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At least 487 records · Page 27Linked to original sources
PubMed2000

A high-fructose diet induces changes in pp185 phosphorylation in muscle and liver of rats.

Insulin stimulates the tyrosine kinase activity of its receptor resulting in the tyrosine phosphorylation of pp185, which contains insulin receptor substrates IRS-1 and IRS-2. These early steps in insulin action are essential for the metabolic effects of insulin. Feeding animals a high-fructose diet results in insulin resistance. However, the exact molecular mechanism underlying this effect is unknown. In the present study, we determined the levels and phosphorylation status of the insulin receptor and pp185 (IRS-(1/2)) in liver and muscle of rats submitted to a high-fructose diet evaluated by immunoblotting with specific antibodies. Feeding fructose (28 days) induced a discrete insulin resistance, as demonstrated by the insulin tolerance test. Plasma glucose and serum insulin and cholesterol levels of the two groups of rats, fructose-fed and control, were similar, whereas plasma triacylglycerol concentration was significantly increased in the rats submitted to the fructose diet (P<0.05). There were no changes in insulin receptor concentration in the liver or muscle of either group. However, insulin-stimulated receptor autophosphorylation was reduced to 72 +/- 4% (P<0.05) in the liver of high-fructose rats. The IRS-1 protein levels were similar in both liver and muscle of the two groups of rats. In contrast, there was a significant decrease in insulin-induced pp185 (IRS-(1/2)) phosphorylation, to 83 +/- 5% (P<0.05) in liver and to 77 +/- 4% (P<0.05) in muscle of the high-fructose rats. These data suggest that changes in the early steps of insulin signal transduction may have an important role in the insulin resistance induced by high-fructose feeding.

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↗
PubMed1995

A fructose-rich diet decreases insulin-stimulated glucose incorporation into lipids but not glucose transport in adipocytes of normal and diabetic rats.

To study the cellular mechanisms underlying fructose-induced insulin resistance in rats, the effects of fructose feeding on insulin-stimulated glucose transport, oxidation and incorporation into lipids in epididymal adipocytes were evaluated in 27 normal and 27 noninsulin-dependent diabetic male Sprague-Dawley rats. Diabetes was induced by streptozotocin injection 2 d after birth. At 5 wk of age, both normal and diabetic rats were fed a diet containing 62% carbohydrate as fructose, dextrose or cornstarch. Fructose feeding for 6 wk induced glucose intolerance in normal rats (P < 0.05) and aggravated that of diabetic rats (P < 0.05). Plasma triacylglycerol concentration was higher in fructose-fed than in starch-fed or dextrose-fed rats (P < 0.05). Adipocytes of fructose-fed rats had significantly lower maximum insulin-stimulated glucose incorporation into total lipids than those of rats fed starch, and tended (P = 0.22) to have lower production of CO2 from glucose than adipocytes of the other dietary groups. Glucose transport in adipocytes of dextrose-, starch- and fructose-fed rats did not differ. We conclude that in both normal and diabetic rats, a chronic fructose-rich diet induced hypertriacylglycerolemia, glucose intolerance and insulin resistance of adipocytes.

Adipocytes↗
PubMed2002

Taurine modulates antioxidant potential and controls lipid peroxidation in the aorta of high fructose-fed rats.

High dosage of fructose induces insulin resistance, glucose intolerance and alterations in plasma lipid profile in normal rats. Recently, it has been shown that these rats also develop oxidative stress, which plays a prominent role in diabetic pathology. We now report the effect of taurine on the susceptibility of the aorta to lipid peroxidation and also on the activities of enzymic and non-enzymic antioxidants in rats fed a high fructose-diet for 4 weeks. Fructose-fed rats were more susceptible to lipid peroxidation as measured by thiobarbituric acid reactivity, and antioxidant status was significantly lower. Taurine supplementation caused a significant reduction in the production of thiobarbituric acid--reactive substances and significant rises in antioxidant enzyme activities. The levels of lipid peroxides, diene conjugates, lipofuscin and hydroperoxides were significantly higher in fructose-fed rats. When these rats received taurine in drinking water, no peroxidative changes were observed. Increased aorta lipid peroxidation could play a role in the pathology associated with fructose-feeding, and taurine reduces the lipid peroxidation by inducing antioxidant enzymes.

