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EN
Melatonin (MEL) plays a role of an important enterehormone in the gastrointestinal tract. Although more than fifty years have already passed since the moment of its isolation from the pineal gland by Aaron Lerner in 1958, we still reveal new aspects of its action. A number of researchers confirmed the high MEL concentration in the gut tissues, several times surpassing its concentration in peripheral blood. The changes of MEL secretion and metabolism have been described in many gastrointestinal disorders. They can be the consequence of the diseases, but they also do not remain without an effect on the clinical picture of these disorders. With increasing knowledge about physiological function of melatonin and the role of its disturbed homeostasis in the pathogenesis of many gastrointestinal diseases, the indications for its therapeutic use in the supportive treatment of many functional and organic gastrointestinal diseases are being widened. In this paper the authors present a comprehensive review on the role of MEL in the selected diseases of the gut.
PL
Melatonina (MEL) pełni rolę bardzo waŜnego enterohormonu w przewodzie pokarmowym. Pomimo, Ŝe od momentu jej wyizolowania z szyszynki przez Aarona Lernera w 1958 roku minęło ponad 50 lat wciąŜ poznajemy nowe aspekty jej działania. Wielu badaczy potwierdziło wysokie stęŜenia MEL w tkankach przewodu pokarmowego, wielokrotnie przewyŜszające wartości stęŜeń we krwi obwodowej. W szeregu schorzeń układu trawiennego opisano zmiany sekrecji i metabolizmu MEL. Są one często następstwem tych chorób, ale z drugiej strony w istotny sposób mogą takŜe wpływać na ich obraz kliniczny. W miarę poznawania funkcji fizjologicznych MEL oraz roli zaburzeń jej homeostazy w patogenezie wielu schorzeń poszerzamy równieŜ moŜliwości jej terapeutycznego wykorzystania w leczeniu wspomagającym wielu chorób czynnościowych i organicznych przewodu pokarmowego. W pracy przedstawiono zbiorczo informacje dotyczące roli MEL w wybranych chorobach przewodu pokarmowego.
EN
Introduction: A chronic or recurrent pain and discomfort in the upper abdomen occurs frequently in depressive patients. The pathogenesis of these symptoms is complex and not fully understood. The aim of the study was to estimate the gastric myoelectrical activity in this group of patients. Material and methods: The study group consisted of 90 subjects, including 71 women and 19 men (mean age – 38.0±8.1). Among them three groups were divided: healthy subjects (K, n=30), depressive patients with dyspepsia (group II, n=30) and depressive patients with Helicobacter pylori infection (group III, n=30). All the subjects completed Hamilton Depression Scale and the gastric myoelectrical activity examination with Polygraph–Medtronic A/S (Denmark) was done before and after a liquid meal for 120 minutes. Results: Preprandial normogastria in depressive patients (group II, III) compared to healthy subjects (group K) was lower 79.5±8.1% vs 73.6±8.7% (p<0.01) and 79.5±8.1% vs 68.4±9.9 (p<0.001). The similar differences were recorded during postprandial time. Power ratio scale (PR) was also lower in depressive patients than in healthy subjects: 3.5±0.7 (K), 1.6±0.7 (group II), 1.7±0.8 (group III) – p<0.001, p<0.001 respectively. Conclusions: In depressive patients gastric myoelectrical activity is disturbed and probably causes chronic dyspepsia symptoms.
EN
In postmenopausal women various psychosomatic disorders concerning mood and appetite occur. The reason is not only estrogen deficiency, but also other hormones and neurotransmitters. The aim of the study was to estimate serotonin and melatonin levels and myoelectrical activity and gastric motor in postmenopausal women in relation to their nutritional status. The study was conducted in three 30-person groups of women: premenopausal (group I), postmenopausal with a normal body mass (group II), postmenopausal overweight (group III). Compared with group I, in group II there were no significant differences, while in group III serotonin level was lower respectively 156.5±40.2 ng/ml and 83.4±32.5 ng/ml (p<0.01), as well as the percentage of normogastria – 82.9±5.6% and 66.9±8.2 (p<0.05) and gastric emptying half-time 43.6±14.7 min and 27.4±12.2 min (p<0.01). Moreover, a negative correlation between body mass index and serotonin (r = -0.4744) and melatonin (r = -0.7146) levels was observed. The study results indicate the involvement of serotonin and melatonin in the pathogenesis of eating disorders in postmenopausal women.
