[Hormones of counter-regulation and metabolism of carbohydrates].
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Biomedical subjects
Publications and source records attributed to A Luyckx.
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1. Twenty-two maturity-onset type diabetics treated with oral hypoglycaemic agents entered a single-blind crossover study using placebo (periods A and C, 2 months each) and clofibrate (2 g/day; period B; 2 months). 2. In thirteen patients, under reasonably good control, clofibrate did not reduce fasting or post-prandial blood glucose, nor 24 h glycosuria; no improvement was noted in the M-value, an index of diabetes control. 3. In contrast, in nine patients, with poor diabetes control, clofibrate reduced 24 h glycosuria and significantly improved the M-value. 4. In all patients, clofibrate therapy was associated with a significant 19-23% reduction in plasma fibrinogen. 5. It is suggested that addition of clofibrate may be useful in maturity-onset diabetics not adequately controlled by diet combined with oral hypoglycaemic agents.
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The effect of a 14 day-administration of butylbiguanide was investigated in a group of 10 obese patients with mild-to-moderate glucose intolerance. Glucose tolerance was significantly improved, while fasting blood glucose and plasma levels of free fatty acids, insulin and glucagon remained unchanged. The estimation of the amount of the oral glucose load oxidized into CO2 was performed by means of a recently described procedure using "naturally labelled 13C-glucose" as tracer. The curves depicting the oxidation of the exogenous glucose load were similar in shape and magnitude before and after administration of the biguanide; in the latter case, however, slightly higher rates of oxidation of exogenous glucose were recorded during the 2nd, 3rd and 4th hours of the test. These data do not provide evidence that the biguanide-induced improvement in glucose tolerance in patients with mild-to-moderate glucose intolerance is associated with any inhibiting or delaying effect of this type of drug on intestinal absorption (and subsequent oxidation) of the exogenous glucose load. On the contrary, a slight, but statistically significant, increase in the oxidation of exogenous glucose has been observed after butylbiguanide.
The distribution of substrates utilized during prolonged exercise was investigated in normal human volunteers with an without ingestion of 100 g exogenous glucose. The energy provided by protein oxidation was derived from urinary nitrogen excretion and the total energy provided by carbohydrates and lipids was calculated from respiratory quotient (RQ) determinations. The contribution of exogenous glucose to the energy supply was determined by an original procedure using "naturally labeled 13C-glucose" as metabolic tracer. Protein oxidation provided between 1 and 2% of the total energy requirement; this amount was not affected by glucose ingestion. In the absence of exogenous glucose ingestion, carbohydrate were progressively replaced by lipids as source of energy. Exogenous glucose contributed markedly to total carbohydrate oxidation and decreased the percentage of energy derived from lipids. In addition, ingestion of exogenous glucose resulted in a significant economy of endogenous carbohydrates and permitted to prolong the duration of exercise.
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Maize glucose was used as a natural tracer for studies of metabolism. It is richer in 13C than common vegetables and foods derived from these, and the C02 formed from it is consequently richer in 13C than the CO2 expired by man fed on a diet of common vegetables. The quantitative results, obtained by measurement of delta 13C of the expired CO2 and of VCO2 during the oxidation of an exogenous glucose load (about 100 g) in eight normal subjects over 7 hr, have shown a consumption of 28.64 +/- 1.44 g of glucose (mean +/- SEM), which represents about 30% of the load given. A comparison is made with the results obtained from other methods and the originality and usefulness of this new quantitative procedure is outlined.
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The aim of the present study was to reconsider the problem of the haematological consequences of biguanide treatment by evaluating serum vitamin B 12 and folic acid levels as well as classical haematological parameters in 30 diabetics treated by metformin. For purpose of comparison, similar evaluations were done in diabetics treated with insulin (27 patients) or sulfonylureas (13 patients). Results indicated that mean serum levels of vitamin B 12 were significantly lower in patients receiving metformin than in both other groups. In the metformin-treated group, five patients had serum levels of vitamin B 12 below 270 pg/ml and five had borderline values. No difference was found in the mean serum folic acid levels between the three groups. Similarly, there were no differences in the red blood cell counts, volumes or haemoglogin concentrations nor in the mean values of serum iron and lacticodeshydrogenase levels between the three groups. Since the haematologic and neurologic complications of vitamin B 12 deficiency may only appear after the deficiency had existed for 10-15 years, the lack of haematological alteration may be explained by the fact that the vitamin B 12 deficiency was not present for a sufficient period of time. We conclude that it may be wise to monitor the haematological values as well as vitamin B 12 levels at regular intervals in diabetic patients treated with metformin so that B 12 hypovitaminosis and its complications can be prevented.
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