Animals↗
PubMedDate not supplied

Effects of oral fructose in normal, diabetic, and impaired glucose tolerance subjects.

We studied the acute effects of oral ingestion of 50-g loads of dextrose, sucrose, and fructose on post-prandial serum glucose, insulin, and plasma glucagon responses in 9 normal subjects, 10 subjects with impaired glucose tolerance, and 17 non-insulin-dependent diabetic subjects. The response to each carbohydrate was quantified when the respective carbohydrate was given alone in a drink or when given in combination with protein and fat in a test meal. The data demonstrate that (1) fructose ingestion resulted in significantly lower serum glucose and insulin responses than did sucrose or dextrose ingestion in all study groups, either when given alone or in the test meal; (2) although fructose ingestion always led to the least glycemic response compared with the other hexoses, the serum glucose response to fructose was increased the more glucose intolerant the subject; (3) urinary glucose excretion during the 3 h after carbohydrate ingestion was greatest after dextrose and least after fructose in all groups. In conclusion, fructose ingestion results in markedly lower serum glucose and insulin responses and less glycosuria than either dextrose or sucrose, both when given alone or as a constituent in a test meal. However, as glucose tolerance worsens, an increasingly greater glycemic response to fructose is seen.

Administration, Oral↗
PubMed1996

Bradykinin may not be involved in improvement of insulin resistance by angiotensin converting enzyme inhibitor.

We have previously demonstrated that captopril ameliorates glucose intolerance by partially preventing the reduction in postprandial skeletal muscle blood flow. The present study was designed to clarify the mechanism by which ACE inhibitors affect glucose metabolism in fructose (FRU)-fed Wistar rats with hypertension, glucose intolerance and hyperinsulinemia. Eight-week-old male rats (n = 51) were divided into six groups. Controls were given a normal chow, while fructose-rich (55%) chow was administered to the remainder for eight weeks. The different groups were administered alacepril (ALA, 30 mg/kg/day) with or without a continuous infusion of Hoe 140, a kinin B2 receptor antagonist (150 micrograms/kg/day), Hoe 140 alone or TCV-116 (1 mg/kg/day), an angiotensin II receptor antagonist, alone. After measuring the body weight and systolic blood pressure (BP), steady-state plasma glucose (SSPG) levels were determined. FRU significantly increased BP from 141 mmHg in controls to 156 mmHg. ALA with or without Hoe 140 decreased BP to 124 mmHg or 117 mmHg, respectively, but Hoe 140 alone did not affect BP. TCV-116 also decreased BP to 116 mmHg. The SSPG levels increased from 7.58 mM in controls to 8.98 mM in FRU-fed rats. This was lowered with both ALA and TCV-116. Hoe 140 alone, however, did not affect SSPG levels. Hoe 140 did not show any effects on ALA-induced improvement of SSPG. These results suggest that the improvement in glucose tolerance observed with ACE inhibitors is not due to the kinins, and angiotensin II receptor antagonists also improve insulin sensitivity.

Angiotensin Receptor Antagonists↗
PubMed1984

Metabolic effects of glucose compared with invertose and a mixture of fructose, glucose and xylitol before and after moderate surgical trauma.

The metabolic and clinical effects of different isocaloric carbohydrate infusions were studied perioperatively in 54 female patients undergoing cholecystectomy. The patients were randomized to six treatment groups, who received infusions only postoperatively (group 1, 2 and 3) or pre- as well as postoperatively (group 4, 5 and 6). One litre was given during 8 h as a 12% infusion solution. Glucose (group 1 and 4) was compared to invertose (group 2 and 5) and to a mixture of fructose, glucose and xylitol 2:1:1 i.e. Triofusin (group 3 and 6). The glycogen content in liver biopsies, taken peroperatively, was significantly higher when infusions were given preoperatively. No significant differences were found between groups, when comparing the different carbohydrate infusions. A minor glucose intolerance was noticed postoperatively, especially in group 4, whereas no fructose or xylitol intolerance was seen. Lactataemia was insignificant and acid-base balance normal in all groups. Serum urea concentrations were lower when preoperative infusions were given but without differences between groups 4, 5 and 6. Electrolytes, creatinine, hemoglobin, hematocrite and liver function tests were unaltered and the clinical course was uncomplicated in all cases. No side effects were observed. It is concluded that the infusion of one litre 12% Triofusin can be used as effectively and safely as 12% glucose and invertose before and after moderate surgical trauma. But no obvious advantage with Triofusin was revealed.

