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PubMed1990

Regulation of L-type pyruvate kinase gene expression by dietary fructose in normal and diabetic rats.

Previous studies have shown that dietary fructose stimulates expression of the L-type pyruvate kinase gene mainly at the post-transcriptional level in diabetic liver, and that this effect may be mediated by a metabolite common to both fructose and glycerol. In the present work, we carried out further studies on the mechanism of fructose induction of L-type isozyme mRNA in the liver, kidney and small intestine of rats. The L-type isozyme mRNA in the kidney of normal and diabetic rats was increased by dietary fructose, the time course of the increase being similar to that observed in the small intestine and liver. The mRNA was not induced in the kidney by dietary glucose or insulin. Glycerol was also a potent inducer of the mRNA in the kidney and liver, but not in the small intestine. These results show that fructose and glycerol induced increase in the mRNA only in organs in which they were metabolized, and thus support the metabolite hypothesis. No other carbohydrates tested increased the level of mRNA in these tissues, except glucose, which increased the level in the small intestine. Thus a molecule that increase the mRNA level may accumulate significantly during metabolism of only certain carbohydrates. Dietary fructose or glycerol slightly stimulated transcription of the gene for the L-type isozyme in diabetic liver, and also in normal and diabetic kidney, but the magnitudes of increase were much lower than those of the mRNA, confirming our previous findings described above. On the other hand, dietary fructose caused marked stimulation of gene transcription in normal rat liver, although the magnitude of its induction of the mRNA was similar to that in diabetic liver. Insulin treatment of fructose-fed diabetic rats also caused a marked increase in the gene transcription without any concomitant change in the mRNA level. Thus, the mechanism of fructose induction of the L-type pyruvate kinase in diabetic liver, which is similar to that found in the kidney, is different from that in normal liver, and this difference is attributable to the difference in the level of insulin.

Animals↗
PubMed1998

Overexpression of vascular endothelin-1 and endothelin-A receptors in a fructose-induced hypertensive rat model.

OBJECTIVE: To examine the temporal relationship between hyperinsulinemia and hypertension in the fructose-hypertensive rat model and to study the function of endothelin-1 (ET-1) in fructose-induced hypertension. DESIGN: Since ET-1 induces insulin resistance in conscious rats, we tested the hypothesis that both hyperinsulinemia and hypertension developed in the fructose-hypertensive rat model might be the sequelae of an elevated tissue content of ET-1 and ET(A) receptors. MATERIALS AND METHODS: Systolic hypertension was induced within 3 weeks in male Sprague-Dawley rats fed on a fructose-rich diet. After continual monitoring of blood pressure and plasma insulin concentrations, the animals were killed at the end of experiment to determine plasma levels of ET-1, the contractile response of aortic rings to ET-1, and ET-1 and ET(A) receptor gene expressions. In a separate experiment, BQ-610 was administered to lower the effect of ET-1 in rats with fructose-induced hypertension. RESULTS: Compared with control rats given normal chow, the fructose-fed rats developed systolic hypertension after 3 weeks of the diet (127+/-3.7 versus 110+/-5.5 mmHg, P < 0.01) and hyperinsulinemia both before (1 07.1+/-32.5 versus 48.5+/-14.3 pmol/l, P < 0.005) and after (96.6+/-63.7 versus 50.4+/-5.6 pmol/l, P< 0.05) they became hypertensive. Although plasma ET-1 levels did not differ between the rat groups, aortic ring contraction-concentration curves, indicating vessel contractility in response to ET-1, were significantly greater in these rats than in controls (F1,72 = 12.34, P< 0.00077). Messenger RNA extracted from the tail arteries and blotted with both ET-1 and ET(A) probes showed that fructose-fed rats had greater ET-1 and ET(A)-receptor gene expression than control rats. Concomitant administration of BQ-610 to rats fed on a fructose diet significantly reduced the hypertension. Conclusions These findings suggest that elevated vascular expression of ET-1 and ET(A) receptor genes may mediate the development of hypertension and hyperinsulinemia in rats fed a fructose-rich diet

Animals↗
PubMed1996

Facilitating effect of amino acids on fructose and sorbitol absorption in children.

