Increased Expression of Cholecystokinin‐A Receptor mRNA in Pancreas and Cholecystokinin‐B Receptor mRNA in Oxyntic Mucosa after Porta‐caval Shunting in Rats

Nylander, Anna‐Greta; Friesen, Cristina Paz von; Monstein, Hans‐Jürg; Yamada, Hironori; Chen, Duan; Boketoft, Åke; Håkanson, R.

doi:10.1111/j.1600-0773.1997.tb00388.x

Cited by 5 publications

(4 citation statements)

References 24 publications

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“…1993). This seems to be the case after portocaval shunt as cholecystokinin B receptor activation on ECL cells associated with enhanced CCK‐B receptor mRNA has recently been described in the oxyntic mucosa of PCA rats (Nylander et al . 1997).…”

Section: Discussionmentioning

confidence: 88%

“…However, under special circumstances ECL cell activity and growth might be controlled by cholecystokinin (CCK) (Chen et al 1993). This seems to be the case after portocaval shunt as cholecystokinin B receptor activation on ECL cells associated with enhanced CCK-B receptor mRNA has recently been described in the oxyntic mucosa of PCA rats (Nylander et al 1997).…”

Section: Discussionmentioning

confidence: 99%

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Neuronal storage of histamine in the brain and tele‐methylimidazoleacetic acid excretion in portocaval shunted rats

Fogel

Michelsen

Granérus

et al. 2002

Journal of Neurochemistry

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Rats with portocaval anastomosis (PCA), an animal model of hepatic encephalopathy (HE), have very high brain histamine concentrations. Our previous studies based on a biochemical approach indicated histamine accumulation in the neuronal compartment. In this study, immunohistochemical evidence is presented which further supports the amine localization in histaminergic neurons. These neurons become pathological in appearance with cisternae frequently seen along histaminergic fibres in many brain areas, including the hypothalamus, amygdala, substantia nigra and cerebral cortex. Such formations were not observed in sham-operated animals. The neuronal deposition is predominant, and unique for histamine. It serves as a mechanism to counterbalance excessive brain neurotransmitter formation evoked by PCA. However, there are other mechanisms. The data provided here show that there is also a significant increase in histamine catabolism in the shunted rats, as reflected by both the higher brain N-telemethylhistamine (t-MeHA) concentration and urinary excretion of N-tele-methylimidazoleacetic acid (t-MeImAA), a major brain histamine end product. The stomach, in addition to the brain, is a site of enhanced histamine synthesis in portocavally shunted subjects. After gastrectomy or food deprivation to eliminate the contribution of the stomach, shunted rats excrete significantly more t-MeImAA, implying the role of the CNS. This last finding suggests that under strictly defined conditions, namely in parenterally fed HE patients with abnormal plasma L-histidine, the measurement of urinary t-MeImAA might provide valuable information concerning putative brain histaminergic activity.

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Section: Discussionmentioning

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Neuronal storage of histamine in the brain and tele‐methylimidazoleacetic acid excretion in portocaval shunted rats

Fogel

Michelsen

Granérus

et al. 2002

Journal of Neurochemistry

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“…PS shunting has also been shown to display significant abnormalities in the biology of inflammation [39]. Second, there is ample evidence of altered gene expression in other organs in PS shunting, such as: skeletal muscle, pancreas, peripheral tissues and liver [38], [40], [41], [42], [43], [44], [45], [46].…”

Section: Discussionmentioning

confidence: 99%

The C57BL/6J Mouse Exhibits Sporadic Congenital Portosystemic Shunts

et al. 2013

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C57BL/6 mice are the most widely used strain of laboratory mice. Using in vivo proton Magnetic Resonance Spectroscopy (1H MRS), we have repeatedly observed an abnormal neurochemical profile in the brains of both wild-type and genetically modified mice derived from the C57BL/6J strain, consisting of a several fold increase in cerebral glutamine and two fold decrease in myo-inositol. This strikingly abnormal neurochemical “phenotype” resembles that observed in chronic liver disease or portosystemic shunting and appeared to be independent of transgene, origin or chow and was not associated with liver failure. As many as 25% of animals displayed the abnormal neurochemical profile, questioning the reliability of this model for neurobiology. We conducted an independent study to determine if this neurochemical profile was associated with portosystemic shunting. Our results showed that 100% of the mice with high brain glutamine displayed portosystemic shunting by concomitant portal angiography while all mice with normal brain glutamine did not. Since portosystemic shunting is known to cause alterations in gene expression in many organs including the brain, we conclude that portosystemic shunting may be the most significant problem associated with C57BL/6J inbreeding both for its effect on the central nervous system and for its systemic repercussions.

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“…The PCS evoked enhancement of the trophic effects of cholecystokinin (CCK)-A receptor activation on the pancreas and of CCK-B receptor activation in the ECL cells in the oxyntic mucosa. This is associated with enchanced expression of CCK-A receptor mRNA in the pancreas and of CCK-B receptor mRNA in the oxyntic mucosa (Nylander et al, 1997).…”

Section: Resultsmentioning

confidence: 99%

Gastrin (g) and enterochromaffin: Like (ecl) cells in the stomach of portocaval-shunted rats: Radioimmunological, immunocytochemical and ultrastructural study

Tatjana¹,

Vera²,

Nikolić³

et al. 2005

Acta vet. (Beogr.)

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The aim of the study was to monitor the changes observed in the concentration of gastrin, as well as the morphological and ultrastructural properties of pyloric G and fundic ECL cells in rats with a portocaval shunt (PCS). Eight weeks after surgery, plasma and pyloric tissue gastrin concentrations were determined by radioimmunoassay. Sections from pyloric mucosa were immunostained for the identification of G cells, while oxyntic mucosa specimens were processed for Sevier-Munger detection of ECL cells. In addition, ultrastructural properties of G and ECL cells were determined by standard transmission electron microscopy. The results showed that the plasma gastrin levels were unchanged, while the pyloric gastrin concentrations were significantly increased in rats with PCS compared to the control animals (p<0.01). The morphometric analysis showed a significant increase in the cell density of antral G cells (p<0.05) and fundic ECL cells (p<0.01), as well as an increased number of these cells per mm2 of mucosa (p<0.01). In addition the ECL cell profile area was increased in rats with PCS. The predominance of very large vesicles and the reduction of normal cytoplasmic granules and vesicles was a prominent subcellular feature of the ECL. G-cells in PCS rats showed the presence of secretory granules of all types (electron-dense electron-lucent and electron-pale). The number of electron dense granules was elevated. These ultrastructural patterns are compatible with the functional activation of G and ECL cells. The present study suggests that PCS results in hyperplasia of G cells, as well as in both hyperplasia and hypertrophia of ECL cells. It is highly probable that the PCS enchances the sensitivity of the ECL cells to gastrin, thereby enabling them to respond to gastrin in an exaggerated manner

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Increased Expression of Cholecystokinin‐A Receptor mRNA in Pancreas and Cholecystokinin‐B Receptor mRNA in Oxyntic Mucosa after Porta‐caval Shunting in Rats

Cited by 5 publications

References 24 publications

Neuronal storage of histamine in the brain and tele‐methylimidazoleacetic acid excretion in portocaval shunted rats

Neuronal storage of histamine in the brain and tele‐methylimidazoleacetic acid excretion in portocaval shunted rats

The C57BL/6J Mouse Exhibits Sporadic Congenital Portosystemic Shunts

Gastrin (g) and enterochromaffin: Like (ecl) cells in the stomach of portocaval-shunted rats: Radioimmunological, immunocytochemical and ultrastructural study

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