Journal Article↗
PubMed2003

Activation of the hexosamine signaling pathway in adipose tissue results in decreased serum adiponectin and skeletal muscle insulin resistance.

Overexpression of the rate-limiting enzyme for hexosamine synthesis (glutamine:fructose-6-phosphate amidotransferase) in muscle and adipose tissue of transgenic mice was previously shown to result in insulin resistance and hyperleptinemia. Explanted muscle from transgenic mice was not insulin resistant in vitro, suggesting that muscle insulin resistance could be mediated by soluble factors from fat tissue. To dissect the relative contributions of muscle and fat to hexosamine-induced insulin resistance, we overexpressed glutamine:fructose-6-phosphate amidotransferase 2.5-fold, specifically in fat under control of the aP2 promoter. Fasting glucose, insulin, and triglycerides were unchanged in the transgenic mice; leptin and beta-hydroxybutyrate levels were 91% and 29% higher, respectively. Fasted transgenic mice have mild glucose intolerance and skeletal muscle insulin resistance in vivo. In fasting transgenic mice, glucose disposal rates with hyperinsulinemia were decreased 27% in females and 10% in males. Uptake of 2-deoxy-D-glucose into muscle was diminished by 45% in female and 21% in male transgenics. Serum adiponectin was also lower in the fasted transgenics, by 37% in females and 22% in males. TNF alpha and resistin mRNA levels in adipose tissue were not altered in the fasted transgenics; levels of mRNA for leptin were increased and peroxisome proliferator-activated receptor gamma decreased. To further explore the relationship between adiponectin and insulin sensitivity, we examined mice that have been refed for 6 h after a 24-h fast. Refeeding wild-type mice resulted in decreased serum adiponectin and increased leptin. In transgenic mice, however, the regulation of these hormones by refeeding was lost for adiponectin and diminished for leptin. Refed transgenic female and male mice no longer exhibited decreased serum adiponectin in the refed state, and they were no longer insulin resistant as by lower or unchanged insulin and glucose levels. We conclude that increased hexosamine levels in fat, mimicking excess nutrient delivery, are sufficient to cause insulin resistance in skeletal muscle. Changes in serum adiponectin correlate with the insulin resistance of the transgenic animals.

3-Hydroxybutyric Acid↗
PubMed1988

Effect of fructose on phenylephrine-induced glucose output in perfused rat liver.

Glucose output induced by phenylephrine in perfused livers of fed rats was decreased by 34% during an infusion of fructose, but was increased by 30% (compared to controls) following cessation of fructose infusion. Corresponding changes in hepatic inorganic phosphate (Pi) were also observed with a 40% decrease and a 48% increase in Pi concentration being measured during and following fructose infusion, respectively. The data suggest that the glycogenolytic response to phenylephrine is dependent on the hepatic Pi concentration. It is also suggested that enhanced hepatic Pi concentrations and glycogenolytic responses observed following fructose infusion may antagonize insulin-induced suppression of hepatic glucose output and thus play a role in the glucose intolerance and insulin resistance associated with sucrose or fructose feeding.

Animals↗
PubMed1998

Cardiovascular kinin-generating capability in hypertensive fructose-fed rats.

