PubMed Health⌕ Search

Biomedical subjects

J Rybka

Publications and source records attributed to J Rybka.

At least 19 recordsLinked to original sources
PubMed1999

Fatty acids and glycerol or lactate are required to induce gluconeogenesis from alanine in isolated rabbit renal cortical tubules.

In isolated rabbit renal cortical tubules, glucose synthesis from 1 mM alanine is negligible, while the amino acid is metabolized to glutamine and glutamate. The addition of 0.5 mM octanoate plus 2 mM glycerol induces incorporation of [U-14C]alanine into glucose and decreases glutamine synthesis, whereas oleate and palmitate in the presence of glycerol are less potent than octanoate. Gluconeogenesis is also significantly accelerated when glycerol is substituted by lactate. In view of an increase in 14CO2 fixation and elevation of both cytosolic and mitochondrial NADH/NAD+ ratios, the activation of glucose formation from alanine upon the addition of glycerol and octanoate is likely due to (i) stimulation of pyruvate carboxylation, (ii) increased availability of NADH for glyceraldehyde-3-phosphate dehydrogenase and (iii) elevation of mitochondrial redox state causing a diminished provision of ammonium for glutamine synthesis. The induction of gluconeogenesis in the presence of alanine, glycerol and octanoate is not related to cell volume changes. The results presented in this paper show the importance of free fatty acids and glycerol for regulation of renal gluconeogenesis from alanine. The possible physiological significance of the data is discussed.

Alanine↗
PubMed1998

[The present and future of treatment with oral antidiabetic agents].

Oral antidiabetics (PAD) are still the most frequent pharmacotherapeutic intervention in NIDDM, characterized by insulin deficiency and in particular by insulin resistance in the liver and peripheral tissues. Depending on the site of action, they are divided into substances retarding carbohydrate breakdown in the small intestine (alpha-glucosidase inhibitors), substances stimulating B-cells of the islets of Langerhans (beta-cytotropic substances) and substances acting in the periphery. The authors discuss PAD, in particular SU and biguanides which have been used for treatment for some years and more recent preparations--acarbose (Glucobay) and miglitol. Attention is paid to perspective preparation which are in the research stage, among them in particular troglitazone which belongs into the group of substances which improve the sensitivity of insulin receptors (insulin sensitizers) which will soon be on the market. As to other possibilities the authors discuss the role of fatty acid oxidation and its inhibitors and new non-sulphonyl urea insulin secretagogues. All these preparations, despite certain limitations, offer exciting therapeutic perspectives. Further research will reveal to what extent this potential can be implemented in practice.

Administration, Oral↗
PubMed1997

The efficacy and safety of miglitol therapy compared with glibenclamide in patients with NIDDM inadequately controlled by diet alone.

OBJECTIVE: To compare the therapeutic effects of the alpha-glucosidase inhibitor miglitol (BAY m 1099), the sulfonylurea glibenclamide, and placebo on parameters of metabolic control and safety in patients with NIDDM that is inadequately controlled by diet alone. RESEARCH DESIGN AND METHODS: After a 4-week placebo run-in period, 201 patients in 18 centers in 4 countries were randomized in a double-blind manner to miglitol (50 mg t.i.d., followed by 100 mg t.i.d.), glibenclamide (3.5 mg q.d/b.i.d.), or placebo for 24 weeks. Efficacy criteria were changes from baseline of HbA1c, fasting and postprandial blood glucose and insulin levels, body weight, and serum triglycerides. RESULTS: Efficacy was assessed in 119 patients who completed the full protocol, and the results were similar to those obtained in 186 patients who fulfilled the validity criteria for analysis. Compared with placebo, mean baseline-adjusted HbA1c decreased by 0.75% (P = 0.0021) and 1.01% (P = 0.0001) in the miglitol and glibenclamide treatment groups, respectively. Blood glucose decreased slightly in the fasting state and considerably in the postprandial state in both treatment groups but not in the placebo group. Fasting insulin levels increased slightly (NS) in all treatment groups; however, postprandial insulin levels decreased with miglitol, while increasing markedly with glibenclamide (P = 0.0001 between all treatment groups). Gastrointestinal side effects (flatulence and diarrhea) occurred mostly in the miglitol-treated patients, while some glibenclamide-treated patients had symptoms suggestive of hypoglycemia. CONCLUSIONS: Miglitol monotherapy is effective and safe in NIDDM patients. Compared with glibenclamide, it reduced HbA1c less effectively and caused more gastrointestinal side effects. On the other hand, glibenclamide, unlike miglitol, tended to cause hypoglycemia, hyperinsulinemia, and weight gain, which are not desirable in patients with NIDDM.

1-Deoxynojirimycin↗
PubMed1997

[Special features of strokes in diabetics].

Diabetes mellitus is a potent risk factor of cerebrovascular episodes. All statistics reveal a markedly higher prevalence in diabetic patients, as compared with non-diabetics, a poorer prognosis, more frequent recurrence and higher mortality. These facts are particularly relevant with regard to the increasing rate of diabetes in this country and in the world and also with regard to data on the rising incidence of cerebrovascular episodes in diabetic subjects, at least as recorded e.g. in the USA. Prevention is the concern of diabetologists, specialists in internal medicine and all doctors who are in contact with diabetic patients. Essentially it is identical with systematic diabetological care focused on maintaining a normal blood pressure and normal blood lipid values and acceptable blood sugar values in diabetics patients. Principles of secondary prevention must include monitoring of the arteries of the neck by auscultation and instruments and early correction of revealed serious atherosclerotic changes. Unfortunately this is the rule so far.

