Plasma D-Glucose, D-Fructose and Insulin Responses after Oral Administration of D-Glucose, D-Fructose and Sucrose to Normal Rats

Prieto, Pablo G.; Cancelas, Jesús; Villanueva-Peñacarrillo, María Luisa; Valverde, Isabel; Malaisse, Willy

doi:10.1080/07315724.2004.10719386

Cited by 26 publications

(20 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The majority of ingested fructose passes via the portal circulation to the liver where it is rapidly cleared. Very little of this escapes the liver first-pass, limiting peak peripheral fructose levels to high micromolar or low millimolar concentrations [11, 16]. Intracellularly, fructose is rapidly phosphorylated by Ketohexokinase (KHK) into fructose 1-phosphate (F1P) (Figure 1).…”

Section: Biochemistry Of Fructose Metabolismmentioning

confidence: 99%

The Sweet Path to Metabolic Demise: Fructose and Lipid Synthesis

Herman

Samuel

2016

Trends in Endocrinology & Metabolism

180

143

View full text Add to dashboard Cite

Epidemiological studies link fructose consumption with metabolic disease, an association attributable in part to fructose mediated lipogenesis. The mechanisms governing fructose-induced lipogenesis and disease remain debated. Acutely, fructose increases de novo lipogenesis through the efficient and uninhibited action of Ketohexokinase and Aldolase B, which yields substrates for fatty-acid synthesis. Chronic fructose consumption further enhances the capacity for hepatic fructose metabolism via activation of several key transcription factors (i.e. SREBP1c and ChREBP), which augment expression of lipogenic enzymes, increasing lipogenesis, further compounding hypertriglyceridemia, and hepatic steatosis. Hepatic insulin resistance develops from diacylglycerol-PKCε mediated impairment of insulin signaling and possibly additional mechanisms. Initiatives that decrease fructose consumption and therapies that block fructose mediated lipogenesis are needed to avert future metabolic pandemics.

show abstract

Section: Biochemistry Of Fructose Metabolismmentioning

confidence: 99%

The Sweet Path to Metabolic Demise: Fructose and Lipid Synthesis

Herman

Samuel

2016

Trends in Endocrinology & Metabolism

180

143

View full text Add to dashboard Cite

show abstract

“…From the physiological standpoint, a recent study revealed that both the immediate and delayed effects of D-fructose, as compared to D-glucose, upon secretory activity may differ in insulin-, somatostatinand glucagon-producing cells (10). The possible participation of D-fructose insulinotropic action in the improvement of Dglucose tolerance evoked in vivo by the ketohexose was also investigated (11). Last, in terms of the perturbation of islet function in type 2 diabetes, several studies aimed at comparing the fate of D-fructose in islets obtained from either control rats or animals currently used as models for this disease (12)(13)(14).…”

Section: Introductionmentioning

confidence: 99%

Fructokinase activity in rat liver, ileum, parotid gland, pancreas, pancreatic islet, B and non-B islet cell homogenates

Giroix

Jijakli²,

Courtois³

et al. 2006

Int J Mol Med

View full text Add to dashboard Cite

Abstract. The presence of fructokinase (ketohexokinase) in rat pancreatic islet homogenates was previously documented. However, no information was so far available on the activity of this enzyme in islets relative to that in other tissues and on the respective contribution of insulin-producing B cells and non-B islet cells. The present study provides such an information. The activity of fructokinase, as assessed by the phosphorylation of 1.0 mM D-fructose, was compared to that of hexokinase isoenzyme(s), as measured in the presence of 1.0 mM Dglucose, and further characterized by its heat-resistance, K + dependency and resistance to the inhibitory action of D-mannoheptulose. As judged from the results obtained in heated homogenates, the activity of fructokinase, expressed relative to protein content (nmol/min per mg protein) was highest in liver (21.5±2.5; n=11) and lowest in parotid gland (0.16±0.09; n=3), with in-between values in ileum (2.45±0.53; n=3), pancreas (0.82±0.11; n=11) and pancreatic islets (0.46±0.07; n=6). The paired ratio between fructokinase and hexokinase isoenzyme activity was also highest in liver (548±45%; n=8) and lowest in parotid gland (0.93±0.52%; n=3). Such a ratio was not significantly different in pancreas, islets and purified B or non-B islet cells, with an overall mean value of 2.57±0.46% (n=12). The present findings thus unambiguously document the presence of fructokinase activity in all cell types under consideration, except possibly parotid cells, with the following hierarchy: liver > ileum > pancreas. Relative to paired hexokinase activity, no obvious difference was found for fructokinase activity in B versus non-B islet cells.

show abstract

“…Changes in the fructose concentration in the peripheral blood after oral fructose administration have been examined in rats by using an enzymatic method [16] and in human subjects by using a colorimetric method [17–21]. In the case of these methods, other reducing substances in the blood complicate the interpretation of the fructose analysis; for example, high glucose content interferes with the measurement of fructose concentrations.…”

Section: Discussionmentioning

confidence: 99%

Eucalyptus Leaf Extract Suppresses the Postprandial Elevation of Portal, Cardiac and Peripheral Fructose Concentrations after Sucrose Ingestion in Rats

Sugimoto

Hosotani

Kawasaki

et al. 2010

J. Clin. Biochem. Nutr.

View full text Add to dashboard Cite

Overintake of sucrose or fructose induces adiposity. Fructose undergoes a strong Maillard reaction, which worsens diabetic complications. To determine whether Eucalyptus globulus leaf extract (ELE) suppresses the postprandial elevation of serum fructose concentrations (SFCs) in the portal, cardiac, and peripheral blood after sucrose ingestion, we performed gas chromatography/mass spectrometry (GC/MS) and measured SFC without any interference by contaminating glucose in the samples. Fasting Wistar rats were orally administered water (control group) or ELE (ELE group) before sucrose ingestion. Blood was collected from the portal vein, heart, and tail. The increase in the SFCs in the portal and cardiac samples 30 min after sucrose ingestion was lower in the ELE group than in the control group. The coefficient of correlation between the SFCs in the portal and cardiac samples was 0.825. The peripheral SFC in the control group progressively increased and was 146 µmol/L at 60 min. This increase was significantly lower in the ELE group. In contrast, the serum glucose concentrations in the 2 groups were similar. ELE suppressed postprandial hyperfructosemia in the portal, cardiac, and peripheral circulations. ELE may counteract glycation caused by high blood fructose concentrations induced by the consumption of fructose-containing foods or drinks.

show abstract

Plasma D-Glucose, D-Fructose and Insulin Responses after Oral Administration of D-Glucose, D-Fructose and Sucrose to Normal Rats

Cited by 26 publications

References 14 publications

The Sweet Path to Metabolic Demise: Fructose and Lipid Synthesis

The Sweet Path to Metabolic Demise: Fructose and Lipid Synthesis

Fructokinase activity in rat liver, ileum, parotid gland, pancreas, pancreatic islet, B and non-B islet cell homogenates

Eucalyptus Leaf Extract Suppresses the Postprandial Elevation of Portal, Cardiac and Peripheral Fructose Concentrations after Sucrose Ingestion in Rats

Contact Info

Product

Resources

About