OBJECTIVE: The hypertensive state is often associated with metabolic abnormalities, including glucose intolerance. Tissue kallikrein, a potent kinin-generating enzyme, is present in the vascular wall and heart tissue. High dietary fructose consumption is reported to induce hyperinsulinemia, hypertriglyceridemia and hypertension. The objective of the present study was to examine the status of kallikrein in vascular and cardiac tissue from highly fructose-fed rats and to delineate the effect of kinins and the angiotensin converting enzyme inhibitor ramipril in this animal model of glucose intolerance. DESIGN AND METHODS: Male Wistar rats (350 g body weight) were divided into four groups of 10 rats each: (1) controls; (2) oral ramipril at 500 microg/kg per day for the last 2 study weeks; (3) fructose in drinking water as a 10% (w/v) solution for 4 weeks; and (4) fructose + ramipril, with fructose administered as in group 3 plus the administration of ramipril for the last 2 study weeks. Systolic blood pressure (tail-cuff method), glucose tolerance (2 g/kg body weight intraperitoneally) and metabolic parameters were recorded. Kallikrein activity in tail artery and heart tissue homogenates was estimated at the end of the 4th study week from measurements of kininogenase activity and kinins generated by a radioimmunoassay. RESULTS: The area under the curve for the glucose tolerance test increased from 1265 +/- 103 mmol/l after 120 min in the control and 1152 +/- 36 mmol/l in the ramipril group (NS) to 2628 +/- 143 mmol/l in the fructose group (P<0.01). The administration of ramipril to fructose-treated rats in group 4 improved glucose tolerance (2160 +/- 100 mmol/l; P<0.05 versus group 3). Blood pressure increased significantly in fructose-fed rats but fell markedly in fructose-fed rats treated with ramipril (P<0.01). Kallikrein activity measured in the heart and vessels increased as a consequence of fructose administration (P<0.05), but the administration of ramipril increased this parameter to a much greater extent (P<0.01 versus control group), which correlated closely with the decrease in blood pressure and the improvement in glucose tolerance observed in the fructose + ramipril group. CONCLUSIONS: The administration of fructose as a solution in the drinking water induced glucose intolerance and increased blood pressure. Treatment with the angiotensin converting enzyme inhibitor ramipril improved glucose tolerance and significantly diminished blood pressure. Cardiovascular kinin-generating capability increased in treated animals and this increase was even higher when rats were treated with ramipril, suggesting that kinins, acting as a paracrine hormonal system, can exert cardiovascular protection and contribute to the beneficial effects of angiotensin converting enzyme inhibitor.

Animals↗
PubMed2000

Overexpression of glutamine: fructose-6-phosphate amidotransferase in the liver of transgenic mice results in enhanced glycogen storage, hyperlipidemia, obesity, and impaired glucose tolerance.

To examine the effect of increased hexosamine flux in liver, the rate-limiting enzyme in hexosamine biosynthesis (glutamine:fructose-6-phosphate amidotransferase [GFA]) was overexpressed in transgenic mice using the PEPCK promoter. Liver from random-fed transgenic mice had 1.6-fold higher GFA activity compared with nontransgenic control littermates (276 +/- 24 pmol x mg(-1) x min(-1) in transgenic mice vs. 176 +/- 18 pmol x mg(-1) x min(-1) in controls, P < 0.05) and higher levels of the hexosamine end product UDP-N-acetyl glucosamine (288 +/- 11 pmol/g in transgenic mice vs. 233 +/- 10 pmol/g in controls, P < 0.001). Younger transgenic mice compared with control mice had lower fasting serum glucose (4.8 +/- 0.5 mmol/l in transgenic mice vs. 6.5 +/- 0.8 mmol/l in controls, P < 0.05) without higher insulin levels (48.0 +/- 7.8 pmol/l in transgenic mice vs. 56.4 +/- 5.4 pmol/l in controls, P = NS); insulin levels were significantly lower in transgenic males (P < 0.05). At 6 months of age, transgenic animals had normal insulin sensitivity by the hyperinsulinemic clamp technique. Hepatic glycogen content was higher in the transgenic mice (108.6 +/- 5.2 pmol/g in transgenic mice vs. 32.8 +/- 1.3 micromol/g in controls, P < 0.01), associated with an inappropriate activation of glycogen synthase. Serum levels of free fatty acids (FFAs) and triglycerides were also elevated (FFAs, 0.67 +/- 0.03 mmol/l in transgenic mice vs. 0.14 +/- 0.01 in controls; triglycerides, 1.34 +/- 0.15 mmol/l in transgenic mice vs. 0.38 +/- 0.01 in controls, P < 0.01). Older transgenic mice became heavier than control mice and exhibited relative glucose intolerance and insulin resistance. The glucose disposal rate at 8 months of age was 154 +/- 5 mg x kg(-1) x min(-1) in transgenic mice vs. 191 +/- 6 mg x kg(-1) x min(-1) in controls (P < 0.05). We conclude that hexosamines are mediators of glucose sensing for the regulation of hepatic glycogen and lipid metabolism. Increased hexosamine flux in the liver signals a shift toward fuel storage, resulting ultimately in obesity and insulin resistance.

Adenosine Triphosphate↗
PubMedDate not supplied

Carbohydrate malabsorption in clinical routine: a prospective observational study.

