Histology and histopathology · 2006
Zinc ions in the endocrine and exocrine pancreas of zinc deficient rats.
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Søndergaard L G, Stoltenberg M, Doering P, Flyvbjerg A, Rungby J
Аннотация
OBJECTIVE: Zinc deficiency is a problem world-wide. Zinc and insulin are intimately related, and a reduced zinc intake may affect glucose metabolism. The present study investigates how subclinical zinc deficiency in rats affects glucose metabolism and zinc distribution in the pancreas.
METHODS: Glucose metabolism was evaluated by blood-glucose, serum insulin, homeostasis model assessment (HOMA), and intraperitoneal glucose tolerance tests. Immersion zinc-sulphide autometallography (iZnSAMG) was used to describe zinc ion distribution.
RESULTS: After 4 weeks on a zinc deficient diet (<10 ppm), the zinc deficient rats had a slightly impaired glucose metabolism characterized by significantly increased blood-glucose levels. No differences in serum insulin, insulin resistance, beta-cell function were observed. The zinc deficient rats had significantly decreased serum zinc without any clinical signs of zinc deficiency. Zinc ion staining intensity of the islets of Langerhans was unaffected by the zinc deficiency. In contrast, the acinar cells in the exocrine pancreas appeared depleted of iZnSAMG grains in the zinc deficient rats when compared with their controls. Though statistically non-significant, a reduction in total zinc of the pancreas was found.
CONCLUSIONS: The present findings suggest that the endocrine pancreas is able to compensate for the subclinical zinc deficiency as it maintains an adequate zinc ion level in the secretory vesicles for insulin storage. The exocrine pancreas lacks this ability; it exhibits decreased levels of zinc ion staining as a consequence of 4 weeks of reduced zinc intake.
METHODS: Glucose metabolism was evaluated by blood-glucose, serum insulin, homeostasis model assessment (HOMA), and intraperitoneal glucose tolerance tests. Immersion zinc-sulphide autometallography (iZnSAMG) was used to describe zinc ion distribution.
RESULTS: After 4 weeks on a zinc deficient diet (<10 ppm), the zinc deficient rats had a slightly impaired glucose metabolism characterized by significantly increased blood-glucose levels. No differences in serum insulin, insulin resistance, beta-cell function were observed. The zinc deficient rats had significantly decreased serum zinc without any clinical signs of zinc deficiency. Zinc ion staining intensity of the islets of Langerhans was unaffected by the zinc deficiency. In contrast, the acinar cells in the exocrine pancreas appeared depleted of iZnSAMG grains in the zinc deficient rats when compared with their controls. Though statistically non-significant, a reduction in total zinc of the pancreas was found.
CONCLUSIONS: The present findings suggest that the endocrine pancreas is able to compensate for the subclinical zinc deficiency as it maintains an adequate zinc ion level in the secretory vesicles for insulin storage. The exocrine pancreas lacks this ability; it exhibits decreased levels of zinc ion staining as a consequence of 4 weeks of reduced zinc intake.