scholarly journals Interactions of Gut Endocrine Cells with Epithelium and Neurons

2018 ◽  
pp. 1019-1030
Author(s):  
Rodger A. Liddle
Keyword(s):  
Endocrine Cells ◽  
Gut Endocrine Cells

The effect of pancreatic mesenchyme on the differentiation of endocrine cells from gastric endoderm

Development ◽  
1987 ◽  
Vol 100 (4) ◽  
pp. 661-671 ◽  
Author(s):  
B. Kramer ◽  
A. Andrew ◽  
B.B. Rawdon ◽  
P. Becker
Keyword(s):  
Endocrine Cell ◽  
Endocrine Cells ◽  
Cell Types ◽  
The Other ◽  
Chick Embryos ◽  
Cell Type ◽  
Pancreatic Insulin ◽  
Somatostatin Cells ◽  
Regional Specificity ◽  
Gut Endocrine Cells

To determine whether mesenchyme plays a part in the differentiation of gut endocrine cells, proventricular endoderm from 4- to 5-day chick or quail embryos was associated with mesenchyme from the dorsal pancreatic bud of chick embryos of the same age. The combinations were grown on the chorioallantoic membranes of host chick embryos until they reached a total incubation age of 21 days. Proventricular or pancreatic endoderm of the appropriate age and species reassociated with its own mesenchyme provided the controls. Morphogenesis in the experimental grafts corresponded closely to that in proventricular controls, i.e. the pancreatic mesenchyme supported the development of proventricular glands from proventricular endoderm. Insulin, glucagon and somatostatin cells and cells with pancreatic polypeptide-like immunoreactivity differentiated in the pancreatic controls. The latter three endocrine cell types, together with neurotensin and bombesin/gastrin-releasing polypeptide (GRP) cells, developed in proventricular controls and experimental grafts. The proportions of the major types common to proventriculus and pancreas (somatostatin and glucagon cells) were in general similar when experimental grafts were compared with proventricular controls but different when experimental and pancreatic control grafts were compared. Hence pancreatic mesenchyme did not materially affect the proportions of these three cell types in experimental grafts, induced no specific pancreatic (insulin) cell type and allowed the differentiation of the characteristic proventricular endocrine cell types, neurotensin and bombesin/GRP cells. However, an important finding was a significant reduction in the proportion of bombesin/GRP cells, attributable in part to a decrease in their number and in part to an increase in the numbers of endocrine cells of the other types. This indicates that mesenchyme may well play a part in determining the regional specificity of populations of gut endocrine cells.

The distribution of endocrine cell progenitors in the gut of chick embryos

Development ◽  
1984 ◽  
Vol 82 (1) ◽  
pp. 131-145
Author(s):  
B. B. Rawdon ◽  
Beverley Kramer ◽  
Ann Andrew
Keyword(s):  
Gastrointestinal Tract ◽  
Progenitor Cells ◽  
Digestive Tract ◽  
Pancreatic Polypeptide ◽  
Endocrine Cell ◽  
Endocrine Cells ◽  
Chick Embryos ◽  
Intact Embryo ◽  
Pancreatic Endocrine Cells ◽  
Gut Endocrine Cells

The aim of this experiment was to find out whether or not, at early stages of development, progenitors of the various types of gut endocrine cells are localized to one or more specific regions of the gastrointestinal tract. Transverse strips of blastoderm two to four somites in length were excised between the levels of somites 5 and 27 in chick embryos at 5- to 24-somite stages and were cultured as chorioallantoic grafts. The distribution of endocrine cells in the grafts revealed confined localization of progenitor cells only in the case of insulinimmunoreactive cells. Theprogenitors of cells with somatostatin-, pancreatic polypeptide-, glucagon-, secretin-, gastrin/CCK-, motilin-, neurotensin- and serotonin-like immunoreactivity were distributed along the length of the presumptive gut at the time of explantation; indeed, in many cases they were more widespread than are their differentiated progeny in normal gut of the same age. This finding indicates that conditions in grafts must differ from those that operate in the intact embryo. Also it may explain the occurrence of ectopic gut or pancreatic endocrine cells in tumours of the digestive tract.

Co-localisation of substance P-, bombesin-and peptide histidine isoleucine (PHI)-like peptides in gut endocrine cells of the dogfish Scyliorhinus stellaris

1989 ◽  
Vol 179 (6) ◽  
pp. 605-614 ◽  
Author(s):  
V. Cimini ◽  
S. Noorden ◽  
J. M. Polak
Keyword(s):  
Substance P ◽  
Endocrine Cells ◽  
Gut Endocrine Cells

scholarly journals Gut chemosensing: Interactions between gut endocrine cells and visceral afferents

2010 ◽  
Vol 153 (1-2) ◽  
pp. 41-46 ◽  
Author(s):  
Helen E. Raybould
Keyword(s):  
Endocrine Cells ◽  
Visceral Afferents ◽  
Gut Endocrine Cells

scholarly journals An Immunohistochemical and Ultrastructural Study of Segi's Cap, a Large Aggregation of Gut Endocrine Cells, in Bovine Fetuses

