Return to Normal of Blood-Glucose, Plasma-Insulin, and Weight Gain in New Zealand Obese Mice After Implantation of Islets of Langerhans

Gates, R J; Smith, R. V.; Hunt, Madison; Lazarus, N R

doi:10.1016/s0140-6736(72)91960-5

Cited by 51 publications

(34 citation statements)

References 6 publications

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“…Although earlier studies suggested a possible defect in the development of pancreatic peptide-positive (PP) cells in the islets of NZO/Wehi mice (Gates and Lazarus, 1977;Gates et al, 1972Gates et al, , 1974, we observed numerous granulated PP-cells, as well as glucagoncontaining alpha cells. Although less numerous, somatostain containing delta cells were also demonstrable by immunochemical staining (Fig.…”

Section: Junger Et Alcontrasting

confidence: 92%

The Diabetes-Prone NZO/Hl Strain. II. Pancreatic Immunopathology

Junger¹,

Herberg²,

Jeruschke³

et al. 2002

Laboratory Investigation

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SUMMARY:We report the first combined light and electron microscopic analysis of the pancreas during the development of type 2 diabetes in the New Zealand Obese (NZO) mouse. As in most other polygenic rodent models of type 2 diabetes, hyperglycemia associated with beta cell destruction is male sex-limited. Increasing degrees of hyperinsulinemia and transition to diabetes were clearly reflected by the islet volume fraction, by the beta cell granulation state, and by ultrastructural changes, primarily of the endoplasmic reticulum. One of the unusual histopathologic features of NZO mice of both sexes was the presence of B-lymphocyte enriched leukocytic aggregates in the pancreas. Immunocytochemical analysis of the pancreas of 52-week-old diabetic males indicated enrichment for CD19 ϩ B lymphocytes. Staining of adjacent sections for CD3 and CD5 indicated CD5 coexpression on some of the CD19 ϩ cells, suggesting the presence of the B1-B subset associated with generation of natural autoantibodies in other autoimmune-prone New Zealand mouse strains. In addition, plasma cells in peri-insular leukocytic infiltrates were identified by electron microscopy. Hence, although autoimmunity has previously proven to be a secondary manifestation of beta cell destruction in most rodent models of type 2 diabetes, the present observations suggest that B lymphocyte function, in association with male gender, may contribute to the development of insulin resistance and chronic hyperglycemia in the NZO model. (Lab Invest 2002, 82:843-853).

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Section: Junger Et Alcontrasting

confidence: 92%

The Diabetes-Prone NZO/Hl Strain. II. Pancreatic Immunopathology

Junger¹,

Herberg²,

Jeruschke³

et al. 2002

Laboratory Investigation

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“…When NZO mice are implanted intraperitoneally with Millipore diffusion chambers containing islets isolated from normal albino mice the hyperglycaemia and hyperinsulinaemia, associated with NZO mice, return to levels similar to that of non-obese mice [1]. This finding indicates that the genetic lesion responsible for the NZO state lies within the islets of Langerhans.…”

Section: Discussionmentioning

confidence: 87%

“…Islets were isolated by a collagenase technique, sealed in diffusion chambers constructed from nylonreinforced Millipore membranes and implanted intraperitoneally as described elsewhere [1].…”

Section: Islet Isolation and Implantation Proceduresmentioning

confidence: 99%

Further studies on the amelioration of the characteristics of New Zealand Obese (NZO) mice following implantation of islets of Langerhans

1974

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Summary. New Zealand Obese (NZO) mice are eharaeterised by hyperglyeaemia, hyperinsulinaemia and obesity. The blood glucose and plasma insulin levels of these mice can be lowered to levels approaching those normally associated with non-obese mice, by the intraperitoneal implantation of pancreatic islets from albino mice which have had their fl-cells selectively destroyed by streptozotocin. Removal of these implanted islets causes the animals to revert to their original state. It would seem, therefore, that the genetic lesion responsible for the NZO state lies within the islets of Langerhans but not within the beta-cell. Its exact location is as yet unknown.

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“…Insulin resistance in the obesehyperglycaemic mouse has been attributed to several factors. (1) The number of insulin-binding sites on the membranes of the liver (Kahn et al, 1972(Kahn et al, , 1973a and adipose tissue (Freychet et al, 1972a) (1968,1970) and Gates et al (1972) have shown that after transplantation of islet cells from normal animals into ob/ob animals and NZO mice respectively the body weight and the concentrations of glucose and insulin decreased and glucose tolerance was improved. That the hyperinsulinism itself may be a factor in the production of insulin resistance is indicated by the work of Solomon & Mayer (1962) and by that of Mahler & Szabo (1971), who showed that injections of alloxan into the ob/ob mouse resulted in lower blood glucose concentrations accompanied by a decreased resistance to exogenous insulin and regranulation of the islet cells.…”

mentioning

confidence: 99%

The effect of oxytetracycline on insulin resistance in obese mice

Bégin–Heick

Bourassa

Heick

1974

Biochemical Journal

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1. Chronic oxytetracycline treatment was found to improve the insulin resistance of the obese-hyperglycaemic mouse. 2. The improved response to insulin was accompanied by decreased concentrations of circulating insulin and glucose, by a decrease in the lipid content of the liver and by an increase in the insulin-receptor sites of the liver and adipose tissue. 3. The increase in insulin-receptor sites preceded the fall in blood glucose. 4. Comparable studies done on food-restricted animals indicated that although chronic food restriction corrected the hyperinsulinaemia it did not restore the insulin-receptor sites or the hyperglycaemia.The obese-hyperglycaemic mouse is characterized by obesity, non-ketotic hyperglycaemia, hyperinsulinism, islet-cell hyperplasia and resistance to exogenous insulin. Insulin resistance in the obesehyperglycaemic mouse has been attributed to several factors.(1) The number of insulin-binding sites on

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Return to Normal of Blood-Glucose, Plasma-Insulin, and Weight Gain in New Zealand Obese Mice After Implantation of Islets of Langerhans

Cited by 51 publications

References 6 publications

The Diabetes-Prone NZO/Hl Strain. II. Pancreatic Immunopathology

The Diabetes-Prone NZO/Hl Strain. II. Pancreatic Immunopathology

Further studies on the amelioration of the characteristics of New Zealand Obese (NZO) mice following implantation of islets of Langerhans

The effect of oxytetracycline on insulin resistance in obese mice

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