Abstract
Fructose accumulates in tissue and body fluids of patients affected by hereditary fructose intolerance (HFI), a disorder caused by the deficiency of aldolase B. We investigated the effect of acute fructose administration on the biochemical profile and on the activities of the Krebs cycle enzymes in the cerebral cortex of young rats. Rats received a subcutaneous injection of NaCl (0.9 %; control group) or fructose solution (5 μmol/g; treated group). Twelve or 24 h after the administration, the animals were euthanized and the cerebral cortices were isolated. Peripheral blood (to obtain the serum) and cerebral spinal fluid (CSF) from the animals were also collected. It was observed that albumin levels were decreased and cholesterol levels were increased in CSF of animals 12 h after the administration of fructose. In addition, serum lactate levels were increased 12 h after the administration, as compared to control group. Furthermore, malate dehydrogenase activity was increased in cerebral cortex from treated group 24 h after the administration of this carbohydrate. Herein we demonstrate that fructose administration alters biochemical parameters in CSF and serum and bioenergetics parameters in the cerebral cortex. These findings indicate a possible role of fructose on brain alterations found in HFI patients.
Highlights
Fructose (β-D-fructofuranose) is a glucose epimer widely found in food, especially fruits and honey (Hardinge et al 1965, Somogyi and Trautner 1974).There are several studies showing toxic effect of fructose per se (Yokozawa et al 2008, Fan et al 2014, Yeh et al 2014) or by inducing glyoxal and methylglyoxal formation (Maruf et al 2015)
Previous studies from our group described an animal model of fructosemia induced chemically by administrating fructose acutely to rats (Monteiro et al 2012, Lopes et al 2014). By using this experimental model, we evaluated the biochemical profile in cerebral spinal fluid (CSF) and serum and the activities of Krebs cycle enzymes in the cerebral cortex of young rats
We first investigated biochemical parameters in CSF of rats submitted to acute fructose administration
Summary
Fructose (β-D-fructofuranose) is a glucose epimer widely found in food, especially fruits and honey (Hardinge et al 1965, Somogyi and Trautner 1974).There are several studies showing toxic effect of fructose per se (Yokozawa et al 2008, Fan et al 2014, Yeh et al 2014) or by inducing glyoxal and methylglyoxal formation (Maruf et al 2015). HFI (OMIM 229600) is an autosomal recessive inborn error of fructose metabolism caused by the deficiency of the enzyme fructose1-fosfato aldolase (EC 4.1.2.7.), known as aldolase B. This enzyme is present in liver, kidney, and small intestine (Van den Berghe 1986). The deficiency leads to the accumulation of fructose in biological fluids and tissues of patients (Steinmann et al 2001). Continuous exposure of patients affected by HFI to fructose during infancy may result in liver damage, mental retardation, and even death (Gopher et al 1990, Steinmann et al 2001). Hyperuricemia, hypophosphatemia, hyperlactatemia, and metabolic acidosis (Cornblath et al 1963, Perheetupa et al 1972, Froesch 1976, 1978)
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
