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V Lassmann

Publications and source records attributed to V Lassmann.

24 records · Page 2Linked to original sources
PubMed1978

[Multiple hepatic cysts in rat rendered diabetic by streptozotocin and treated by islets of Langerhans grafts: the role of streptozotocin].

This study is based on the investigation by light and electron microscopy of hepatic biopsies from 14 rats rendered diabetic by streptozotocin and treated by portal embolization of islets of Langerhans. Macroscopically, voluminous projecting cysts were observed, sometimes occupying a whole lobe. By light microscopy, the cysts were lined with canalicular-type epithelium. Ultrastructural studies confirmed the canalicular nature of these cells and cilia were frequently observed. The presence of identical cysts in rats rendered diabetic by streptozotocin but not treated by embolization proves that this product is the agent responsible for the induction of this adenomatosis.

Animals↗
PubMedDate not supplied

Islet transplantation in diabetic rats. Long-term follow-up of glucose tolerance.

Inbred Lewis rats made diabetic by streptozotocin were transplanted with 430-870 islets from syngenic donors via the portal vein. Though fasting plasma glucose was normal, the tolerance to glucose given intraperitoneally (IPGTT) or orally (OGTT) remained impaired one month after transplantation. The higher the number of islets, however, the better the glucose tolerance. The results of IPGTT and OGTT in each animal correlated. Fasting plasma insulin levels were within the normal range suggesting that the action of insulin on the liver and its degradation by the liver is impaired due to the limited number of hepatocytes subjected to high insulin concentrations. Eight months after transplantation, the plasma insulin and glucose responses to OGTT were still unchanged while those of the less physiological IPGTT were worse. Thus, the functional capacity of the transplanted endocrine tissue does not appear to change with time.

Animals↗
PubMedDate not supplied

Sustained initial remission induced by intensive insulin treatment in type I diabetes. Possible role of the genetic background.

A remission defined by the possibility of temporarily discontinuing insulin therapy while blood glucose remains normal is not infrequently observed after intensive insulin therapy in newly diagnosed acute type I diabetes in the South of France. In order to analyze possible factors of such a remission, 47 newly diagnosed ketotic diabetics under 35 years of age and of Caucasian origin were enrolled in a prospective study. They were given continuous s.c. insulin infusion for two weeks and oral agents were introduced on day 8. In 16 patients insulin could not be withdrawn. In 31 insulin was stopped for more than 3 months (mean 12.3, range 3-35) while blood glucose remained below 6 mmol/l fasting (mean 5.3) and 7.8 post-prandial (mean 5.1) and glycosylated Hb below 8.5% (mean 6). At presentation, diabetics who later went into remission and those who did not, showed no difference in age (22.3 vs 23.1 years), sex ratio, apparent duration of symptoms (1.4 vs 1.6 months), glycosylated hemoglobin (12.0 vs 13.1%) and basal or post-prandial C-peptide values or presence of islet cell antibodies. No differences were observed in the frequency of DR3 and DR4 antigens in the two groups but diabetics who developed a remission bore the A 19.2 antigen (9/31 vs 1/16) and the B18 one (11/31 vs 1/16) more frequently, A 19.2 and B18 being associated in 7 cases of this group. This increased frequency in the remission group of HLA antigens, more often observed in diabetics of Mediterranean origin, suggests that differences in the genetic background may be associated with a difference in the evolution of the disease.

Administration, Oral↗