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Biomedical subjects

I Klimes

Publications and source records attributed to I Klimes.

At least 55 records · Page 3Linked to original sources
PubMed1997

Fatty acid composition in fractions of structural and storage lipids in liver and skeletal muscle of hereditary hypertriglyceridemic rats.

The fatty acid (FA) compositions of liver and skeletal muscle structural lipids, overall phospholipids and phosphatidylcholine, and triglycerides (TG) were determined in the hereditary hypertriglyceridemic (HTG) rat, a nonobese animal model of the insulin resistance syndrome. Four groups of HTG rats and four groups of control animals were fed equal-energy diets for two weeks: basal (B), high-sucrose (HS), or fish oil-supplemented basal (BFO) or high-sucrose (HSFO) diets. In the liver of HTG rats, a decrease of n-6 long-chain polyunsaturated FA (PUFA), especially in 20:4n-6, in comparison with controls was found. Moreover, a concomitant accumulation of 18:2n-6 in structural lipids was observed. These differences were more pronounced in liver than in skeletal muscle. HS feeding raised the proportion of 18:1n-9 and decreased 18:2n-6 in lipid fractions. In both tissues and in both strains, the amounts of long-chain n-3 PUFA, as well as the level of total C20-22 PUFA, went up after fish oil feeding. However, the effects were somewhat less pronounced in the HTG rats. The increase in n-3 PUFA occurred mainly at the expense of reduced levels of 18:2n-6 in structural lipids and of 18:1n-9 in triglycerides. These changes were associated, in companion studies reported in this volume, with improved insulin action in HTG rats. In conclusion, the FA composition in lipid subclasses of HTG rats differs significantly from the controls mainly in liver structural lipids, suggesting the impairment of PUFA desaturation. Dietary change effected a similar modulation of FA profile across both strains, with fish oil increasing the levels of long-chain PUFA toward control values in the NTG rats. The HTG rat thus provides an interesting animal model for the study of impaired fatty acid metabolism.

Animals↗
PubMed1997

Structural changes in the aorta of the hereditary hypertriglyceridemic rat.

Structural changes in the ascending thoracic aorta of hereditary hypertriglyceridemic (hHTG), insulin-resistant, and hypertensive rats were studied using transmission electron microscopy. Normotensive Wistar rats were used as controls. The most-pronounced morphological changes were observed in the tunica intima. Endothelial cells of hHTG rats formed a continual layer around the whole circumference. Subendothelial space was enlarged. Some endothelial cells were delaminated from the subendothelial space by big lipid droplets that were often present in the subendothelial space, and the endothelial cells bulged out towards the lumen. Big electron-lucent lipid droplets were present in the majority of the endothelial cells and occupied the main part of the cytoplasm. Degenerative microvesicular and membranous material was present in the cytoplasm. Increased numbers of vesicles of Golgi apparatus and cisternae of endoplasmic reticulum were found. Similar morphological alterations, but in less-extended form, were observed in smooth muscle cells. The organization and orientation of smooth muscle cells were essentially intact. In muscle cells, lipid droplets were localized in close relation to Golgi complex and in dilated cisternae of the sarcoplasmic reticulum. Lipid droplets, degenerative material, myelin figures, myelinoid membranes, and vesicular components were also sporadically found in the intercellular space among muscle cells. This pilot morphological investigation provides further arguments for a thorough and more-focused electron microscopy study of conductance arteries of the hHTG rats.

Animals↗
PubMed1997

The effect of hyperlipidemia on serum fatty acid composition in type 2 diabetics.

Fatty acid (FA) profiles of total serum lipids were determined by capillary gas chromatography in Type 2 diabetic patients (NIDDM) with diverse types of hyperlipidemia. In patients with hypertriglyceridemia (DM-HTG) and combined hypertriglyceridemia and hypercholesterolemia (DM-HLP), a significantly different total FA composition was found compared with healthy controls or diabetics with normal serum lipids. In particular, the proportions of saturated and monounsaturated FA were increased and the proportions of n-6 polyunsaturated FA were decreased. In DM-HLP patients, PUFA n-6 metabolites and C20-C22 PUFA were also decreased. Thus, hyperlipidemia shifts significantly the serum FA composition in NIDDM patients into an atherogenic profile. More study is needed, however, to understand if serum FA changes may contribute to the increased atherogenesis commonly found in these patients.