PL
U kobiet po menopauzie występują różnorodne zaburzenia psychosomatyczne, w tym dotyczące nastroju i łaknienia. Przyczyną tego jest niedobór estrogenów, ale także innych hormonów i neurotransmiterów. Celem badania było określenie stężenia serotoniny i melatoniny oraz czynności mioelektrycznej i motorycznej żołądka u kobiet po menopauzie w odniesieniu do ich stanu odżywienia. Badania przeprowadzono w trzech 30-sto osobowych grupach kobiet: przed menopauzą (grupa I), po menopauzie z prawidłową masą ciała (grupa II), po menopauzie ze współistniejącą nadwagą (grupa III). W porównaniu z grupą I, w grupie II nie stwierdzono istotnych różnic, natomiast w grupie III niższe było stężenie serotoniny, odpowiednio 156,5±40,2 ng/mL i 83,4±32,5 ng/mL (p<0,01), a także niższy był odsetek prawidłowej czynności mioelektrycznej żołądka (normogastrii) – 82,9±5,6% i 66,9±8,2 (p<0,05) oraz krótszy był czas połowicznego opróżniania żołądka (43,6±14,7 min. i 27,4±12,2 min.; p<0,01. Ponadto stwierdzono odwrotną zależność między wskaźnikiem masy ciała a stężeniem serotoniny (r = -0,4744) i melatoniny (r = -0,7146). Wyniki badań wskazują na udział serotoniny i melatoniny w patogenezie zaburzeń odżywiania u kobiet po menopauzie.
EN
Inflammatory bowel diseases (IBDs), mainly ulcerative colitis (UC) and Crohn's disease (CD), are characterized by chronic and idiopathic inflammatory conditions of gastrointestinal tract that are immunologically mediated. Stromal cell-derived factor 1 (CXCL12) has been demonstrated to be involved in the pathophysiology of IBD.The aim of the study was to investigate whether the CXCL12 -G/A polymorphism (rs1801157) is associated to IBD in a sample of Polish population.Material and methods. A total of 188 patients with IBD including 103 patients with CU and 72 patients with CD and 184 controls were enrolled in the study. Both groups came from the Polish population. The G/A polymorphism of CXCL12 was determined by PCR-RFLP analysis.Results. There was no association between G/A polymorphism at position -801 promoter region of CXCL12 gene and increased risk of IBD. The study population was not found a difference in genotype distribution between the control group and with both CD and CU patients.Conclusions. These results suggest that G/A polymorphism at position -801 promoter region of CXCL12 gene relates neither to the risk of the development of inflammatory bowel disease nor to the clinical subtypes of IBD in the Polish population. Whether this polymorphism truly contributes to disease susceptibility needs to be further addressed, and should stimulate additional studies in other populations.
EN
Inflammatory bowel diseases (IBD) are disorders originated from immune disturbances.The aim of the study was to evaluate the association between the -2518 A/G MCP-1 polymorphism and the risk of IBD development.Material and methods. Genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. Study group consisted of 197 subjects with IBD (120 with ulcerative colitis and 77 with Crohn's disease) as well as 210 healthy controls.Results. The presence of the -2518 G/G MCP-1 genotype in the investigated groups seems to be connected with higher risk of inflammatory bowel disease as well as Crohn's disease only (OR 2.26; 95% CI 1.44-3.54 and OR 2.08; 95% CI 1.21-3.46, respectively).Conclusions. Our data showed that the -2518 A/G MCP-1 polymorphism might be associated with the IBD occurrence and might be used as predictive factor of these diseases in a Polish population.
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