Response of plasma pancreatic and gastrointestinal hormones and growth hormone to oral and intravenous glucose and insulin hypoglycaemia in Chagas's disease.

Long, Richard; Albuquerque, R. H.; Prata, A. B.; Barnes, Alan; Adrian, Thomas E.; Christofides, Nicos; Bloom, Stephen R.

doi:10.1136/gut.21.9.772

Cited by 31 publications

(24 citation statements)

References 21 publications

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“…In conclusion, these data indicate that T. cruzi infection downregulates PRL and GH production, in keeping with previous data showing decreased GH levels in Chagas patients in response to glucose or insulin compared with healthy subjects [15] , but in contrast to a recent report on pulmonary tuberculosis patients, who exhibit higher levels of circulating GH than age-matched normal subjects [16] .…”

Section: Decreased Endocrine Activity In Gh3-infected Cells: Correlatcontrasting

confidence: 33%

Modulation of Growth Hormone and Prolactin Secretion in <i>Trypanosoma cruzi</i>-Infected Mammosomatotrophic Cells

Correa-de-Santana

Paez-Pereda

Theodoropoulou

et al. 2009

Neuroimmunomodulation

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Objective: In a previous study, we reported an imbalance in the hypothalamus-pituitary-adrenal axis of mice acutely infected with the protozoan parasite Trypanosoma cruzi, the causative agent of Chagas disease. Methods: Possible effects of this parasitic infection on the endocrine function of other pituitary cell types were studied, in particular regarding the production of prolactin (PRL) and growth hormone (GH). Results: In the mammosomatotrophic cell line GH3, both GH and PRL secretion were decreased, reflecting the diminished PRL concentrations in the pituitary glands of infected mice. Additionally, expression of extracellular matrix proteins, e.g. laminin, was increased in T. cruzi-infected GH3 cells, which may be related to the diminished secretory function of these cells. Lastly, the expression of Pit-1, a major transcription factor for the PRL and GH genes, is also decreased in T. cruzi-infected cultures. Conclusion: T. cruzi infection downregulates PRL and GH production. Combined with our previous data showing increased glucocorticoid levels following T. cruzi infection, the immunosuppression induced by T. cruzi infection may be partially related to multiple endocrine changes involving the hypothalamus-pituitary axis and corresponding target endocrine glands.

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Section: Decreased Endocrine Activity In Gh3-infected Cells: Correlatcontrasting

confidence: 33%

Modulation of Growth Hormone and Prolactin Secretion in <i>Trypanosoma cruzi</i>-Infected Mammosomatotrophic Cells

Correa-de-Santana

Paez-Pereda

Theodoropoulou

et al. 2009

Neuroimmunomodulation

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“…It is possible that the gastroenteric-pancreatic hormones may also play some role in the changes of PI density and size described here. There are several reports in the literature, experimental 34 and clinical 8,11,22,24,40,46,47 of functional alterations of the pancreas in Chagas' disease including glycemia, glucagon, and insulin responses.…”

Section: Discussionmentioning

confidence: 99%

“…According to the concept of the enteroinsular axis (EIA), the PI should have important connections with the intestinal tube via the nervous, peptidergic, and substrate routes 37,38 . Increases in neuroendocrine system cell count 39 and gastrin serum levels [40][41][42] associated with reduction of pancreatic polypeptide (PP) levels have been reported 40,42 . Gastrin may act as a growth factor, performing direct trophic actions at various sites including the gastrointestinal mucus and the pancreas [43][44][45] .…”

Section: Discussionmentioning

confidence: 99%

Morphologic and morphometric evaluation of pancreatic islets in chronic Chagas' disease

Saldanha

Santos²,

Reis³

et al. 2001

Rev. Hosp. Clin.

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Purpose: Hyperglycemia and abnormal glucose tolerance tests observed in some patients with chronic Chagas' disease suggest the possibility of morphological changes in pancreatic islets and/or denervation. The purpose of this study was to describe the morphology and morphometry of pancreatic islets in chronic Chagas' disease.Methods: Morphologic and computerized morphometric studies were performed in fragments of the head, body, and tail regions of the pancreas obtained at necropsies of 8 normal controls and 17 patients with chronic Chagas' disease: 8 with the digestive form (Megas) and 9 with the congestive heart failure form.Results: The Megas group had a larger (p < 0.05) pancreatic islet area in the tail of the pancreas (10649.3 ± 4408.8 µm 2 ) than the normal control (9481.8 ± 3242.4 µm 2 ) and congestive heart failure (9475.1 ± 2104.9 µm 2 ) groups; likewise, the density of the pancreatic islets (PI) was greater (1.2 ± 0.7 vs. 0.9 ± 0.6 vs. 1.9 ± 1.0 PI/mm 2 , respectively). In the tail region of the pancreas of patients with the Megas form, there was a significant and positive correlation (r = +0.73) between the area and density of pancreatic islets. Discrete fibrosis and leukocytic infiltrates were found in pancreatic ganglia and pancreatic islets of the patients with Chagas' disease. Trypanosoma cruzi nests were not observed in the examined sections. Individuals with the Megas form of Chagas' disease showed increased area and density of pancreatic islets in the tail of the pancreas.Conclusion: The observed morphometric and morphologic alterations are consistent with functional changes in the pancreas, including glycemia and insulin disturbances.

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“…Intramural denervation would be expected to have some effect on this secretion. However, it was observed that Chagasic patients with clear impairment of the digestive tract shown by megaesophagus did not present any abnormality in motilin, enteroglucagon or gastric inhibitor peptide levels either under basal conditions or after stimulation by an oral or intravenous glucose overload or by insulin hypoglycemia 27 . In another study on this same type of patients, no changes in cholecystokinin, motilin or enteroglucagon levels were detected in the basal state or after intravenous administration of secretin associated or not with duodenal instillation of phenylalanine 43 .…”

Section: Figure 1 -Recordings Of Fasting Small Intestine Motility In mentioning

confidence: 92%

Chagasic enteropathy

Meneghelli

2004

Rev. Soc. Bras. Med. Trop.

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Involvement of the hollow organs of the digestive apparatus can occur in patients in RESUMO O comprometimento dos órgãos ocos do aparelho digestivo pode ocorrer nos portadores da fase crônica da doença de Chagas. O mecanismo básico é a destruição dos neurônios do sistema nervoso entérico. Conquanto o megaesôfago e o megacólon sejam as expressões mais notáveis e estudadas da forma digestiva da doença de Chagas, o envolvimento do intestino delgado (enteropatia chagásica) é menos freqüente e menos conhecido do que o das duas entidades

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Response of plasma pancreatic and gastrointestinal hormones and growth hormone to oral and intravenous glucose and insulin hypoglycaemia in Chagas's disease.

Cited by 31 publications

References 21 publications

Modulation of Growth Hormone and Prolactin Secretion in <i>Trypanosoma cruzi</i>-Infected Mammosomatotrophic Cells

Modulation of Growth Hormone and Prolactin Secretion in <i>Trypanosoma cruzi</i>-Infected Mammosomatotrophic Cells

Morphologic and morphometric evaluation of pancreatic islets in chronic Chagas' disease

Chagasic enteropathy

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