Cerebrovascular Disorders↗
PubMed1996

[Diabetic dyslipidemia and its treatment].

A review on the lipid metabolism in IDDM and NIDDM. The paper deals with quantitative and qualitative lipid changes and their relationship with macrovascular diseases. Part of the paper is devoted also to practical problems of dietetic and medicamentous treatment of lipid disorders in diabetes and different hypolipidaemic agents are discussed in detail.

Diabetes Complications↗
PubMed1995

[New aspects of pharmacologic and general prophylactic care of the diabetic foot].

Ischaemia, neuropathies and infections are predisposing factors for the development of ulceration of the diabetic foot. Diabetics have evidently a disposition for affections of the peripheral circulation and impaired regulation of the microcirculation as a result of autonomic neuropathy. The lower the driving pressure (in critical ischaemia), the more important are rheological factors and drugs which can influence them. These preparations include e.g. Trental (pentoxiphilline), Prostavasin (prostaglandin E1), Vessel due F (sulodexide). In advanced stages of ischaemic extremities oedema is a very adverse factor. Non-cardiac oedema can be very effectively handled by manual lymphatic drainage combined with intermittent one-segment pneumatic compression which was successfully used by the authors in ulcerations of the diabetic foot. One of the main general protective measures is adequate care of the foot and protective footwear for diabetics. After 3.5 years' use of protective footwear the authors recorded, consistent with data in the literature, a 50% reduction of relapses of ulcerations (and amputations). By examination on an EMED II apparatus abnormally high local pressures on the sole of risk patients can be detected and at the some time the protective effect of materials used for protective insoles can be tested. Active pharmacological and generally protective care of diabetic foot leads to a reduced number of amputations, in particular supracondylar ones by 50 or more per cent.

Diabetic Foot↗
PubMed1994

[The present, something from the past and the future of therapy of type II diabetes (NIDDM). II].

Insulin resistance which is the typical sign of NIDDM and the metabolic "X" syndrome is the basic problem of successful treatment of NIDDM. The author discusses therapeutic possibilities--biguanides, some new perspective pharmaceutical preparations and possibilities of combined treatment with PAD and insulin. Although it is not quite clear so far which treatment is the best, prevention of late diabetic complications, intensive NIDDM treatment must be focused on perfect control of the blood sugar level as well as on correction of associated metabolic abnormalities, as much as possible.

Diabetes Mellitus, Type 2↗
PubMed1994

[Evidence of the value of good compensation in diabetes (conclusions of the Diabetes Control and Complications Trial)].

The Diabetes Control and Complications Trial--DCCT--is the longest and largest perspective study in the history of diabetes which provides evidence that reduction of the blood sugar level delays or prevents the development of late diabetic complications. The main conclusions of DCCT proved that correct metabolic control reduces the risk of late diabetes, and to the majority of patients with IDDM intensified treatment should be recommended. DCCT confirmed also the correctness of therapeutic recommendations given in the Saint Vincent declaration.

Blood Glucose↗
PubMed1994

[Recent findings on type II non-insulin-dependent diabetes (epidemiologic data, etiopathogenesis)].

Although NIDDM is by far the most frequent form of diabetes, the pathogenesis is less clear and even more controversial than in IDDM. There is a heterogeneity of IDDM and NIDDM and there are reasons why the two types should be considered different diseases although we do not know exactly why. NIDDM is the result of a disbalance between insulin sensitivity and insulin secretion. Fully developed NIDDM syndrome calls for the concurrent existence of both main defects, i.e. insulin resistance and deteriorated B-cell function. It is important that the two defects must occur simultaneously, only then marked glucose intolerance develops. Concurrent hyperglycaemia and hyperinsulinaemia on fasting suggest severe insulin resistance. Investigations provide evidence that hyperinsulinaemia is a predictor of the final development of IGT and IDDM and it was demonstrated that hyperglycaemia is a predictor of development of NIDDM in Caucasians.

Diabetes Mellitus, Type 2↗
PubMed1994

[The past, present and future of treatment of type II diabetes mellitus].

Diabetes mellitus type II-NIDDM--is characterized by insulin insufficiency and insulin resistance. The main therapeutic aim is to mitigate symptoms, achieve and maintain desirable body weight, achieve a normal blood sugar level and treat complications. The main principle of NIDDM therapy remains an adequate dietary programme with reduction of the total energy intake. The greatest problem of successful therapy remains dietary non-compliance of the patient. Oral antidiabetics--in particular sulphonyl urea, have been the basis of therapy for more than 30 years. But even on this point there are some controversial views. The author discusses some problems of the pharmacodynamics and pharmacokinetics of SU, clinical effectiveness, reasons for primary and secondary failure and presents a list of sulphonyl urea derivatives of the second generation.

Diabetes Mellitus, Type 2↗