The facilitating effect of glucose on free fructose absorption has been suggested to be due to a sucrase-related transport mechanism. In contrast, the conditions influencing the absorption of sorbitol have hardly been investigated. As amino acids promote transcellular water flow, we investigated their effects on the absorption of fructose and sorbitol. We studied 15 healthy children using breath hydrogen tests following the ingestion of fructose and sorbitol, alone and in combination with glucose or amino acids. Similarly, the effect of acarbose pretreatment on sucrose and fructose-glucose absorption was investigated. The inhibition of sucrase isomaltase by acarbose impedes the absorption of sucrose but not of the fructose-glucose mixture. Fructose absorption is enhanced by glucose and by the amino acids L-alanine, L-glutamine, L-phenylalanine, and L-proline. Similarly, the absorption of sorbitol is facilitated by glucose and L-alanine. These results are not in concordance with a sucrase-related fructose-transport system and suggest another mechanism for glucose-induced enhancement of fructose (and sorbitol) absorption. We hypothesize that the absorption of fructose and sorbitol may be stimulated by the increased water flux induced by active absorption of glucose as well as amino acids.

Adolescent↗
PubMed2003

Effects of fructose on hepatic glucose metabolism.

PURPOSE OF REVIEW: The liver plays an important role in glucose tolerance. A number of studies have suggested fructose improves glucose tolerance especially in insulin resistant settings. This review summarizes the recent work suggesting that fructose enhances glucose tolerance by augmenting liver glucose uptake. This increase may be mediated by the translocation and activation of hepatic glucokinase. RECENT FINDINGS: Catalytic quantities of fructose (<10% of total carbohydrate flux) enhance liver glucose uptake in a dose dependent manner. The primary fate of the glucose is glycogen synthesis. The ability of fructose to augment liver glucose uptake is not impaired by the presence of marked insulin resistance such as in type 2 diabetes or infection. In addition, it is able to further enhance liver glucose uptake in the normal adapted setting of total parenteral nutrition and reverse the infected-induced decrease in liver glucose uptake. Studies also demonstrate that the beneficial effects of fructose on liver glucose uptake during chronic nutritional support do not persist. SUMMARY: Fructose is a potent acute regulator of liver glucose uptake and glycogen synthesis. Inclusion of catalytic quantities of fructose in a carbohydrate meal improves glucose tolerance. This improvement is primarily mediated by the activation of hepatic glucokinase and consequent facilitation of liver glucose uptake. The improvement in glucose tolerance is most evident in insulin resistant settings (e.g. Type 2 diabetes and infection). The beneficial effect of fructose on hepatic glucose disposal, however, does not persist if fructose is given continuously such as in total parenteral nutrition.

Area Under Curve↗
PubMed1975

Existence of two alternative pathways for fructose and sorbitol metabolism in Bacillus subtilis Marburg.

Strains of Bacillus subtilis mutated for fructose phosphotransferase system (fruA), fructose-1-phosphate kinase (fruB), fructokinase (frucC) have been tested for their catabolism of sorbitol and fructose. It is shown that the previously known pathways of sorbitol and fructose degradation in B. subtilis, e.g.: (see article) may metabolize intracellular fructose produced either by sorbitol oxidation or by fructose-1-phosphate dephosphorylation. The intracellular fructore degradation via fructose-1-phosphate kinase has been found to require the fructose phosphotransferase system which ensures a vectorial transport of fructose.

Bacillus subtilis↗
PubMed1978

Ethanol oxidation by isolated rat-liver cells. Stimulatory effects of fructose.