Aged↗
PubMed1997

A controlled trial of cognitive behavioural therapy for non-cardiac chest pain.

BACKGROUND: The majority of patients presenting to cardiac clinics with chest pain who are reassured they do not have heart disease or other serious physical disorder continue to experience symptoms, worry about heart disease and restrict their activities. This randomized trial investigated the effectiveness of psychological treatment within routine cardiac care. METHODS: Consecutive patients presenting with chest pain and reassured by a cardiologist they do not have heart disease were reassessed 6 weeks later. Those with persistent limiting symptoms were offered the opportunity to participate in a trial of cognitive behavioural therapy. RESULTS: Thirty-seven subjects agreed to take part. A number of subjects were unenthusiastic about psychological intervention or, following explanation of the study, regarded further treatment as not being necessary. At 3 months there were significant differences between the treatment group and the control group on key outcome measures of symptoms, mood and activity. At 6 months there were fewer differences but significant advantages of treatment in terms of limitation of activities and worry about physical symptoms. CONCLUSION: We conclude that there is a need for 'stepped' further care following reassurance in the cardiac clinic and that cognitive behavioural treatment is effective with those with persistent disabling symptoms.

Adult↗
PubMed1996

Regulation of gene expression for lipogenic enzymes in the liver and adipose tissue of hereditary hypertriglyceridemic, insulin-resistant rats: effect of dietary sucrose and marine fish oil.

Hypertriglyceridemia is closely linked to insulin resistance. Increased dietary intake of n-3 polyunsaturated fatty acids reverses both hypertriglyceridemia and insulin resistance. To evaluate molecular mechanisms responsible for the hypotriglyceridemic effects of n-3 polyunsaturated fatty acids, the expression of genes for lipogenic enzymes in liver and white and brown adipose tissue was estimated in hereditary hypertriglyceridemic rats which underwent an euglycemic hyperinsulinemic clamp. Before the clamp, animals were fed a basal or a high (63%) sucrose diet with or without fish oil for two weeks. Results were compared to data obtained from control animals subjected to the identical protocol. In hereditary hypertriglyceridemic rats, gene expression for malic enzyme was increased in liver and in brown adipose tissue but not in white adipose tissue. The high sucrose diet raised malic enzyme mRNA levels in liver of both hereditary hypertriglyceridemic and control rats, and this effect was more pronounced in brown adipose tissue. Supplementing the high sucrose diet with fish oil led to a suppression of malic enzyme gene expression in liver and brown adipose tissue of control rats. However, this inhibitory effect was not as pronounced in the hereditary hypertriglyceridemic rats. Raised levels of fatty acid synthase mRNA in liver and brown adipose tissue of control rats fed high sucrose diet were suppressed by consumption of diet high in n-3 fatty acids. On the other hand, in hereditary hypertriglyceridemic rats fed high sucrose diet, fish oil supplementation failed to suppress increased levels of fatty acid synthase mRNA in liver and in brown adipose tissue. It appears that hereditary hypertriglyceridemic rats have elevated levels of mRNA for lipogenic enzymes in liver and brown adipose tissue and dietary control leading to an alteration of hypertriglyceridemia influences gene expression of lipogenic enzymes only under special dietary circumstances.

Adipose Tissue↗
PubMed1996

Cognitive behaviour therapy for the chronic fatigue syndrome: a randomized controlled trial.

OBJECTIVE: To evaluate the acceptability and efficacy of adding cognitive behaviour therapy to the medical care of patients presenting with the chronic fatigue syndrome. DESIGN: Randomised controlled trial with final assessment at 12 months. SETTING: An infectious diseases outpatient clinic. SUBJECTS: 60 consecutively referred patients meeting consensus criteria for the chronic fatigue syndrome. INTERVENTIONS: Medical care comprised assessment, advice, and follow up in general practice. Patients who received cognitive behaviour therapy were offered 16 individual weekly sessions in addition to their medical care. MAIN OUTCOME MEASURES: The proportions of patients (a) who achieved normal daily functioning (Karnofsky score 80 or more) and (b) who achieved a clinically significant improvement in functioning (change in Karnofsky score 10 points or more) by 12 months after randomisation. RESULTS: Only two eligible patients refused to participate. All randomised patients completed treatment. An intention to treat analysis showed that 73% (22/30) of recipients of cognitive behaviour therapy achieved a satisfactory outcome as compared with 27% (8/30) of patients who were given only medical care (difference 47 percentage points; 95% confidence interval 24 to 69). Similar differences were observed in subsidiary outcome measures. The improvement in disability among patients given cognitive behaviour therapy continued after completion of therapy. Illness beliefs and coping behaviour previously associated with a poor outcome changed more with cognitive behaviour therapy than with medical care alone. CONCLUSION: Adding cognitive behaviour therapy to the medical care of patients with the chronic fatigue syndrome is acceptable to patients and leads to a sustained reduction in functional impairment.

