Glucose may be a suitable replacement sugar.

Adult↗
PubMed1977

Stimulation of neutral amino acid transport by fructose in epithelial cells isolated from rat intestine.

Interest in the nutritional and physiological implications of the high dietary intakes of fructose from sucrose and isomerized corn sweeteners has directed attention to the specific metabolic properties of this monosaccharide. Epithelial cells isolated from the small intestine of Wistar rats fed a stock diet showed 24% to 57% higher transport of 1 mM leucine, isoleucine, valine, alanine, phenylalanine tryptophan and histidine in the presence of 10 mM fructose than in its absence. In contrast, 10mM glucose generally inhibited the transport of these amino acids and 10mM sorbose had no effect on leucine transport. Fructose failed to consistently stimulate the transport of basic amino acids and generally inhibited the transport of glucose and galactose, indicating that the stimulation was relatively specific for neutral amino acids. Cells preloaded with fructose optimally stimulated leucine transport in the absence of extracellular fructose. Ouabain and dinitrophenol inhibited the stimulation of leucine transport by intracellular fructose after 2 minutes. A stimulation mediated by an exchange transport mechanism was rejected on the basis of the failure of 1 mM neutral amino acids either to inhibit the transport of 10 mM fructose or to accelerate the movement of fructose out of fructose-loaded cells. Although the mechanism remains unknown, these results demonstrate a specific effect of fructose at the intestinal level that produces a stimulation of neutral amino acid transport.

Amino Acids↗
PubMed2002

Substituting honey for refined carbohydrates protects rats from hypertriglyceridemic and prooxidative effects of fructose.

Recent findings indicate that a high fructose diet has a prooxidant effect in rats compared with a starch diet. Because honey is rich in fructose, the aim of this study was to assess the effect of substituting honey for refined carbohydrates on lipid metabolism and oxidative stress. Rats were fed for 2 wk purified diets containing 65 g/100 g carbohydrates as wheat starch or a combination of fructose and glucose or a honey-based diet prepared by substituting honey for refined carbohydrates (n = 9/group). The same amount of fructose was provided by the honey and fructose diets. The hypertriglyceridemic effect of fructose was not observed when fructose was provided by honey. Compared with those fed starch, fructose-fed rats had a lower plasma alpha-tocopherol level, higher plasma nitrite and nitrate (NOx) levels and were less protected from lipid peroxidation as indicated by heart homogenate TBARS concentration. Compared with those fed fructose, honey-fed rats had a higher plasma alpha-tocopherol level, a higher alpha-tocopherol/triacylglycerol ratio, lower plasma NOx concentrations and a lower susceptibility of heart to lipid peroxidation. Further studies are required to identify the mechanism underlying the antioxidant effect of honey but the data suggest a potential nutritional benefit of substituting honey for fructose in the diet.

Animals↗
PubMed2003

Fructose and its effect on turkey plasma uric acid levels and productive performance.

Previous studies have shown that addition of fructose to the diet of broilers raises plasma uric acid (PUA) concentration and improves productive performance. The purpose of this experiment was to establish the effect of feeding fructose on turkey PUA concentration and productive performance. Turkey poults (n = 64) were weighed and randomly assigned to diets containing 0 (control), 5, 10, and 15% fructose with four replicates of four poults each per treatment. All diets were isocaloric and isonitrogenous. Feed and water were offered ad libitum for 14 wk. Body weights were measured biweekly throughout the study, and blood samples were drawn from wk 8 to 10 for determination of PUA concentration, leukocyte oxidative activity (LOA), and differential leukocyte counts. Relative liver size (g/kg BW) was also determined. The heaviest body weights were recorded from turkeys fed 10% fructose diet (P < 0.05). Supplemental fructose had no effect on the feed to gain ratio, relative liver size, or PUA concentrations. LOA increased in poults fed the 15% fructose diet. Turkeys fed 10 and 15% fructose diets had higher monocyte and lower polymorphonuclear lymphocyte counts (P < 0.05) compared to those fed control and 5% fructose diets. Feeding fructose to turkeys at 10% of the diet improved productive performance. However, dietary fructose had no effect on PUA or, consequently, LOA.

