Impact of the short-term, intense exercise on postprandial glycemia in type 2 diabetic patients treated with gliclazide.

BACKGROUND: Physical activity is crucial for treatment of diabetes. However, intensive exercise brings the risk for metabolic decompensation; therefore, predicting its effect on glycemia is of great importance. MATERIALS AND METHODS: Fourteen type 2 diabetic patients (47.9+/-1.6 years; mean+/-S.E.M.), treated with gliclazide, and 14 healthy controls (45.1+/-1.0 years) were subjected to standard graded submaximal (90% HR(max)) exercise treadmill testing for 2 h after standardized breakfast. Blood glucose, lactate, insulin, and proinsulin concentrations were measured on fasting and during the periexercise period up to 120 min after the effort. Glucagon, growth hormone, cortisol, and catecholamines were determined up to 60 min of the recovery period. RESULTS: After exercise, glycemia decreased from the preexercise value of 11.3+/-1.4 to 8.0+/-1.1 mmol/l at 120 min (P<.001) in the diabetic group, while in controls, it did not change significantly. Shift in glycemia during and after exercise in the diabetic group was dependent on preexercise glycemia, according to the quadratic polynomial regression model, whereas a simple negative correlation between these indices was found in the control group. Insulinemia tended to decrease from the midexercise maximum of 488+/-116 to 261+/-71 pmol/l at the 120th min in diabetic patients. Neither hypoglycemia nor deficit in response of counterregulatory hormones was observed. CONCLUSIONS: In the type 2 diabetic patients treated with gliclazide, short-term, intensive, submaximal exercise, performed 2 h after a meal, causes reduction of hyperglycemia during the recovery period. Preexercise glycemia was found to be a primary predictor of the shift in glycemia under the exercise, according to the polynomial regression model.

[Hyperammonemia type II as an example of urea cycle disorder]. / Hiperamonemia typu ii jako przyklad choroby cyklu mocznikowego.

Ornithine transcarbamylase deficiency is the most common inherited urea cycle disorder. Its clinical manifestations as lethargy, vomites, coma and cerebral edema are the effect of the higher concentration of the ammonia in plasma. Hyperammonemia, caused by mutation in ornithine transcarbamylase gene, is often considered as a reason of coma by pediatricians but skipped by internist, although it is the third reason of hepatic coma in adults. This article is the recapitulation of published studies and their implication on everyday clinical practice.