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Brunerova L.,Centrum Vyzkumu Diabetu | Andel M.,Centrum Vyzkumu Diabetu
Diabetologie Metabolismus Endokrinologie Vyziva | Year: 2013

The review article summarizes the principles of hedonic regulation of food intake which represents the food intake independent on the maintenance of homeostasis. The theory describing hedonic regulation, so called Incentive Saliance Theory, comprises three major processes: liking (positive attribution to food stimulus), wanting (motivation to gain it) and learning (identification of these stimuli and distinguishing them from those connected with aversive reaction). Neuronal reward circuits are the anatomical and functional substrates of hedonic regulation. They react to gustatory and olfactory (or visual) stimuli associated with food intake. A food item is preferred in case its consumption is connected with a pleasant feeling thus promoting the behavioural reaction. The probability of this reaction after repetitive exposure to such a stimulus is increased (learned preference). On the contrary, learned aversion after repetitive exposure is connected with avoidance of a food item associated with a negative feeling. Main mediators of hedonic regulation are endocannabinoids, opioids and monoamines (dopamine, serotonin). Dopamine in dorsal striatum via D2 receptors generates food motivation as a key means of survival, however in ventral striatum (nucleus accumbens) is responsible for motivation to food bringing pleasure. Serotonin via its receptors 5-HT1A a T-HT2C decreases intake of palatable food. It plays a significant role in the pathogenesis of eating disorders, particulary mental anorexia. There, a food restriction represents a kind of automedication to constitutionally pathologically increased serotonin levels. Detailed understanding of processes regulating food intake is a key to new pharmacological interventions in eating disorders.


Brunerova L.,Centrum Vyzkumu Diabetu | Andel M.,Centrum Vyzkumu Diabetu
Vnitrni Lekarstvi | Year: 2013

The review article summarizes a very complex process of appetite regulation: the part focused on homeostatic regulation of food intake. The aim of homeostatic regulation is to achieve energy balance, stabile weight and optimal nutrient intake, in contrast to hedonic regulation of food intake, in which emotional and motivational factors are involved. Homeostatic regulation could be divided into short-term and long-term regulation and comprises mainly gastrointestinal peptides, fat tissue hormones and central mechanisms localized in hypothalamus. It is a resultant of the action of orexigenic factors (increasing appetite and food intake) and anorexigenic factors (decreasing appetite and thus food intake), respectively. The anorexigenic factors include gastrointestinal peptides (e.g. cholecystokinin, glucagon-like peptide 1, bombesin, peptide YY and others), hormone of fat tissue leptin and centrally acting melanocortin system. On the contrary, orexigenic factors comprise of gastric ghrelin and centrally acting system of neuropeptide Y/Agouti-related peptide. Understanding the principles of the regulation of food intake is essential for comprehension of pathogenesis of eating disorders and obesity, whose prevalence has been recently increasing, and it provides potential targets for pharmacological interventions.


Andel M.,Centrum Vyzkumu Diabetu | Nemcova V.,Centrum Vyzkumu Diabetu | Pavlikova N.,Centrum Vyzkumu Diabetu | Urbanova J.,Centrum Vyzkumu Diabetu | And 10 more authors.
Diabetologie Metabolismus Endokrinologie Vyziva | Year: 2014

Insulin secretion in patients with manifested diabetes mellitus tends to disappear months to decades after the diagnosis, which is a clear sign of a gradual loss of pancreatic islet beta-cells. In our sample of 30 type 2 diabetic patients, whose disease manifested between 30 and 45 years of age, about a half have retained or even increased insulin secretion 30 years later, while the other half exhibit a much diminished or lost insulin secretion. Factors that can damage or destroy beta-cells can be divided into the following groups: Metabolic factors: hyperglycemia and glucotoxicity, lipotoxicity, hypoxia, reactive oxygen species; Pharmacological factors: antimicrobial medication pentamidine, SSRI antidepressants; Factors realted to impaired insulin secretion: MODY type diabetes; Environmental toxic factors: rat poison Vacor, streptozotocin, polychlorinated and polybrominated hydrocarbons; Disorders of the exocrine pancreas: tumor infiltration, fibroous infiltration, chronic pancreatitis, cystic fibrosis; Infections, inflammation, autoimmunity, viral factors: Coxsackie viruses, H1N1 influenza, enteroviruses. We are currently working on finding other factors leading to beta-cell damage, studying their effect on apoptosis and necrosis and looking for possible protective factors to prevent this damage. We our increasing knowledge about the mechanisms of beta-cell damage and destruction we come ever closer to suggest measures for their prevention. In this review we offer a brief and simplified summary of some of the findings related to this area.