1983 ◽  
Vol 46 (5) ◽  
pp. 701-711 ◽  
Author(s):  
Hirofumi KURAMOTO ◽  
Junzo YAMADA ◽  
Nobuo KITAMURA ◽  
Tadayuki YAMASHITA ◽  
Noboru YANAIHARA
Keyword(s):  
Ultrastructural Study ◽  
Endocrine Cells ◽  
Large Aggregation ◽  
Bovine Fetuses ◽  
Gut Endocrine Cells

scholarly journals Interaction between ingested nutrients and gut endocrine cells in patients with irritable bowel syndrome (Review)

2014 ◽  
Vol 34 (2) ◽  
pp. 363-371 ◽  
Author(s):  
MAGDY EL-SALHY ◽  
ODD HELGE GILJA ◽  
DORIS GUNDERSEN ◽  
JAN G. HATLEBAKK ◽  
TRYGVE HAUSKEN
Keyword(s):  
Irritable Bowel Syndrome ◽  
Endocrine Cells ◽  
Gut Endocrine Cells ◽  
Irritable Bowel

Enterostatin in gut endocrine cells—Immunocytochemical evidence

Peptides ◽  
1996 ◽  
Vol 17 (4) ◽  
pp. 609-614 ◽  
Author(s):  
M. Sörhede ◽  
C. Erlanson-Albertsson ◽  
J. Mei ◽  
T. Nevalainen ◽  
A. Aho ◽  
...  
Keyword(s):  
Endocrine Cells ◽  
Gut Endocrine Cells

Gut endocrine cells in rat stomach carcinoma induced by N-methyl-N?-nitro-N-nitrosoguanidine

1986 ◽  
Vol 111 (2) ◽  
pp. 87-92 ◽  
Author(s):  
Wataru Yasui ◽  
Hiromichi Sumiyoshi ◽  
Jotaro Hata ◽  
Kohichi Mandai ◽  
Eiichi Tahara
Keyword(s):  
Endocrine Cells ◽  
Rat Stomach ◽  
Stomach Carcinoma ◽  
Gut Endocrine Cells

scholarly journals GUT ENDOCRINE CELLS IN INSECTS: THE ULTRASTRUCTURE OF THE ENDOCRINE CELLS IN THE COCKROACH MIDGUT

1981 ◽  
Vol 2 (1) ◽  
pp. 30-44 ◽  
Author(s):  
JUNKO NISHIITSUTSUJI-UWO ◽  
YASUHISA ENDO
Keyword(s):  
Endocrine Cells ◽  
Gut Endocrine Cells

scholarly journals Case Report: Severe Hypocalcemic Episodes Due to Autoimmune Enteropathy

2021 ◽  
Vol 12 ◽  
Author(s):  
Inbal Halabi ◽  
Marie Noufi Barohom ◽  
Sarit Peleg ◽  
Phillippe Trougouboff ◽  
Ghadir Elias-Assad ◽  
...  
Keyword(s):  
Endocrine Cells ◽  
Oral Candidiasis ◽  
Diabetes Mellitus Type 1 ◽  
Intestinal Biopsy ◽  
Disease Course ◽  
Autoimmune Enteropathy ◽  
Appropriate Therapy ◽  
Gut Endocrine Cells ◽  
Normal Calcium

Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) is a rare monogenic disorder, associated with endocrine deficiencies and non-endocrine involvement. Gastrointestinal (GI) manifestations appear in approximately 25% of patients and are the presenting symptom in about 10% of them. Limited awareness among pediatricians of autoimmune enteropathy (AIE) caused by destruction of the gut endocrine cells in APECED patients delays diagnosis and appropriate therapy. We describe an 18-year-old female presenting at the age of 6.10 years with hypoparathyroidism, oral candidiasis and vitiligo. The clinical diagnosis of APECED was confirmed by sequencing the autoimmune regulator-encoding (AIRE) gene. Several characteristics of the disease—Hashimoto’s thyroiditis, Addison’s disease, diabetes mellitus type 1 and primary ovarian insufficiency—developed over the years. She had recurrent episodes of severe intractable hypocalcemia. Extensive GI investigations for possible malabsorption, including laboratory analyses, imaging and endoscopy with biopsies were unremarkable. Revision of the biopsies and chromogranin A (CgA) immunostaining demonstrated complete loss of enteroendocrine cells in the duodenum and small intestine, confirming the diagnosis of AIE. Management of hypocalcemia was challenging. Only intravenous calcitriol maintained calcium in the normal range. Between hypocalcemic episodes, the proband maintained normal calcium levels, suggesting a fluctuating disease course. Repeated intestinal biopsy revealed positive intestinal CgA immunostaining. The attribution of severe hypocalcemic episodes to AIE emphasizes the need for increased awareness of this unique presentation of APECED. The fluctuating disease course and repeated intestinal biopsy showing positive CgA immunostaining support a reversible effect of GI involvement. CgA immunostaining is indicated in patients with APECED for whom all other investigations have failed to reveal an explanation for the malabsorption.

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