Serotonin-producing enterochromaffin (EC) cells of gastrointestinal mucosa in dexamethasone-treated rats

Koko, Vesna; Todorovic, Vesna; Drndarević, Neda; Cvijic̀, Gordana

doi:10.1016/j.regpep.2006.04.019

Cited by 20 publications

(6 citation statements)

References 32 publications

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“…Generally, the observed changes in the number, density and ultrastructure of the gut endocrine cells in our previous reports (KOKO et al, 2001;GLIŠIĆ et al, 2006;KOKO et al, 2008;GLIŠIĆ et al, 2011) as well as the changes in the ENS in the dexamethasone-treated rats, presented in this study, indicate a likely disturbed bowel motility and secretion. The disturbance of the gut motility and secretion interfere with normal metabolic processes of food digestion, which may lead to impaired glucose homeostasis and the development of other symptoms and complications of diabetes mellitus type 2.…”

Section: Discussionsupporting

confidence: 79%

“…The dexamethasone-treated animals in the present study, developed diabetes similar to human diabetes mellitus type 2 (GLIŠIĆ et al, 2006) and changes in the enteric innervation occurred, likely in the direction to neuronal regeneration. This is consistent with the literature data (ADEGHATE et al, 2003;CHANDRASEKHARAN and SRINIVASAN, 2007).…”

Section: Discussionsupporting

confidence: 58%

“…Given that gastrointestinal disorders involving motility impairment are relatively common in diabetic patients, this study (as a part of the wider research) was designed to investigate the alterations in the intensity of the ENS innervation of defined regions of small and large intestine, using animal model of dexamethasone-induced prediabetes/diabetes type 2 (MULDER, 1997). Based on the previously reported results (KOKO et al, 2001;GLIŠIĆ et al, 2006), which emerged from the above-mentioned comprehensive research, we already showed that same treatment caused hypoglycemia, glycosuria, increase in plasma and pancreatic insulin levels, as well as the strong hypertrophy and hyperplasia of the pancreatic B cells, together indicating the impaired glucose tolerance and diabetic state.…”

Section: Discussionmentioning

confidence: 99%

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Immunohistochemical study of enteric nervous system in dexamethasone-treated rats

Glišić¹,

Čakić-Milošević²,

Ukropina³

2018

Kragujevac J Science

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The gut is supplied with its own nervous system, referred to as the enteric nervous system (ENS). It regulates the various functions of a digestive system such as motility, secretion and digestion and has close interactions with the enteric immune system. The aim of this study was to investigate the alterations of the ENS in dexamethasone-treated rats using two general neuroendocrine markers: protein gene product 9.5 (PGP 9.5) and synaptophysin (SY). As concluded from the changes in a pattern of immunoexpression of the markers applied, some remodeling of the ENS occured. Further investigations are needed to elucidate in more details its nature and importance with respect to gastrointestinal complications seen in diabetes.

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Section: Discussionsupporting

confidence: 79%

Section: Discussionsupporting

confidence: 58%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Immunohistochemical study of enteric nervous system in dexamethasone-treated rats

Glišić¹,

Čakić-Milošević²,

Ukropina³

2018

Kragujevac J Science

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“…Several previous reports clearly indicated that the number of EC in the mammalian gut can be changed. A dramatic change in EC amount (correlated with alterations in serotonin content) has been noted in numerous diseases including diabetes induced by dexamethasone or streptozotocin treatment (9,29), irritable bowel syndrome (18), colitis induced by TNBS or dextran sodium sulfate treatment (14,20), as well as parasite infection (19).…”

Section: Discussionmentioning

confidence: 99%

Red kidney bean (Phaseolus vulgaris) lectin stimulation increases the number of enterochromaffin cells in the small intestine of suckling piglets

Zacharko-Siembida¹,

Piedra

Strzałka³

et al. 2014

Bulletin of the Veterinary Institute in Pulawy

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The quantities and distribution patterns of serotonin-immunoreactive (serotonin-IR) enterochromaffin cells (EC) were studied immunohistochemically in the small intestine of suckling piglets stimulated with red kidney bean lectin, and in nonstimulated, control animals. The co-expression patterns of serotonin with somatostatin (SOM) or corticotropin releasing-factor (CRF) were also studied. After the lectin treatment, the increased numbers of EC were noted in the duodenum of experimental animals. Lectin stimulation did not change the proportions of EC in the jejunum and ileum. In the duodenal epithelium of the lectin-stimulated piglets, the vast majority of serotonin-IR EC were distributed at the basis of crypts. After the lectin administration, the proportions of serotonin-IR/SOM-IR EC were statistically similar in all sections of the small intestine. No upregulation of CRF was found in duodenal, jejunal, and ileal EC of lectin-treated animals. The findings demonstrated that red kidney bean lectin increased the serotonin reservoir in the duodenum, and thus may be an effective stimulant of the gut maturation in suckling mammals.

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“…Serotonin, which is otherwise known as ‘the happy hormone’, is a known neurotransmitter involved in regulating appetite and mood. Enterochromaffin cells in the gut-lining produce 95% of the body's serotonin (Glišić et al, 2006; Young and Leyton, 2002), and it is carried by platelets and mast-cells to the site of inflammation (Dürk et al, 2013; Peckett et al, 2011; Sepiashvili et al, 2013). In cases of chronic psychological stress, stress hormones like cortisol can induce adipocyte hypertrophy (Spesivtseva et al, 1979) and adipose tissue inflammation (Lee and Aich, 2002), making adipose tissue an ideal site for the dumping of serotonin by mast cells and platelets.…”

Section: Introductionmentioning

confidence: 99%

Role of murine macrophage in temporal regulation of cortisol and serotonin induced adipogenesis in pre-adipocytes when grown together

2018

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Regulation of adipogenesis, the root cause for obesity, is very poorly understood. However, studies have presented evidence of immuno-metabolic regulation of adipose tissue during periods of chronic psychological stress, leading to adverse conditions related to stress manifestation, including visceral obesity and atherosclerosis. Despite pronounced association of hormonal markers of stress with dys-regulated metabolic states, the contributing signalling events are yet to be established. It is apparent that to understand contributing signalling events we need a model. Although an in vivo model is preferred, it is difficult to establish. The current report, therefore, presents an in vitro model system for the simulation of adipose tissue in a chronic stress micro-environment by growing pre-adipocytes with macrophages in the presence and absence of stress hormones. In this report, effects of cortisol and serotonin on the kinetics of immune and metabolic changes in adipocytes and macrophage (alone and co-cultured) was studied through whole genome transcriptome profiling. A transition from pro- to anti-inflammatory response in the immune profile of pre-adipocytes, with increasing time in co-culture with macrophages, was observed. This transition was reversed by stress hormones cortisol and/or serotonin.

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Serotonin-producing enterochromaffin (EC) cells of gastrointestinal mucosa in dexamethasone-treated rats

Cited by 20 publications

References 32 publications

Immunohistochemical study of enteric nervous system in dexamethasone-treated rats

Immunohistochemical study of enteric nervous system in dexamethasone-treated rats

Red kidney bean (Phaseolus vulgaris) lectin stimulation increases the number of enterochromaffin cells in the small intestine of suckling piglets

Role of murine macrophage in temporal regulation of cortisol and serotonin induced adipogenesis in pre-adipocytes when grown together

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