The Concentrations of Fructose, Glucose and Lactate in the Splanchnic Blood Vessels of Rats Absorbing Fructose

Topping, David L.; Mayes, Peter A.

doi:10.1159/000175352

Cited by 66 publications

(39 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In our experiments [unpublished results), we found in peripheral blood (mixed blood from the neck vessels) of rats fed for 3 weeks the fruc tose diet fructose concentrations of 1.7 and 2.2 mg/100 ml in two experimen tal series. Similar concentrations of fructose in the blood were recorded recently by T o p p in g and M ayes [21] in rats after acute administration of fructose. The maximum fructose concentration in their experiments was 20-40 mg/100ml intheportal blood, but only 2-6mg/lOOml in the aortal blood.…”

Section: Discussionsupporting

confidence: 86%

Effect of Dietary Fructose on Fatty Acid Synthesis in Adipose Tissue and on Triglyceride Concentration in Blood in the Rat

Vrána

Fábry

Kazdová³

1973

Ann Nutr Metab

View full text Add to dashboard Cite

Experiments where the inhibition of lipid synthesis from glucose in adipose tissue of rats fed sucrose was analyzed led to the following conclusions:The nutritional factor leading to inhibited fatty acid synthesis from glucose in adipose tissue is fructose, ingested either as such or as part of sucrose. A high fructose intake inhibits in addition to glucose incorporation also acetate incorporation into fatty acids. This indicates that fructose-induced inhibition of fatty acid synthesis in adipose tissue takes place in some step(s) between acetate and fatty acids. Inhibition of fatty acid synthesis in adipose tissue is not caused by the direct effect of the fructose molecule on adipose tissue, but is probably the result of hypertriglyceridemia and the ensuing enhanced supply of fatty acids from triglycerides of blood lipoproteins. The chronological course of changes of hypertriglyceridemia and fatty acid synthesis in adipose tissue, as well as experiments where the effect of diets with a rising fructose ratio was investigated, provide indirect evidence that the factor which determines quantitatively the inhibitory effect of fructose ingestion is probably rather the actual uptake of preformed fatty acids in adipose tissue than the magnitude of hypertriglyceridemia per se.

show abstract

Section: Discussionsupporting

confidence: 86%

Effect of Dietary Fructose on Fatty Acid Synthesis in Adipose Tissue and on Triglyceride Concentration in Blood in the Rat

Vrána

Fábry

Kazdová³

1973

Ann Nutr Metab

View full text Add to dashboard Cite

show abstract

“…Infusion of fructose at this rate has been shown to elicit a steady-state plasma fructose concentration lower than 2.0 mM (28), which is comparable to the concentrations reported in postprandial circulation (29,30) and in our in vitro experiments. A bolus injection of fructose (0.3 g/kg) did not alter plasma glucose or insulin, suggesting that a moderate increase in circulating fructose alone is not sufficient to stimulate insulin release (Fig.…”

Section: Postprandial Concentrations Of Fructose Potentiate Gsis Via supporting

confidence: 86%

Sweet taste receptor signaling in beta cells mediates fructose-induced potentiation of glucose-stimulated insulin secretion

Kyriazis

Soundarapandian

Tyrberg

2012

Proc. Natl. Acad. Sci. U.S.A.

202

186

View full text Add to dashboard Cite

Postprandial insulin release is regulated by glucose, but other circulating nutrients may target beta cells and potentiate glucosestimulated insulin secretion via distinct signaling pathways. We demonstrate that fructose activates sweet taste receptors (TRs) on beta cells and synergizes with glucose to amplify insulin release in human and mouse islets. Genetic ablation of the sweet TR protein T1R2 obliterates fructose-induced insulin release and its potentiating effects on glucose-stimulated insulin secretion in vitro and in vivo. TR signaling in beta cells is triggered, at least in part, in parallel with the glucose metabolic pathway and leads to increases in intracellular calcium that are dependent on the activation of phospholipase C (PLC) and transient receptor potential cation channel, subfamily M, member 5 (TRPM5). Our results unveil a pathway for the regulation of insulin release by postprandial nutrients that involves beta cell sweet TR signaling.saccharin | G-protein coupled receptor | T1R3 | glucagon-like peptide-1 | MIN6

show abstract

“…When ingested by mouth, fructose is initially absorbed by the small intestine and flows through the liver (1). As a consequence of the high rate of extraction of fructose by liver, correspondingly low fructose concentrations are found in systemic blood vessels after meals (11). Several previous studies have examined serum and urinary fructose concentrations in patients with diabetes.…”