Isolated liver cells from starved or fed rats were used to examine the mechanisms by which fructose stimulates hepatic ethanol oxidation, particularly in relation to the role of intercompartmental hydrogen transfer. The presence of added fructose stimulated ethanol oxidation, the degree of stimulation being directly related to the initial fructose concentration up to a level of 10--20 mM. In the presence of fructose and ethanol, sorbitol, glycerol and glycerol 3-phosphate accumulated. The stimulation of ethanol oxidation by fructose could be attributed to its ability to promote the oxidation of cytoplasmic NADH by the provision both of cytoplasmic hydrogen sinks and components of the glycerol 3-phosphate shuttle. Shuttles mediated by malate dehydrogenase were unimportant for fructose-stimulated ethanol oxidation. Rates of respiration and gluconeogenesis were similar over a fructose range of 5--20 mM although ethanol oxidation was faster at higher fructose concentrations. Hence the stimulation of ethanol oxidation by fructose is not merely a direct function of the energy demands of gluconeogenesis.

Animals↗
PubMed1990

Spinach cytosolic fructose-1,6-bisphosphatase. Purification, enzyme properties and structural comparisons.

Cytosolic fructose-1,6-bisphosphatase from spinach leaves was purified to homogeneity and characterized. The pure enzyme has a subunit mass of 38 kDa, its Km values for fructose 1,6-bisphosphate and Mg2+ are 1.5 microM and 260 mM, respectively, and its Vmax is 110-120 units/mg. It is inhibited by fructose 2,6-bisphosphate and AMP with Ki values of 0.07 microM and 120 microM, respectively. About 90% of the primary structure of the spinach cytosolic fructose-1,6-bisphosphatase has been determined by amino-acid sequencing. The sequence data demonstrate that the cytosolic enzyme lacks the sequence insert characteristic of chloroplast fructose-1,6-bisphosphatase. The data include also the sequences of peptides containing all seven cysteine residues. Only two of the seven cysteines are conserved between the two isozymes, none of which is believed to be involved with the light regulation of the chloroplast enzyme. Sequence comparisons between the spinach cytosolic enzyme and gluconeogenic fructose-1,6-bisphosphatases from other species reveal similarity ranging over 47-54%, which is higher than the 40-45% similarity between the chloroplast enzyme and gluconeogenic fructose-1,6-bisphosphatases. However, similarity between these isozymes and Escherichia coli fructose-1,6-bisphosphatase are 44% and 47% for the cytosolic and chloroplast enzymes, respectively. Similarity between the cytosolic and chloroplast counterparts is 52%, indicating wide divergence between these two fructose-1,6-bisphosphatases.

Amino Acid Sequence↗
PubMed2001

Characterization of FruR as a putative activator of the fructose operon of Spiroplasma citri.

The role of fruR, the first gene of the Spiroplasma citri fructose operon, was investigated. In vivo transcription of the fructose operon is greatly enhanced by the presence of fructose in the growth medium while glucose has no effect. When fruR is not expressed, transcription of the fructose operon is not stimulated by fructose, and fructose fermentation is decreased, indicating that FruR is an activator of the fructose operon. The promoter of the fructose operon was localized by primer extension, and a direct T-rich repeat was found to overlap the -35 box. This repeat could be the binding site of FruR. The presence of fructose in the culture medium also decreases the toxicity of methyl alpha-glucoside, however FruR is not involved in this regulation. This is the first description of transcription regulation of a mollicute operon.

Bacterial Proteins↗
PubMed1998

Identification and characterization of human fructose or glucose taste variants with hypogeusia for one monosaccharide but not for the other.