Animal Nutritional Physiological Phenomena↗
PubMed2000

Fructose utilization and phytopathogenicity of Spiroplasma citri.

Spiroplasma citri is a plant-pathogenic mollicute. Recently, the so-called nonphytopathogenic S. citri mutant GMT 553 was obtained by insertion of transposon Tn4001 into the first gene of the fructose operon. Additional fructose operon mutants were produced either by gene disruption or selection of spontaneous xylitol-resistant strains. The behavior of these spiroplasma mutants in the periwinkle plants has been studied. Plants infected via leafhoppers with the wild-type strain GII-3 began to show symptoms during the first week following the insect-transmission period, and the symptoms rapidly became severe. With the fructose operon mutants, symptoms appeared only during the fourth week and remained mild, except when reversion to a fructose+ phenotype occurred. In this case, the fructose+ revertants quickly overtook the fructose- mutants and the symptoms soon became severe. When mutant GMT 553 was complemented with the fructose operon genes that restore fructose utilization, severe pathogenicity, similar to that of the wild-type strain, was also restored. Finally, plants infected with the wild-type strain and grown at 23 degrees C instead of 30 degrees C showed late symptoms, but these rapidly became severe. These results are discussed in light of the role of fructose in plants. Fructose utilization by the spiroplasmas could impair sucrose loading into the sieve tubes by the companion cells and result in accumulation of carbohydrates in source leaves and depletion of carbon sources in sink tissues.

Animals↗
PubMed1999

Dietary modulation of intestinal fructose transport and GLUT5 mRNA expression in hypothyroid rat pups.

BACKGROUND: Intestinal fructose transport rates or GLUT5 mRNA levels typically show a two- to threefold increase after weaning in rats allowed to wean normally but can be enhanced precociously by high-fructose diets during early weaning. Developmental increases in serum thyroxine levels coincide with the onset of weaning and have been linked to changes in intestinal sucrase and lactase activities. METHODS: Rat pups were made hypothyroid by giving the dam 0.01% propylthiouracil as drinking water from day 18 of gestation. The hypothyroid pups and age-matched euthyroid control pups were then fed high-fructose or high-glucose solutions by gavage, twice a day starting at 17 days of age for 3 days, and then killed at 20 days of age. RESULTS: Serum thyroxine levels were five times lower in the hypothyroid pups. Rates of intestinal fructose uptake in the proximal and middle small intestine were 2.0 to 2.5 times higher in the hypothyroid and euthyroid pups fed high-fructose solution than in littermates fed high-glucose solution or those allowed to wean normally with the dam. Intestinal glucose uptake also increased in hypothyroid but not in euthyroid pups fed high-fructose or high-glucose solutions. GLUT5 mRNA levels increased in euthyroid and hypothyroid pups fed high fructose and paralleled the increase in fructose uptake. CONCLUSION: During weaning, dietary fructose can precociously enhance intestinal fructose uptake and GLUT5 mRNA expression, independent of developmental increases in serum thyroxine levels. Modest changes in glucose transport rates indicate that nonspecific mechanisms may provide a minor contribution to diet-induced changes in nutrient absorption in hypothyroid pups.

Animals↗
PubMed2006

Metabolic effects of fructose.

PURPOSE OF REVIEW: Fructose is consumed in significant amounts in Western diets. An increase in fructose consumption over the past 10-20 years has been linked with a rise in obesity and metabolic disorders. Fructose/sucrose produces deleterious metabolic effects in animal models. This raises concern regarding the short-term and long-term effects of fructose and its risk in humans. RECENT FINDINGS: In rodents, fructose stimulates lipogenesis and leads to hepatic and extrahepatic insulin resistance, dyslipidaemia and high blood pressure. Insulin resistance appears to be related to ectopic lipid deposition. In humans, short-term fructose feeding increases de-novo lipogenesis and blood triglycerides and causes hepatic insulin resistance. There is presently no evidence for fructose-induced muscle insulin resistance in humans. The cellular mechanisms underlying the metabolic effects of fructose involve production of reactive oxygen species, activation of cellular stress pathways and possibly an increase in uric acid synthesis. SUMMARY: Consuming large amounts of fructose can lead to the development of a complete metabolic syndrome in rodents. In humans, fructose consumed in moderate to high quantities in the diet increases plasma triglycerides and alters hepatic glucose homeostasis, but does not appear to cause muscle insulin resistance or high blood pressure in the short term. Further human studies are required to delineate the effects of fructose in humans.