Section: Resultsmentioning

confidence: 99%

“…First, impaired fructose metabolism in the liver might play an important role, given that several studies have shown that the liver metabolizes at least half of all fructose (11,13). Second, the transport system for fructose might be disrupted.…”

mentioning

confidence: 99%

Increased Fructose Concentrations in Blood and Urine in Patients With Diabetes

Kawasaki

Akanuma²,

Yamanouchi³

2002

Diabetes Care

213

173

View full text Add to dashboard Cite

OBJECTIVE -To investigate fructose metabolic changes in patients with diabetes.RESEARCH DESIGN AND METHODS -Serum and urinary fructose concentrations were determined in healthy subjects (n ϭ 23) and in nondiabetic (n ϭ 23) and diabetic patients (n ϭ 26). Fructose was measured using our newly developed method, and 13 C 6 -fructose was used as the internal standard. After adding sample to a fixed amount of internal standard, ion-exchange resins and high-performance liquid chromatography pretreatments were performed. Then, the amount of fructose in the sample was measured by gas chromatography-mass spectrometry.RESULTS -Serum fructose concentrations in patients with diabetes (12.0 Ϯ 3.8 mol/l) were significantly higher than those in healthy subjects (8.1 Ϯ 1.0 mol/l, P Ͻ 0.001) and nondiabetic patients (7.7 Ϯ 1.6 mol/l, P Ͻ 0.001), and daily urinary fructose excretion was significantly greater in patients with diabetes (127.8 Ϯ 106.7 mol/day) than in nondiabetic patients (37.7 Ϯ 23.0 mol/day, P Ͻ 0.001). In patients with diabetes (n ϭ 20), serum fructose concentrations (8.6 Ϯ 1.8 mol/l, P Ͻ 0.001) and daily urinary fructose excretion (63.4 Ϯ 63.8 mol/day, P Ͻ 0.01) significantly decreased by week 2 after admission.CONCLUSIONS -The present results differed from those of previous studies in that we found that the serum and urinary fructose concentrations decreased rapidly, concomitant with an improvement in glycemia. Therefore, hyperglycemia was associated with increased serum and urinary fructose concentrations in patients with diabetes. Diabetes Care 25:353-357, 2002F ructose is an important dietary source of carbohydrates. In Western countries, daily intake of fructose by adults is ϳ100 g (1). Due to its unique metabolic properties, fructose promotes adverse metabolic changes, including glucose intolerance (2,3), hyperlipidemia (2,3), and hyperuricemia (4). Moreover, in light of nonenzymatic fructosylation of proteins (5), polyol pathway, and carbonyl stress, fructose is inferred to have an important role in the pathogenesis of diabetic complications. Therefore, if the measurement of serum fructose levels is clinically significant and available as a biomarker, it could be greatly useful. However, previous studies have reported no significant difference in serum fructose concentrations between diabetic and nondiabetic patients (6 -8). In these studies, the pretreatment of samples was insufficient to remove glucose, which interfered with the measurement of fructose. In this study, we report serum and urinary fructose concentrations measured by a newly developed method that overcomes this problem of glucose interference, and we describe fructose kinetic changes in patients with diabetes. RESEARCH DESIGN ANDMETHODS -Three subsets comprised the present study. First, serum fructose concentrations were determined in 23 healthy subjects and in 26 diabetic (diabetes group) and 23 nondiabetic (nondiabetic group) inpatients. Daily urinary fructose excretion was examined in the diabetes group and in the nondiabetic group. Ser...

show abstract

The Concentrations of Fructose, Glucose and Lactate in the Splanchnic Blood Vessels of Rats Absorbing Fructose

Cited by 66 publications

References 13 publications

Effect of Dietary Fructose on Fatty Acid Synthesis in Adipose Tissue and on Triglyceride Concentration in Blood in the Rat

Effect of Dietary Fructose on Fatty Acid Synthesis in Adipose Tissue and on Triglyceride Concentration in Blood in the Rat

Sweet taste receptor signaling in beta cells mediates fructose-induced potentiation of glucose-stimulated insulin secretion

Increased Fructose Concentrations in Blood and Urine in Patients With Diabetes

Contact Info

Product

Resources

About