Human psychophysical functions for sweetness are similar for sucrose and fructose, but different for glucose, and suggest different mechanisms for fructose and glucose. Drosophila behavioral and electrophysiological data are similar to the human data and indicate separate receptor cell mechanisms for the monosaccharides. Moreover, fructose 'nontasters' (NTs) and glucose NTs have been identified in two Drosophila species. Identification of human NTs would confirm separate mechanisms and could lead to identification of proteins in human sweet taste by molecular genetic techniques. To identify human NTs, we first obtained responses for sucrose, fructose and glucose from 20 subjects. They tasted seven concentrations of each sugar (2-128 mM), paired with water, and indicated the sweeter of each pair. Functions for recognition indices (RIs) (proportion of subjects recognizing the sugar as sweeter) were similar for sucrose and fructose and different for glucose; this result agrees with the previous studies and supports different mechanisms for the monosaccharides. At 128 mM, RIs for all three sugars were 1.0; this result is consistent with the monogeusia reported by Breslin et al. for concentrations higher than those tested here. Eleven rising-phase concentrations (10-35 mM fructose, 10-90 mM glucose) then were tested on 32 subjects. A statistically significant interaction indicated different regression slopes and supported different monosaccharide mechanisms. From these data, positive identification values (PIDs) (lowest concentration at which the sugar always was judged sweeter than the water) were determined for each subject. The fructose log(PID) and glucose log(PID) data were not well correlated; thus separate mechanisms were supported further. Next, NT traits were defined by log(PID)s > or = 2 SD above the mean for one sugar, while the PID for the other remained within 1 SD of the population mean log(PID). Ninety-two subjects were screened to identify 12 glucose NTs and four fructose NTs. Two glucose NTs and three average subjects were tested in six additional sessions. The NTs showed an experience-induced change: there was a statistically significant reduction of glucose PIDs, but not of fructose PIDs. No change occurred in PIDs of the average subjects for either sugar.

Animals↗
PubMed1987

Fructose disposal and oxidation rates in the ovine fetus.

Fructose disposal and oxidation rates were measured in fetal lambs receiving a constant intravenous infusion of D-[U-14C]fructose. Approximately 60% of the infused tracer entered the placenta, but loss of fructose into the maternal circulation was negligible. Fructose was metabolized to lactate and CO2 in both the placenta and fetus, whereas there was no detectable conversion to glucose. In well-fed ewes the fetal disposal and utilization rates of fructose were 2.4 +/- 0.17 and 0.97 +/- 0.09 mg/min. kg, respectively. The umbilical excretion rate of CO2 originating from the oxidation of fetal fructose was 18.1 +/- 1.3 mumol/min. kg or 5.3% of total fetal CO2 production. This excretion rate is one-fifth of the CO2 excretion rate from fetal glucose carbon. In four ewes comparison of fructose metabolism in the fed and fasted states showed a significant decrease of fructose production and oxidation with fasting. Although fructose is present in high concentrations in the fetal blood of ungulates, its contribution to fetal oxidative metabolism is relatively small in comparison to glucose.

Animals↗
PubMed2003

Chemolithoorganotrophic growth of Nitrosomonas europaea on fructose.

The nitrifying bacterium Nitrosomonas europaea can obtain all its carbon for growth from CO(2) and all its energy and reductant for growth from the oxidation of NH(3) and is considered an obligate chemolithoautotroph. Previous studies have shown that N. europaea can utilize limited amounts of certain organic compounds, including amino acids, pyruvate, and acetate, although no organic compound has been reported to support the growth of N. europaea. The recently completed genomic sequence of N. europaea revealed a potential permease for fructose. With this in mind, we tested if N. europaea could utilize fructose and other compounds as carbon sources to support growth. Cultures were incubated in the presence of fructose or other organic compounds in sealed bottles purged of CO(2). In these cultures, addition of either fructose or pyruvate as the sole carbon source resulted in a two- to threefold increase in optical density and protein content in 3 to 4 days. Studies with [(14)C]fructose showed that >90% of the carbon incorporated by the cells during growth was derived from fructose. Cultures containing mannose, glucose, glycerol, mannitol, citrate, or acetate showed little or no growth. N. europaea was not able to grow with fructose as an energy source, although the presence of fructose did provide an energy benefit to the cells. These results show that N. europaea can be grown in CO(2)-free medium by using fructose and pyruvate as carbon sources and may now be considered a facultative chemolithoorganotroph.

