Effects of Intragastric Fructose and Dextrose on Mesenteric Microvascular Inflammation and Postprandial Hyperemia in the Rat
| Autor: | Kurt P. Schropp, James H. Thomas, Leone F. Mattioli, Naomi B. Holloway, John G. Wood |
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| Rok vydání: | 2011 |
| Předmět: |
Male
medicine.medical_specialty Antioxidant medicine.medical_treatment Medicine (miscellaneous) Hyperemia Inflammation Fructose Oxidative phosphorylation medicine.disease_cause Enteral administration Antioxidants Rats Sprague-Dawley chemistry.chemical_compound Venules Internal medicine Cell Adhesion Leukocytes Animals Medicine Mesentery chemistry.chemical_classification Reactive oxygen species Nutrition and Dietetics Thioctic Acid business.industry Postprandial Period Rats Arterioles Oxidative Stress Glucose Postprandial Endocrinology chemistry medicine.symptom business Oxidative stress |
| Zdroj: | Journal of Parenteral and Enteral Nutrition. 35:223-228 |
| ISSN: | 1941-2444 0148-6071 |
| DOI: | 10.1177/0148607110385819 |
| Popis: | Fructose superfused on the mesenteric venules of rats induces microvascular inflammation via oxidative stress. It is unknown whether intragastric fructose exerts a similar effect and whether fructose impairs postprandial hyperemia (PPH). The goals were to determine whether intragastric fructose administration promotes leukocyte adherence and whether fructose, owing to its oxidative properties, may also impair nitric oxide-dependent PPH in the mesenteric microcirculation of rats.Leukocyte adherence to mesenteric venules, arteriolar velocity, and diameter were measured in Sprague-Dawley rats before and 30 minutes after intragastric (1 mL 0.5 M, ~0.3 g/kg) dextrose (n = 5), fructose (n = 6), and fructose after intravenous injection of the antioxidant α-lipoic acid (ALA, n = 6).Only fructose increased leukocyte adherence: control 2.3 ± 0.3 per 100 µm; fructose 9.7 ± 1.4 per 100 µm (P.001). This effect was independent of changes in venular shear rate: control 269 ± 48 s(-1); fructose 181 ± 27 s(-1) (P.05, r(2) = 0.083 for shear rate vs leukocyte adherence). Dextrose had no effect on leukocyte adherence: control 1.52 ± 0.13 per 100 µm; dextrose 2.0 ± 0.7 per 100 µm (P.05). ALA prevented fructose-induced leukocyte adherence: control 1.9 ± 0.2 per 100 µm; fructose + ALA 1.8 ± 0.3 per 100 µm (P.05). Neither fructose nor dextrose induced PPH: arteriolar velocity: control 3.3 ± 0.49 cm/s, fructose 3.06 ± 0.34 cm/s (P.05); control 3.3 ± 1.0 cm/s, dextrose 3.15 ± 1.1 cm/s (P.05); arteriolar diameter: control 19.9 ± 1.10 µm, fructose 19.7 ± 1.0 µm (P.05); control 21.5 ± 2.6, dextrose 20.0 ± 2.7 µm (P.05).Intragastric fructose induced leukocyte adherence via oxidative stress. Neither dextrose nor fructose induced PPH, likely because of the inhibitory effect of anesthesia on splanchnic vasomotor tone. |
| Databáze: | OpenAIRE |
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