BACKGROUND/AIMS: Nonspecific abdominal symptoms are a serious problem throughout the world. Among the multitude of differential diagnoses in carbohydrate malabsorption, only incomplete absorption of lactose is mentioned, while malabsorption of fructose and sorbitol--which occurs much more often, at least in the Western world--is usually not included. METHODOLOGY: During a 6-month period, all patients (n=90; 33 males, median age 45 years, range 10-81; 57 females, median age 47 years, range 15-71) who consecutively presented for H2 exhalation tests were evaluated. In addition to the test results, data were obtained from the referring physicians and from the family doctors responsible for the patients' long-term treatment regarding the role of the test results in the treatment of the patients. Finally, the patients were also asked whether any improvement in their symptoms had followed from the test results. RESULTS: Lactulose tests were normal in only 63% of the patients. As with the other sugars, at least one form of malabsorption was detected in 47 patients (52%). The malabsorption rate was 34% after lactose, 61% after fructose, and 91% after the intake of sorbitol. The referring physicians evaluated the test results as having been important in 52% of the patients, while the family doctors considered that there was some benefit for the patients in 77% of the cases. The patients themselves reported an improvement in 75% of cases. CONCLUSIONS: These data again show that carbohydrate malabsorption is an important differential diagnosis in patients with nonspecific abdominal complaints. However, the data also make it clear that caution is advisable both in establishing the indication for the tests and in interpreting the results. Despite this, carbohydrate malabsorption appears to be an underestimated problem in a considerable number of patients.

Adolescent↗
PubMed1986

Dietary fructose in the management of intractable diarrhea of infancy.

Carbohydrate digestion/absorption was evaluated in 11 infants with intractable diarrhea while they were receiving a carbohydrate-free soy-isolate formula. Seven patients were fed within 48 h of admission. Enteral feedings were initiated in the remainder after they had gained 1 kg while receiving parenteral nutrition. All feedings were initially administered by continuous nasogastric infusion. Nine patients were initially fed formula with polymeric glucose; two received fructose as the carbohydrate source, based on a documented history of polymeric glucose intolerance. Five of the nine developed watery, acidic stools while receiving polymeric glucose. All were switched to fructose, which resulted in improvement in stool pH and consistency. Glucose tolerance was normal 1 month after discharge in all seven fructose-requiring infants. Three of six infants have shown a persistent inability to hydrolyze sucrose. Several putative mechanisms of polymeric glucose intolerance are discussed, as well as the apparent association with primary sucrase-isomaltase deficiency in three of the patients. Fructose is an effective alternative carbohydrate source in infants unable to tolerate polymeric glucose, and early initiation of fructose may obviate the need for total parenteral nutrition and prolonged bowel rest.

Diarrhea, Infantile↗
PubMed2001

Suppressed gene expression of adipocyte resistin in an insulin-resistant rat model probably by elevated free fatty acids.

Resistin, the peptide specifically secreted from adipocytes, is a hormone antagonistic to insulin action and, thus, may serve as a link between human obesity due to adiposity and insulin resistance associated with type 2 diabetes. To test this hypothesis, we studied the gene expression of resistin in adipocytes isolated from rats fed with a fructose diet which induced insulin resistance. Compared to the control rats (C) on a normal chow diet, the fructose-fed rats (F) developed hyperinsulinemia, glucose intolerance, hypertriglyceridemia and hypertension, a profile reminiscent of the syndrome X of patients with non-insulin-dependent diabetes mellitus (NIDDM). The F rats had significantly elevated plasma free fatty acids (FFA), enlarged epididymal fat pads, and increased adipocyte size compared with the C rats. We examined the glucose transport and the relative quantity of resistin mRNA produced in the adipocytes of these two groups of rats. Compared to the C rats, the F rats had a clearly reduced insulin-stimulated glucose transport. The gene expression of resistin and other adipocyte peptides was measured on the mRNA by semiquantitative RT-PCR; the validity of this technique was established in advance with a rat-fasting and then refeeding experiment. The F rats showed a decreased expression of the resistin gene, whereas gene expression of leptin and angiotensinogen in contrast increased. Free fatty acids were found to suppress the expression of resistin gene in normal rat adipocytes. These results demonstrate that an insulin-resistant instance in the fructose diet rat model exists with the decreased gene expression of resistin.

Adipocytes↗