Fructose↗
PubMed2005

Inclusion of low amounts of fructose with an intraportal glucose load increases net hepatic glucose uptake in the presence of relative insulin deficiency in dog.

The effect of small amounts of fructose on net hepatic glucose uptake (NHGU) during hyperglycemia was examined in the presence of insulinopenia in conscious 42-h fasted dogs. During the study, somatostatin (0.8 microg.kg(-1).min(-1)) was given along with basal insulin (1.8 pmol.kg(-1).min(-1)) and glucagon (0.5 ng.kg(-1).min(-1)). After a control period, glucose (36.1 micromol.kg(-1).min(-1)) was continuously given intraportally for 4 h with (2.2 micromol.kg(-1).min(-1)) or without fructose. In the fructose group, the sinusoidal blood fructose level (nmol/ml) rose from <16 to 176 +/- 11. The infusion of glucose alone (the control group) elevated arterial blood glucose (micromol/ml) from 4.3 +/- 0.3 to 11.2 +/- 0.6 during the first 2 h after which it remained at 11.6 +/- 0.8. In the presence of fructose, glucose infusion elevated arterial blood glucose (micromol/ml) from 4.3 +/- 0.2 to 7.4 +/- 0.6 during the first 1 h after which it decreased to 6.1 +/- 0.4 by 180 min. With glucose infusion, net hepatic glucose balance (micromol.kg(-1).min(-1)) switched from output (8.9 +/- 1.7 and 13.3 +/- 2.8) to uptake (12.2 +/- 4.4 and 29.4 +/- 6.7) in the control and fructose groups, respectively. Average NHGU (micromol.kg(-1).min(-1)) and fractional glucose extraction (%) during last 3 h of the test period were higher in the fructose group (30.6 +/- 3.3 and 14.5 +/- 1.4) than in the control group (15.0 +/- 4.4 and 5.9 +/- 1.8). Glucose 6-phosphate and glycogen content (micromol glucose/g) in the liver and glucose incorporation into hepatic glycogen (micromol glucose/g) were higher in the fructose (218 +/- 2, 283 +/- 25, and 109 +/- 26, respectively) than in the control group (80 +/- 8, 220 +/- 31, and 41 +/- 5, respectively). In conclusion, small amounts of fructose can markedly reduce hyperglycemia during intraportal glucose infusion by increasing NHGU even when insulin secretion is compromised.

Animals↗
PubMed2002

Amelioration of high fructose-induced metabolic derangements by activation of PPARalpha.

To elucidate molecular mechanisms of high fructose-induced metabolic derangements and the influence of peroxisome proliferator-activated receptor-alpha (PPARalpha) activation on them, we examined the expression of sterol regulatory element binding protein-1 (SREBP-1) and PPARalpha as well as its nuclear activation and target gene expressions in the liver of high fructose-fed rats with or without treatment of fenofibrate. After 8-wk feeding of a diet high in fructose, the mRNA contents of PPARalpha protein and its activity and gene expressions of fatty acid oxidation enzymes were reduced. In contrast, the gene expressions of SREBP-1 and lipogenic enzymes in the liver were increased by high fructose feeding. Similar high fructose effects were also found in isolated hepatocytes exposed to 20 mM fructose in the media. The treatment of fenofibrate (30 mg.kg(-1).day(-1)) significantly improved high fructose-induced metabolic derangements such as insulin resistance, hypertension, hyperlipidemia, and fat accumulation in the liver. Consistently, the decreased PPARalpha protein content, its activity, and its target gene expressions found in high fructose-fed rats were all improved by fenofibrate treatment. Furthermore, we also found that the copy number of mitochondrial DNA, the expressions of mitochondrial transcription factor A, ATPase-6 subunit, and uncoupling protein-3 were increased by fenofibrate treatment. These findings suggest that the metabolic syndrome in high fructose-fed rats is reversed by fenofibrate treatment, which is associated with the induction of enzyme expression related to beta-oxidation and the enhancement of mitochondrial gene expression.

