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Glucose suppresses the activity of rat oxyntic histidine decarboxylase without affecting gastrin levels
T Kaneko1, Y Nagamachi, S Matsuzaki
1First Department of Surgery, Gunma University School of Medicine, Japan.
Abstract:
Glucose suppressed the activity of oxyntic mucosal histidine decarboxylase within 2 h when given either intragastrically or intraperitoneally to rats fasted for 24 h. Serum levels of gastrin, secretin, glucagon, and somatostatin and oxyntic mucosal levels of gastrin, histamine, and somatostatin showed no significant changes after glucose. Glucose suppressed the aspirin-induced histidine decarboxylase activity without changing serum gastrin. It also suppressed the pentagastrin-induced histidine decarboxylase activity. Neither fructose nor mannitol had such an effect. These results suggest that glucose acts directly on the enterochromaffin-like cells in rat oxyntic mucosa to suppress histidine decarboxylase activation.
Insights
Glucose directly inhibits histidine decarboxylase activity in rat gastric mucosa, independent of hormonal changes. This finding is crucial for understanding glucose
Area of Science:
- Physiology
- Biochemistry
- Gastroenterology
Background:
- Histidine decarboxylase (HDC) activity in the oxyntic mucosa is a key regulator of histamine synthesis.
- Glucose metabolism can influence gastric acid secretion and related enzyme activities.
- Understanding the direct effects of glucose on mucosal enzymes is important for gastrointestinal physiology.
Purpose of the Study:
- To investigate the direct effect of glucose administration on oxyntic mucosal histidine decarboxylase (HDC) activity in rats.
- To determine whether glucose influences HDC activity through hormonal signaling pathways.
- To explore the specificity of glucose's effect compared to other sugars.
Main Methods:
- Rats were fasted for 24 hours and then administered glucose intragastrically or intraperitoneally.
- Oxyntic mucosal HDC activity was measured at 2 hours post-administration.
- Serum and mucosal levels of gastrin, secretin, glucagon, and somatostatin were analyzed.
- The effects of glucose were compared to fructose, mannitol, aspirin, and pentagastrin.
Main Results:
- Glucose significantly suppressed oxyntic mucosal HDC activity within 2 hours.
- No significant changes were observed in serum or mucosal levels of gastrin, secretin, glucagon, or somatostatin.
- Glucose suppressed both basal and stimulated (aspirin- or pentagastrin-induced) HDC activity.
- Fructose and mannitol did not exhibit the same suppressive effect on HDC activity.
Conclusions:
- Glucose directly suppresses histidine decarboxylase activation in rat oxyntic mucosal enterochromaffin-like cells.
- This effect appears to be independent of changes in key gastrointestinal hormones.
- Glucose's direct action on HDC offers new insights into glucose-gastric mucosal interactions.