Bojarova A.,Centrum Vyzkumu Diabetu | Andel M.,Centrum Vyzkumu Diabetu | Trnka J.,Centrum Vyzkumu Diabetu
Diabetologie Metabolismus Endokrinologie Vyziva | Year: 2013

Endothelial cells form the inner layer of the vascular system. They ensure the transport between blood and insterstitium and take part in the regulation of vascular tonus, in the equlibrium of thrombosis/thrombolysis, and in immune processes. Therefore an endothelial cell has very high energetic demands. The most important source of energy for the endothelium, even in aerobic conditions, is the anaerobic glycolysis. That is why endothelial cells are not very sensitive to hypoxia. Intracellular transport of glucose is independent on insulin. Fatty acids, lactate, glutamine, and phosphocreatine can perform as other energetic substrates. Their utilisation rises especially with the insufficiency of glucose. Moreover this condition combined with hypoxia causes the energetic breakdown of the cell.


Urbanova J.,Centrum Vyzkumu Diabetu | Hoffmanova I.,Centrum Vyzkumu Diabetu | Andel M.,Centrum Vyzkumu Diabetu
Diabetologie Metabolismus Endokrinologie Vyziva | Year: 2011

Even before 15 years ago, type 1 diabetes mellitus was rated as a disease affecting children, adolescent and young adults. New knowledge about autoimmune insulitis, the possibilities to investigate routinely plasma C-peptide levels and specific islet antibodies have shown, that type 1 diabetes can affect patients in any age as classical type 1 or LADA. The authors are reporting about the woman, who manifested type 1 diabetes in her 97 years. Her BMI was 22,9 kg/m2, C-peptide plasma level 276 pmol/l and plasma level of specific islets antibodies was significantly positive: GADA 250 IU/ml and IA2A 79,92 IU/ml. According to our knowledge, our patient is the case of the oldest manifestation of type 1 diabetes proved by levels of specific antigens and plasma C-peptide.


Andel M.,Centrum Vyzkumu Diabetu | Nemcova V.,Centrum Vyzkumu Diabetu | Pavlikova N.,Centrum Vyzkumu Diabetu | Urbanova J.,Centrum Vyzkumu Diabetu | And 9 more authors.
Vnitrni Lekarstvi | Year: 2014

Insulin secretion in patients with manifested diabetes mellitus tends to disappear months to decades after the diagnosis, which is a clear sign of a gradual loss of pancreatic islet beta-cells. In our sample of 30 type 2 diabetic patients, whose disease manifested between 30 and 45 years of age, about a half have retained or even increased insulin secretion 30 years later, while the other half exhibit a much diminished or lost insulin secretion. Factors that can damage or destroy beta-cells can be divided into the following groups: Metabolic factors: hyperglycemia and glucotoxicity, lipotoxicity, hypoxia, reactive oxygen species; Pharmacological factors: Antimicrobial medication pentamidine, SSRI antidepressants; Factors related to impaired insulin secretion: MODY type diabetes; Environmental toxic factors: rat poison Vacor, streptozotocin, polychlorinated and polybrominated hydrocarbons; Disorders of the exocrine pancreas: tumor infiltration, fibrous infiltration, chronic pancreatitis, cystic fibrosis; Infections, inflammation, autoimmunity, viral factors: Coxsackie viruses, H1N1 influenza, enteroviruses. We are currently working on finding other factors leading to beta-cell damage, studying their effect on apoptosis and necrosis and looking for possible protective factors to prevent this damage. We our increasing knowledge about the mechanisms of beta-cell damage and destruction we come ever closer to suggest measures for their prevention. In this review we offer a brief and simplified summary of some of the findings related to this area.


Andel M.,Centrum Vyzkumu Diabetu | Skrha P.,Centrum Vyzkumu Diabetu | Trnka J.,Centrum Vyzkumu Diabetu
Vnitrni Lekarstvi | Year: 2013

Type 2 diabetes moderately increases predisposition for manifestation of tumor disease. Both drugs stimulating insulin secretion (insulin secretagogues) and insulin injection therapy also moderately increases risk of tumor manifestation (OR approx 1.3). According to some reports pyoglitazon therapy could be of increased risk of bladder cancer. On the other hand, hunderds of study on isolated cells, experimental animal models and retrospective studies in patients have shown preventive effect of metformin therapy on manifestation tumors of pancreas, breast, colorectum, liver, endometrium and ovary. More over, the prognosis of diabetic cancer patients on metformin therapy seems be better, than in diabetics without metformin treatment. These data are promising for future use of metformin for prevention and therapy of some malignant tumors.


PubMed | Centrum vyzkumu diabetu
Type: Journal Article | Journal: Vnitrni lekarstvi | Year: 2013

Type 2 diabetes moderately increases predisposition for manifestation of tumor disease. Both drugs stimulating insulin secretion (insulin secretagogues) and insulin injection therapy also moderately increases risk of tumor manifestation (OR approx 1.3). According to some reports pyoglitazon therapy could be of increased risk of bladder cancer. On the other hand, hundreds of study on isolated cells, experimental animal models and retrospective studies in patients have shown preventive effect of metformin therapy on manifestation tumors of pancreas, breast, colorectum, liver, endometrium and ovary. More over, the prognosis of diabetic cancer patients on metformin therapy seems be better, than in diabetics without metformin treatment. These data are promising for future use of metformin for prevention and therapy of some malignant tumors.

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