Adaptation, Psychological↗
PubMed1996

Regulation of gene expression and activity of malic enzyme in liver of hereditary hypertriglyceridemic (hHTG) insulin resistant rat: effect of dietary sucrose and marine fish oil.

The effect of increased dietary intake of n-3 polyunsaturated fatty acids (PUFA) on hepatic malic enzyme (EC 1.1.1.40) gene expression and activity was investigated in either hereditary fixed or dietary induced hypertriglyceridemia after euglycemic hyperinsulinemic (6.4 mU/kg/min) clamp. The hereditary hypertriglyceridemic rats (hHTG) were fed for 2 weeks basal (B) or high (63 cal %) sucrose (HS) diet, with or without fish oil (FO, 30 wt % n-3 PUFA). The results were compared with the data obtained in control (C) animals subjected to identical protocol. In hHTG rats, increased gene expression [hHTG: 1.7 +/- 0.1 vs. C: 0.5 +/- 0.05 arbitrary units (AU), P<0.02] for malic enzyme (ME) was not accompanied by increased activity of this enzyme in liver [hHTG: 1.1 +/- 0.1 vs. C: 3.1 +/- 0.4 nkat/mg, P<0.001]. HS feeding raised the activity [HS-hHTG: 4.2 +/- 0.3 nkat/mg, P<0.001; HS-C: 7.5 +/- 0.9 nkat/mg, P<0.001] and mRNA levels [HS-hHTG: 10.4 +/- 0.3 AU, P<0.001; HS-C: 7.7 +/- 0.3 AU, P<0.001] in liver of both hHTG and control rats. The supplementation of HS diet with FO led to striking suppression of activity by 63 % [2.8 +/- 0.5 nkat/mg, P<0.001] and gene expression [2.9 +/- 0.2 AU, P<0.001] for ME in liver of control rats. Such inhibitory effect was not as pronounced in hHTG rats and reached about 50 % in the ME activity [HS+FO: 2.0 +/- 0.06 nkat/mg vs. HS:4.2 +/- 0.3 nkat/mg, P<0.001] or 30 % decrease in ME mRNA levels [HS+FO: 7.5 +/- 0.8 Au vs. HS:10.4 +/- 0.3 AU, P<0.001]. Thus, hHTG rats have markedly elevated levels of mRNA for malic enzyme in liver accompanied by decreased enzymatic activity. Dietary manipulations leading to alteration of hypertriglyceridemia (HS diet, omega-3 PUFA) influenced both the activity of malic enzyme and its transcription in the liver.

Journal Article↗
PubMed1996

[Comparison of insulin loss in treatment of diabetics using the classical syringe or the insulin pen (Novopen II)].

The aim of the study was to investigate changes in insulin wastage when transferring patients from vial insulin to Actraphane HM Penfills and NovoPen II. Twenty four diabetic patients, were treated with Actraphane HM 40 IU/ml vial for 3 months, then transferred to Actraphane HM Penfill and NovoPen II for further 3 months. Wastage 1 (difference between insulin consumption and the total prescribed dose) was higher in vials than in Penfills (268.7 +/- 69.4 IU/3 months/patients vs. -7.6 +/- 30.2 IU/3 months/patient, p < 0.001 mean +/- SEM). Wastage 2 (insulin remaining in the container when discharged) was higher in the Penfills than in vials (214.1 +/- 22.04 IU/3 months/patient vs 45.2 +/- 11.2 IU/3 months/patient). Total wastage was 313.9 +/- 67.8 IU/3 months/patient (3.96 IU/day/patient) when using vials and 206.5 +/- 31.2 IU/3 months/patient (2.52 IU/day/patient) when using Penfills (NS). Higher wastage in vials may relate to a larger volume used for "airshot", and to a larger imprecision in the measured and injected dose when using vials. The latter may also be reflected in a significantly higher average incidence of weighted hypogiycemias in the vial period (15 +/- 4.28/3 months/patient) compared to the Penfill period (5.1 +/- 1.2/3 months/patient, p < 0.01). Total wastage was seen to be 29% smaller by using NovoPen II and therefore saving of insulin seems to be possible (approximately 1.44 IU/day/patient).

