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Pancreatic Beta-cell growth and diabetes mellitus

Pancreatic Beta-cell growth and diabetes mellitus Diabetologia (1992) 35:193-201 Diabetologia 9 Springer-Verlag 1992 Review I. Swenne Departments of Paediatrics and Medical Cell Biology,Uppsala University,Uppsala, Sweden Glucose homeostasis is tightly controlled by, first and foremost, insulin. There is a minute-to-minute regulation of insulin output from the Beta cell to meet changing demands at and between meals. There is also a long-term adaptation of insulin production by changes in total Betacell mass. Diabetes mellitus develops if any one of these processes is insufficient and causes absolute or relative insulin deficiency. The regulation of insulin biosynthesis and release in relation to the aetiology of diabetes has been intensely studied, while the role of Beta-cell growth has met with less interest until recent years. In Type 1 (insulin-dependent) diabetes there is a loss of Beta cells and decompensation of metabolism following autoimmune aggression [1]. Insulin production often reccurs shortly after onset of clinical disease ("honeymoon period") suggesting an effort by the reduced Beta-cell mass to meet insulin demands. In Type 2 (non-insulin-dependent) diabetes pathogenesis is less clear and probably multifactorial but there is evidence to suggest that a reduced insulin secretory response to glucose and a limited capacity for Beta-cell replication predisposes to the disease [2, 3]. Studies http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Diabetologia Springer Journals

Pancreatic Beta-cell growth and diabetes mellitus

Diabetologia , Volume 35 (3) – Mar 1, 1992

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References (93)

Publisher
Springer Journals
Copyright
Copyright © 1992 by Springer-Verlag
Subject
Medicine & Public Health; Human Physiology; Internal Medicine; Metabolic Diseases
ISSN
0012-186X
eISSN
1432-0428
DOI
10.1007/BF00400917
Publisher site
See Article on Publisher Site

Abstract

Diabetologia (1992) 35:193-201 Diabetologia 9 Springer-Verlag 1992 Review I. Swenne Departments of Paediatrics and Medical Cell Biology,Uppsala University,Uppsala, Sweden Glucose homeostasis is tightly controlled by, first and foremost, insulin. There is a minute-to-minute regulation of insulin output from the Beta cell to meet changing demands at and between meals. There is also a long-term adaptation of insulin production by changes in total Betacell mass. Diabetes mellitus develops if any one of these processes is insufficient and causes absolute or relative insulin deficiency. The regulation of insulin biosynthesis and release in relation to the aetiology of diabetes has been intensely studied, while the role of Beta-cell growth has met with less interest until recent years. In Type 1 (insulin-dependent) diabetes there is a loss of Beta cells and decompensation of metabolism following autoimmune aggression [1]. Insulin production often reccurs shortly after onset of clinical disease ("honeymoon period") suggesting an effort by the reduced Beta-cell mass to meet insulin demands. In Type 2 (non-insulin-dependent) diabetes pathogenesis is less clear and probably multifactorial but there is evidence to suggest that a reduced insulin secretory response to glucose and a limited capacity for Beta-cell replication predisposes to the disease [2, 3]. Studies

Journal

DiabetologiaSpringer Journals

Published: Mar 1, 1992

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