Adipose Tissue↗
PubMed1986

Comparison of thermogenic effect of fructose and glucose in normal humans.

After nutrient ingestion there is an increase in energy expenditure that has been referred to as dietary-induced thermogenesis. In the present study we have employed indirect calorimetry to compare the increment in energy expenditure after the ingestion of 75 g of glucose or fructose in 17 healthy volunteers. During the 4 h after glucose ingestion the plasma insulin concentration increased by 33 +/- 4 microU/ml and this was associated with a significant increase in carbohydrate oxidation and decrement in lipid oxidation. Energy expenditure increased by 0.08 +/- 0.01 kcal/min. When fructose was ingested, the plasma insulin concentration increased by only 8 +/- 2 microU/ml vs. glucose. Nonetheless, the increments in carbohydrate oxidation and decrement in lipid oxidation were significantly greater than with glucose. The increment in energy expenditure was also greater with fructose. When the mean increment in plasma insulin concentration after fructose was reproduced using the insulin clamp technique, the increase in carbohydrate oxidation and decrement in lipid oxidation were markedly reduced compared with the fructose-ingestion study; energy expenditure failed to increase above basal levels. To examine the role of the adrenergic nervous system in fructose-induced thermogenesis, fructose ingestion was also performed during beta-adrenergic blockade with propranolol. The increase in energy expenditure during fructose plus propranolol was lower than with fructose ingestion alone. These results indicate that the stimulation of thermogenesis after carbohydrate ingestion is related to an augmentation of cellular metabolism and is not dependent on an increase in the plasma insulin concentration per se.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1997

Effects of dexamethasone on hepatic glucose production and fructose metabolism in healthy humans.

This study was designed to determine whether glucocorticoids alter autoregulation of glucose production and fructose metabolism. Two protocols with either dexamethasone (DEX) or placebo (Placebo) were performed in six healthy men during hourly ingestion of[13C]fructose (1.33 mmol.kg-1.h-1) for 3 h. In both protocols, endogenous glucose production (EGP) increased by 8 (Placebo) and 7% (DEX) after fructose, whereas gluconeogenesis from fructose represented 82 (Placebo) and 72% (DEX) of EGP. Fructose oxidation measured from breath 13CO2 was similar in both protocols [9.3 +/- 0.7 (Placebo) and 9.6 +/- 0.5 mumol.kg-1.min-1 (DEX)]. Nonoxidative carbohydrate disposal, calculated as fructose administration rate minus net carbohydrate oxidation rate after fructose ingestion measured by indirect calorimetry, was also similar in both protocols [5.8 +/- 0.8 (Placebo) and 5.9 +/- 2.0 mumol.kg-1.min-1 (DEX)]. We concluded that dexamethasone 1) does not alter the autoregulatory process that prevents a fructose-induced increase in gluconeogenesis from increasing total glucose production and 2) does not affect oxidative and nonoxidative pathways of fructose. This indicates that the insulin-regulated enzymes involved in these pathways are not affected in a major way by dexamethasone.

Adult↗
PubMed1994

Rapid reversible substrate regulation of fructose transporter expression in rat small intestine and kidney.