Adult↗
PubMed1995

Hereditary hypertriglyceridemic rat: a new animal model of metabolic alterations in hypertension.

Hereditary hypertriglyceridemic rats (hHTg) were developed as a new genetic model for the study of relationships between blood pressure (BP) and metabolic abnormalities. This strain has been produced by selective inbreeding from Wistar rats according to the rise of plasma triglycerides induced by a high-sucrose diet. Though hHTg rats display hypertriglyceridemia, impaired glucose tolerance, hyperinsulinemia, insulin resistance and increased BP even without nutritional stimuli, high sucrose feeding further aggravates these symptoms. High plasma triglycerides levels in hHTg rats seem to be a consequence of their hyperproduction. Impaired insulin action is responsible for the defective glucoregulation in this strain. The loss of insulin responsiveness might be due to a reduction in the number of glucose transporters. Highly significant relationships among plasma triglycerides, ouabain-resistant Na+ transport and BP were demonstrated in the hHTg rats. Segregating populations (F2 hybrids) should be used for genetic analysis of the primary role of lipid and/or ion transport abnormalities in the pathogenesis of this form of genetic hypertension.

Animals↗
PubMed1995

[The importance of diet therapy in the prevention and treatment of manifestations of metabolic syndrome X].

The authors present an account of dietetic principles in the treatment of the metabolic syndrome X (Reaven 1988). Principles valid til recently are compared with the most recent views based on experimental and clinical investigations, using molecular methods. The authors explain in detail the importance of monounsaturated and polyunsaturated fatty acids in the oil of marine fish which are important not only for reducing the blood lipid level but also to improve the insulin resistance and they reduce slightly the blood pressure.

Diabetes Mellitus, Type 2↗
PubMed1995

[Cellular and molecular mechanisms of insulin resistance].

In the submitted review the authors give an account of contemporary knowledge regarding the mechanism of insulin action, including a brief account of pathological conditions associated with insulin resistance. The development of knowledge of problems of insulin resistance syndromes was always very dynamic, and due to the introduction of techniques of molecular biology and genetics at the turn of the eighties and nineties, a further very marked step forward was made. Despite this it will take some time before molecular mechanisms which will confirm (or rule out?) the etiopathogenetic importance of insulin resistance not only for diabetes but also for hypertension, dyslipidaemia, IHD will be revealed.

Humans↗
PubMed1995

[Etofylline clofibrate in the treatment of diabetic dyslipidemia: results of a 6-month period of therapy].

The objective was to investigate the tolerance of ethophylline clofibrate (EPC) and its effectiveness on changes of dyslipidaemia and compensation of diabetes in type II diabetics during six-month administration of the preparation Duolip forte (Merckle). Twenty diabetics with dyslipoproteinaemia IIb and IV according to Frederickson's classification, compensated by diet alone or combined with oral antidiabetics (Glucobene, Merckle) were included in the study consecutively according to uniform basal criteria. The selected hypolipidaemic agent was administered to patients according to the following pattern: the first four weeks 1,000 mg (2 tablets in the evening) the next two weeks 1.5 tablets and then till the end of the investigation 1 tablet in the evening. In all patients treatment with EPC led to a significant reduction of the total cholesterol level (CH) at all time intervals. Changes of ApoB, ApoA1 and Lp(a) serum levels did not attain statistical significance but trends were revealed (e.g. a drop of the ApoB/ApoA1 index) which are consistent with the expected favourable action of EPC on the CH distribution in lipoproteins. The triacylglycerol (TG) serum concentration declined significantly already after one month of treatment and after identification of five patients whose TG were distributed in separate clusters the hypotriacylglycerolaemic effect of EPC persisted still three months after treatment. It may be summarized that treatment of dyslipoproteinaemia of the type II diabetics with ethophylline clofibrate (Duolip forte, Merckle) led a) to a marked reduction (13-15%) of serum cholesterol, which b) diminished (to 8-9%) but persisted still after 6 months of treatment, c) the greatest effect of EPC on the TG serum level was observed one month after treatment, d) all improvements of lipid parameters occurred without affecting the compensation of diabetes, or BMI and were not associated with any side-effects of EPC.

Clofibrate↗