Few data have been published so far on the long-term metabolic and endocrine consequences of intrasplenic islet autografts in dogs and the available information mainly deals with glucose response and, more rarely, insulin secretion during intravenous glucose tolerance tests. The effect of islet transplantation on glucagon levels has never been reported. In this study we measured glucose, insulin, total glucagon, and pancreatic glucagon in dogs before and after (up to 1 year) intrasplenic islet autografts. Pancreata were retrieved from 21 adult dogs and the islets were isolated by collagenase digestion. The endocrine tissue was transplanted into the spleen by direct pulp injection. Autografts resulted in normoglycaemia in 19 out of 21 dogs (90%). Among the successfully transplanted dogs, the percentage of functioning grafts was 71% at 1 year. The metabolic and hormonal results of the follow-up showed that fasting glucose and insulin concentrations did not differ significantly before and after transplantation. However, glucose tolerance and insulin secretion on intravenous glucose tolerance testing were significantly reduced in transplanted animals. Fasting total and pancreatic glucagon, and their integrated releases during the test did not change significantly after islet transplantation. These results demonstrate that: 1) long-term function of intrasplenic canine islet autografts can be achieved in high percentages; 2) autotransplanted animals have normal or near normal fasting glucose and insulin levels, but reduced glucose disappearance and insulin secretion on intravenous glucose tolerance tests; 3) normal glucagon secretion is a feature of successful islet grafts.

Animals↗

PubMedDate not supplied

[Carcinoma of the bladder: progress in the preservation of the organ?].

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Chemotherapy, Adjuvant↗

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[Zinc deficiency in liver cirrhosis: a curiosity or a problem?].

This article reviews the literature on the role of zinc in liver cirrhosis and dietary zinc supplementation for cirrhotic patients with hepatic encephalopathy. Zinc is a trace metal found in many proteins and enzymes having catalytical, cocatalytical and structural functions. Zinc deficiency has been demonstrated in cirrhotic patients, and dietary supplementation of this metal could benefit the urea cycle, glucose and protein metabolism, and central nervous system neurotransmission in these subjects. After some brief considerations on normal zinc metabolism, the role zinc plays in the central nervous system, and its conduct in patients with hepatic encephalopathy, possible links between zinc deficiency and the pathophysiology of central nervous system dysfunction in cirrhotic patients are discussed. The article concludes with a critical review of favorable and unfavorable evidence for zinc supplementation in patients with hepatic encephalopathy.

Central Nervous System↗