Hyperglycemia induces intestinal sucrase activity in subtotally pancreatectomized rats.

Abstract

The effects of experimental diabetes, hypertonic glucose infusion, and subsequent insulin administration on the sucrase activity of the small intestine were studied using intestinal segments completely excluded from luminal continuity by construction of Thiry-Vella fistulas in rats. Eight weeks after subtotal pancreatectomy, the rats contracted insulin-deficient diabetes mellitus, and sucrase activity was enhanced in both the Thiry-Vella loop and in the proximal jejunum in continuity. Subcutaneous injections of insulin during the last 4 weeks maintained the enzyme activity in the control range in both segments. There was a positive correlation between sucrase activity and blood glucose level in the pancreatectomized rats. Hyperglycemia in normal rats induced by intravenous infusion of 30% glucose solution over 48 hours enhanced the sucrase activity in the jejunum. Furthermore, insulin administration with a glucose solution inhibited the enhancement of enzyme activity. These findings suggest that hyperglycemia itself might play an important role in the diabetic increment of sucrase activity.

• Authors: T Takeguchi, K Mori, S Takano, M Akagi
• Journal: Gastroenterologia Japonica (Gastroenterol Jpn) Vol. 20 Issue 1 Pg. 20-7 (Feb 1985) ISSN: 0435-1339 [Print] Japan
• PMID: 4018494 (Publication Type: Comparative Study, Journal Article)

Chemical References

• Blood Glucose
• Insulin, Long-Acting
• Sucrase
• Glucose

Topics

• Animals
• Blood Glucose (analysis)
• Diabetes Mellitus, Experimental (enzymology, etiology)
• Enzyme Induction (drug effects)
• Glucose (administration & dosage)
• Hyperglycemia (enzymology, etiology)
• Insulin, Long-Acting (administration & dosage)
• Intestine, Small (enzymology)
• Male
• Pancreas (physiology)
• Pancreatectomy
• Rats
• Rats, Inbred Strains
• Splenectomy
• Sucrase (biosynthesis)