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PubMedDate not supplied

[Clinical heterogeneity in fructose intolerance].

We observed eight infants with hereditary fructose intolerance which had been diagnosed by the fructose tolerance test and an aldolase assay on biopsied liver. None of these had been diagnosed before their admission to our department. The most frequent symptoms were vomiting and failure to thrive. All the patients had hepatomegaly. Laboratory findings were indicative of disturbed hepatic function. Hypoglycemia was found in only 3 out of 8 patients. The course was lethal in 2 patients; the 6 survivors are doing well following a fructose-free diet. The importance of practising paediatricians having the detailed nutritional history of the patient and precise knowledge of infant food formulae is stressed. The danger of using fructose continuing solutions for infusion therapy is pointed out. We also report a case of F-1,6-diphosphatase deficiency.

Carbohydrate Metabolism, Inborn Errors↗
PubMed1995

[Effects of vanadate on glucose metabolism in the lens of rats with streptozotocin-induced diabetes--ketohexokinase and aldolase activity].

The effects of vanadate, an oxidized form of vanadium, on glucose metabolism of the lens in diabetic rats were studied. Five-week-old male Sprague-Dawley rats were rendered diabetic with intraperitoneal injection of streptozotocin (50 mg/kg). One week later, the diabetic rats were given 0.2 g/l NaVO3 -5g/l NaCl solution in drinking water ad libitum for 2 weeks and biochemical parameters in their lenses were determined. Blood glucose levels significantly decreased in the vanadate-administered diabetic rats (DV group), compared with the diabetic rats given no vanadate (D group). In the DV group, a significant decrease was observed in lens fructose content compared with the D group. Lens ketohexokinase activity tended to be higher and lens aldolase activity was significantly higher in the DV group than in the D group. These results indicate that vanadate accelerates the metabolic reaction from sorbitol pathway to glycolysis.

Animals↗
PubMedDate not supplied

Peripheral nerve protein glycation and muscle fructolysis: evidence of abnormal carbohydrate metabolism in ALS.

Conversion of glucose to fructose via sorbitol depends upon the enzymes aldose reductase and sorbitol dehydrogenase and is called the polyol pathway. It is particularly active in muscle from patients with X-linked muscular dystrophies (15). This investigation shows enhanced metabolism of glucose to fructose in muscle from patients with ALS. Evidence is also presented showing increased activities of ketohexokinase and F-1-P splitting aldolase, which suggests that further metabolism of fructose may occur via a fructolytic pathway. Investigation of protein glycation, by an adapted fructosamine assay, in post mortem muscle, sural nerve and blood indicates that there is an increased concentration of glucose in muscle and nerve in the period prior to sampling, but blood glucose concentrations were within normal limits. The implications of fructolysis and the relationship of altered glucose metabolism in ALS are discussed.

Amyotrophic Lateral Sclerosis↗
PubMed1996

Protection of astrocytes by fructose 1,6-bisphosphate and citrate ameliorates neuronal injury under hypoxic conditions.

Fructose 1,6-bisphosphate (FBP) protects astrocytes from hypoxic injury in vitro. To determine whether FBP and citrate (inhibitors of phosphofructokinase) ameliorate hypoxia-induced injury to neurons and, if they do, whether the protective effects are a direct result of their actions on neurons or a consequence of their actions on astrocytes, we added FBP or citrate to the media of normoxic and hypoxic 'pure', mixed and co-culture systems. FBP (3.5 mM) and citrate (10 microM-2 mM) decreased release of LDH from astrocytes following 24 h of hypoxia. Eight hours of hypoxia killed pure neuronal cultures and neither FBP nor citrate prevented this death. However, in mixed and co-culture systems, FBP and citrate increased neuronal viability (as determined by the ratio of live-to-total cells), even after 47 h of hypoxia. In co-culture, following 24 h of hypoxia, both FBP and citrate reduced neuronal release of LDH and neuronal death. Fluorocitrate, a suicidal-inhibitor of aconitase, also protected astrocytes, but not neurons, from hypoxia in 'pure' culture, presumably by increasing intracellular citrate concentrations through inhibition of the catalysis of citrate to isocitrate We conclude that FBP and citrate attenuate hypoxic neuronal injury through their effects on astrocytes.

Animals↗
PubMed1997

The effect of diazepan and exercise training on selected biochemical and histochemical properties of rat skeletal muscle.

The effects of chronic diazepam (D) treatment and exercise training on total body mass (TBM), microsomal protein yield (MPY), calcium uptake by fragmented sarcoplasmic reticulum (SR), muscle fibre cross-sectional area, and both PFK and SDH activities were investigated in the tibialis anterior (TA), soleus (Sol), and plantaris (Plt) muscles of 50 male albino Sprague-Dawley rats. Rats were assigned randomly to control (C), sprint-trained (S), or endurance-trained (E) groups. Training was of 12 weeks duration. One-half of each group received daily intraperitoneally D doses of 5 mg kg-1 of TBM. Exercise reduced TBM (p < 0.05); increased the relative BM of the TA (E = 2.02 +/- 0.02, p < 0.01) and Plt (E = 1.15 +/- 0.02, p < 0.01; S = 1.13 +/- 0.03, p < 0.01), as well as the Ca++ uptake of the Sol SR (C = 0.08 +/- 0.02, E = 0.16 +/- 01, p < 0.05). MPY was elevated in S-Sol (C = 1.12 +/- 0.6, S = 1.52 +/- 0.1, p < 0.01). D elevated Sol MPY as well as TA PFK. S-trained animals had lower mean fibre areas than the E-trained (D-treated and untreated) animals. The elevated relative masses of TA and Plt are explained by a decreased TBM with exercise. The increased Ca++ uptake of the Sol indicates that E enhances this function, and the increased MPY probably implies an increased SR. The D could be responsible for the D-elevated Sol MPY as well as the TA PFK. El D did not reduce neuromuscular activity to a level adversely affecting oxidative enzyme activity, but in the case of PFK activity in the TA muscle, such a reduction was evident.

Analysis of Variance↗