Blood Glucose↗
PubMed2000

Fructose operon mutants of Spiroplasma citri.

Fructose-negative mutants of Spiroplasma citri wild-type strain GII-3 were selected by two methods. The first method is based on the selection of spontaneous xylitol-resistant mutants, xylitol being a toxic fructose analogue. Five such mutants were obtained, but only one, xyl3, was unable to use fructose and had no phosphoenolpuryvate:fructose phosphotransferase system (fructose-PTS) activity. Amplification and sequencing of the fructose permease gene of mutant xyl3 revealed the presence of an adenylic insertion leading to a truncated permease. The second method is based on inactivation of fruA and/or fruK by homologous recombination involving one crossing-over between the chromosomal genes and inactivated genes carried by replicative plasmids. Fructose-negative mutants were obtained at a frequency of about 10%. Fructose-PTS activity and 1-phosphofructokinase activity were not detected in four representative mutants that were characterized (H31, H45, E38 and E53). In strain H31, Southern blot analysis and PCR showed that the result of homologous recombination was, as expected, the presence in the chromosome of two mutated fruA-fruK copies with the plasmid sequence in between. Only the mutated copy, under control of the fructose operon promoter, was transcribed. This work describes for the first time the use of two methods to obtain fructose-auxotrophic mutants of S. citri. The method involving homologous recombination is a general procedure for gene disruption in S. citri.

Amino Acid Sequence↗
PubMed1976

Control of the sequential utilization of glucose and fructose by Escherichia coli.

In Escherichia coli (ATCCI5224; ML308), glucose and fructose phosphotransferase systems (PT-systems) are constitutive but activities are increased five and 10-fold respectively by aerobic growth on their respective substrates in defined media. In mixtures, glucose is used preferentially and the fructose PT-system activity is kept at its minimum; but, on glucose exhaustion, it overshoots its steady-state level and growth continues on fructose without lag. Cyclic AMP prevents overshoot. Continuous cultures operating as turbidostats on mixtures of glucose and fructose do not use fructose if sufficient glucose is present to support growth. If less glucose is available, it is all used and sufficient fructose is metabolized concurrently to maintain the growth rate characteristic of glucose. Both PT-systems are inhibited by hexose phosphates. Presence of homologous substrate specifically sensitizes each PT-system to inactivation by N-ethylmaleimide (NEM). Glucose diminishes the ability of fructose to sensitize its PT-system to NEM. This effect parallels the inhibition of fructose utilization by glucose and suggests that glucose denies fructose access to the fructose-specific part of the PT-system.

Aerobiosis↗
PubMed1977

Fructose transport in Bacillus subtilis.

The transport of fructose in Bacillus subtilis was studied in various mutant strains lacking the following activities: ATP-dependent fructokinase (fruC), the fructose 1-phosphate kinase (fruB) the phosphofructokinase (pfk), the enzyme I of the phosphoenolpyruvate phosphotransferase system (the thermosensitive mutation ptsI1), and a transport activity (fruA). Combinations of these mutations indicated that the transport of fructose in Bacillus subtilis is tightly coupled to its phosphorylation either in fructose 1-phosphate, identified in vivo and in vitro or in fructose 6-phosphate identified by indirect lines of evidence. These steps of fructose metabolism were shown to depend on the activity of the enzyme I of the phosphoenolpyruvate phosphotransferase systems. The fruA mutations affect the transport of fructose when the bacteria are submitted to catabolite repression. The mutations were localized on the chromosome of Bacillus subtilis in a cluster including the fruB gene. When grown in a medium supplemented by a mixture of potassium glutamate and succinate the fruA mutants are able to carry on the two vectorial metabolisms generating fructose 6-phosphate as well as fructose 1-phosphate. A negative search of strictly negative transport mutants in fruA strains indicated that more than two structural genes are involved in the transport of fructose.