To understand the regulation of fructose transport in the small intestine and kidney, we provided rats with "control" diets (46% glucose as starch) and with diets enriched in fructose, glucose, or sucrose (60% each of simple carbohydrate) and measured the concentration of facilitative glucose transporter isoform (GLUT5) protein and mRNA in these tissues. The fructose-enriched diet resulted in a five- and eightfold increase in GLUT5 protein at 1 and 7 days, respectively, in the small intestine, which declined rapidly with reversion to control diet. No change in GLUT5 protein levels was seen after glucose- or sucrose-enriched diets. Glucose, and to a lesser extent fructose, feeding resulted in an increase in the basolateral GLUT2 protein. Feeding glucose to the rats caused a rise in sodium-dependent glucose transporter isoform (SGLT1) protein levels compared with the control diet. There was a transient increase in the small intestine GLUT5 mRNA 1 day after fructose feeding, which returned to normal by 7 days. In the kidney, both fructose and sucrose increased GLUT5 protein levels three- to fourfold, whereas glucose had no effect. Fructose-enriched diet did not increase the levels of GLUT5 protein or mRNA in a segment of small intestine that was isolated from the rest of the small intestine but continued to have mesenteric blood supply. The results suggest that the levels of GLUT5 protein are regulated by fructose, its in vivo substrate, in both the small intestine and kidney, and the regulation requires fructose to interact with the brush border of the small intestine, possibly stabilizing the protein.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2005

Differential regulation of insulin resistance and hypertension by sex hormones in fructose-fed male rats.

Differences in gender are in part responsible for the development of insulin resistance (IR) and associated hypertension. Currently, it is unclear whether these differences are dictated by gender itself or by the relative changes in plasma estrogen and/or testosterone. We investigated the interrelationships between testosterone and estrogen in the progression of IR and hypertension in vivo in intact and gonadectomized fructose-fed male rats. Treatment with estrogen significantly reduced the testosterone levels in both normal chow-fed and fructose-fed rats. Interestingly, fructose feeding induced a relative increase in estradiol levels, which did not affect IR in both intact and gonadectomized fructose-fed rats. However, increasing the estrogen levels improved insulin sensitivity in both intact and gonadectomized fructose-fed rats. In intact males, fructose feeding increased the blood pressure (140 +/- 2 mmHg), which was prevented by estrogen treatment. However, the blood pressure in the fructose-fed estrogen rats (125 +/- 1 mmHg) was significantly higher than that of normal chow-fed (113 +/- 1 mmHg) and fructose-fed gonadectomized rats. Estrogen treatment did not affect the blood pressure in gonadectomized fructose-fed rats (105 +/- 2 mmHg). These data suggest the existence of a threshold value for estrogen below which insulin sensitivity is unaffected. The development of hypertension in this model is dictated solely by the presence or absence of testosterone. In summary, the development of IR and hypertension is governed not by gender per se but by the interactions of specific sex hormones such as estrogen and testosterone.

Animals↗
PubMed2000

Effects of intraduodenal glucose and fructose on antropyloric motility and appetite in healthy humans.

Oral fructose empties from the stomach more rapidly and may suppress food intake more than oral glucose. The purpose of the study was to evaluate the effects of intraduodenal infusions of fructose and glucose on antropyloric motility and appetite. Ten healthy volunteers were given intraduodenal infusions of 25% fructose, 25% glucose, or 0.9% saline (2 ml/min for 90 min). Antropyloric pressures, blood glucose, and plasma insulin, gastric inhibitory peptide (GIP), and glucagon-like peptide-1 (GLP-1) were measured concurrently; a buffet meal was offered at the end of the infusion. Intraduodenal fructose and glucose suppressed antral waves (P < 0. 0005 for both), stimulated isolated pyloric pressure waves (P < 0.05 for both), and increased basal pyloric pressure (P = 0.10 and P < 0. 05, respectively) compared with saline, without any significant difference between them. Intraduodenal glucose increased blood glucose (P < 0.0005), as well as plasma insulin (P < 0.0005) and GIP (P < 0.005) more than intraduodenal fructose, whereas there was no difference in the GLP-1 response. Intraduodenal fructose suppressed food intake compared with saline (P < 0.05) and glucose (P = 0.07). We conclude that, when infused intraduodenally at 2 kcal/min for 90 min 1) fructose and glucose have comparable effects on antropyloric pressures, 2) fructose tends to suppress food intake more than glucose, despite similar GLP-1 and less GIP release, and 3) GIP, rather than GLP-1, probably accounts for the greater insulin response to glucose than fructose.

Adult↗