Bacillus subtilis↗
PubMed1982

Enzymes related to fructose utilization in Pseudomonas cepacia.

Growth of Pseudomonas cepacia on fructose, mannitol, or sorbitol depended on formation of an inducible fructokinase (forming fructose-6-phosphate) and the presence of enzymes of the Entner-Doudoroff pathway. Mutants deficient in any of these enzymes failed to utilize the aforementioned carbohydrates. Fructokinase deficiency did not affect growth of the bacteria on glucose. Fructose was accumulated intracellularly by active transport. Mutants blocked in transport of fructose grew normally on mannitol or sorbitol despite their inability to utilize fructose. Growth on either of these hexitols or on galactitol was accompanied by induction of two hexitol dehydrogenases, one active primarily with mannitol and the other active with sorbitol and galactitol. As expected, a mutant deficient in mannitol dehydrogenase failed to utilize mannitol as a carbon and energy source but grew normally on sorbitol and galactitol. Extracts of bacteria grown on fructose, mannitol, or sorbitol and higher levels of phosphoglucose isomerase than extracts of bacteria grown on alternate carbon sources such as citrate or phthalate. The higher levels were due to appearance of a second phosphoglucose isomerase species not present in cells with the lower activity. The results indicate that the initial steps in fructose utilization by P. cepacia differ from those of most other pseudomonads, which transport fructose by phosphoenolpyruvate-dependent translocation, forming fructose-1-phosphate, and suggest that degradation of fructose, mannitol, and sorbitol occurs primarily via the Entner-Doudoroff pathway.

Aldehyde-Lyases↗
PubMed1990

Regulation of fructose metabolism and polymer synthesis by Fusobacterium nucleatum ATCC 10953.

Energy for the anaerobic growth of Fusobacterium nucleatum ATCC 10953 can be derived from the fermentation of sugar (fructose) or amino acid (glutamate). During growth on fructose, the cells formed large intracellular granules which after extraction yielded glucose by either acid or enzymatic hydrolysis. The endogenous polymer was subsequently metabolized, and after overnight incubation of the cells in buffer, the glucan granules were no longer detectable by electron microscopy. Anaerobically, washed cells grown previously on fructose fermented this sugar to a mixture of lactic, acetic, and butyric acids, and little intracellular glucan was formed. Aerobically, the cells slowly metabolized fructose to acetate. Provision of glutamic acid as an additional energy (ATP) source elicited rapid synthesis of polymer by glycolyzing cells. Intracellular granules were not present in glutamate-grown cells, and under anaerobic conditions, the resting cells failed to metabolize [14C] fructose. However, the addition of glutamic acid to the suspension resulted in the rapid accumulation of sugar by the cells. Approximately 15% of the 14C-labeled material was extractable with boiling water, and by 31P nuclear magnetic resonance spectroscopy, this phosphorylated derivative was identified as [14C]fructose-1-phosphate. The nonextractable material represented [14C]glucan polymer. Fructose-1-phosphate kinase activity in fructose-grown cells was fivefold greater than that in glutamate-grown cells. We suggest that the activity of fructose-1-phosphate kinase and the availability of ATP regulate the flow of fructose into either the glycolytic or polymer-synthesizing pathway in F. nucleatum.

Cytoplasmic Granules↗
PubMed1984

Incomplete intestinal absorption of fructose.

Intestinal D-fructose absorption in 31 children was investigated using measurements of breath hydrogen. Twenty five children had no abdominal symptoms and six had functional bowel disorders. After ingestion of fructose (2 g/kg bodyweight), 22 children (71%) showed a breath hydrogen increase of more than 10 ppm over basal values, indicating incomplete absorption: the increase averaged 53 ppm, range 12 to 250 ppm. Four of these children experienced abdominal symptoms. Three of the six children with bowel disorders showed incomplete absorption. Seven children were tested again with an equal amount of glucose, and in three of them also of galactose, added to the fructose. The mean maximum breath hydrogen increases were 5 and 10 ppm, respectively, compared with 103 ppm after fructose alone. In one boy several tests were performed with various sugars; fructose was the only sugar incompletely absorbed, and the effect of glucose on fructose absorption was shown to be dependent on the amount added. It is concluded that children have a limited absorptive capacity for fructose. We speculate that the enhancing effect of glucose and galactose on fructose absorption may be due to activation of the fructose carrier. Apple juice in particular contains fructose in excess of glucose and could lead to abdominal symptoms in susceptible children.

Adolescent↗
PubMed1991

Phosphocreatine protects ATP from a fructose load in transgenic mouse liver expressing creatine kinase.

The effects of an intraperitoneal dose of fructose on hepatic metabolism in transgenic mice expressing creatine kinase in liver were investigated using phosphorus-31 nuclear magnetic resonance (31P-NMR). Transgenic mice were fed diets containing varying amounts of creatine (Cr; 0-12%). It has previously been shown that 31P-NMR spectra of transgenic mice have a peak due to phosphocreatine (PCr), the intensity of which was proportional to the amount of Cr in the diet. No PCr peak was detected in control mice or transgenic mice not fed Cr. In the present study NMR spectra were collected before and for a 1-h recovery period after infusion of 0.15 mmol/10 g body wt fructose. In all mice infusion of fructose resulted in a two- to threefold elevation of phosphomonoesters. In control and non-Cr-fed transgenic mice this was accompanied by a 60% reduction of the inorganic phosphate (Pi) and a 50% fall in ATP. In transgenic mice fed Cr, the extent of reduction of Pi was dependent on the level of PCr and was markedly reduced compared with controls. Falls in Pi of 46, 24, and 6% were detected 12.5 min after fructose infusion in low, intermediate, and high PCr-containing livers, respectively. The presence of PCr also protected hepatic ATP levels from a fructose load. Transgenic mice fed on high or intermediate Cr diets showed no significant loss of ATP. However, livers with low levels of PCr lost ATP during a fructose challenge. From the equilibrium established by creatine kinase, free ADP levels were calculated throughout the fructose dose. Fructose caused a 2.5-fold increase in free ADP. This rise in ADP was independent of the total Cr or whether Pi and ATP were reduced by fructose infusion. These results indicate that an increase in ADP is not sufficient to cause depletion of ATP during a fructose challenge.

Adenosine Triphosphate↗
PubMed1975

Effects of intravenously administered fructose and glucose on splanchnic amino acid and carbohydrate metabolism in hypertriglyceridemic men.

Splanchnic metabolism was studied in the fed state during prolonged intravenous administration (30 g/h) of either fructose or glucose to hypertriglyceridemic men who had been maintained on a high-carbohydrate diet for 2 wk. Splanchnic exchange of amino acids and carbohydrates was quantified by measurement of splanchnic flow and of blood or plasma arteriohepatic venous concentration gradients. Results obtained in subjects receiving fructose were compared with those obtained in (a) similar subjects receiving glucose and (b) postabsorptive controls maintained on isocaloric, balanced diets. Mean arterial plasma levels of alanine, glycine, serine, threonine, methionine, proline, valine, leucine, histidine, lysine, and ornithine were significantly higher in subjects given fructose than in those give glucose (P less than 0.05). The mean arterial concentration and splanchnic uptake of alanine were significantly higher in subjects given fructose than in postabsorptive controls, despite a significantly lower fractional extraction of alanine in the former (P less than 0.05). The mean arterial plasma levels of serine and ornithine were significantly lower in subjects receiving fructose than in postabsorptive controls (P less than 0.05). About half of the administered fructose or glucose was taken up in the splanchnic region, where approximately 15% was converted to CO2 and 10% to lactate. Half of the fructose taken up in the splanchnic region was converted to glucose released from the liver. The amount of hexose carbon remaining for hepatic synthesis of liquids in subjects given fructose was less than half of that of subjects given glucose. These studies demonstrate that fructose and glucose have divergent effects on amino acid metabolism and that during hypercaloric infusion of glucose (as with fructose), the human liver is a major site of lactate production.

Adult↗
PubMed1985

Myosin isoenzyme distribution and Ca+2-activated myosin ATPase activity in the rat heart is influenced by fructose feeding and triiodothyronine.

Studies were conducted to determine if the level of cardiac Ca+2-activated myosin ATPase activity and ventricular myosin isoenzyme distribution are influenced by both T3 administration and fructose feeding. Previous studies have shown that in the cardiac ventricle of hypothyroid rats, only myosin V3 is present, and the Ca+2-activated myosin ATPase activity is markedly decreased. Hypothyroid [thyroidectomized (Tx)] rats were fed a diet containing 60% fructose or a regular diet (47% complex carbohydrates) for 4 weeks. Fructose feeding of hypothyroid rats led to a significant increase in Ca+2-activated myosin ATPase activity (Tx regular diet, 0.33 +/- 0.02 mumol Pi/mg protein X min; Tx fructose diet, 0.54 +/- 0.04 mumol Pi/mg protein X min). In addition, myosin V1 was detectable in the heart of fructose-fed Tx rats, but was absent in Tx rats on the regular diet. To determine if fructose had an effect of similar magnitude in animals of different thyroid states, Tx rats were injected with 0.075, 0.150, 0.225, and 0.300 micrograms T3/100 g BW daily and placed on fructose or regular diets. The fructose-induced increase in Ca+2-myosin ATPase activity was between 24-27% in Tx rats receiving 0-0.15 micrograms T3/100 g BW daily. In animals receiving 0.225 and 0.300 micrograms T3/100 g BW daily, fructose feeding did not induce a significant increase in myosin ATPase activity. This is due to the fact that the Ca+2-activated myosin ATPase activities of euthyroid and hyperthyroid animals are not significantly different from each other. In hypothyroid rats receiving a 60% glucose diet, Ca+2-myosin ATPase activity showed a significant 20% increase above the value in regular diet-fed Tx rats. Fructose- and glucose-induced changes in Ca+2-myosin ATPase activity occurred in the absence of changes in thyroid hormone or insulin levels. Our findings may indicate that cardiac carbohydrate consumption influences the predominance of ventricular myosin isoenzymes in the rat heart.

Animals↗
PubMed1992

Metabolic effects of dietary fructose in diabetic subjects.

OBJECTIVE: To assess the metabolic effects of chronic dietary fructose consumption in diabetic subjects. RESEARCH DESIGN AND METHODS: Six type I and 12 type II diabetic subjects consumed, in random order, two isocaloric study diets for 28 days. In one diet, 20% of energy was derived from fructose. In the other diet, < 3% of energy came from fructose, and carbohydrate energy was derived primarily from starch. Both study diets were composed of common foods. All meals were prepared in a metabolic kitchen where all foods were weighed during meal preparation. RESULTS: Mean plasma glucose, urine glucose, and serum glycosylated albumin values were lower during the fructose diet than during the starch diet, but the differences achieved only marginal statistical significance. The day-28 value for mean plasma glucose was 12.5% lower (P = 0.03) during the fructose diet than during the starch diet. At days 14, 21, and 28, fasting serum cholesterol and LDL cholesterol were both significantly higher during the fructose diet than during the starch diet. The day-28 values for serum cholesterol and LDL cholesterol during the fructose diet were 6.9% (P = 0.008) and 10.9% (P = 0.002) higher, respectively, than the corresponding values during the starch diet. No differences were observed between the study diets in fasting serum HDL cholesterol, fasting serum triglycerides, peak postprandial serum triglycerides, or fasting serum lactate. Peak postprandial serum lactate was significantly higher during the fructose diet. Type I and type II diabetic subjects responded to the diets in a consistent way, but type I subjects experienced significantly more hypoglycemia during the fructose diet than during the starch diet. CONCLUSIONS: A high-fructose diet may result in reduced glycemia in diabetic subjects but at the expense of increased fasting serum total and LDL cholesterol.

Adult↗