The Discovery of Type 1 Diabetes

Gale, E. A. M.

doi:10.2337/diabetes.50.2.217

Cited by 125 publications

(75 citation statements)

References 90 publications

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“…This goal has proved elusive (74). Given the complexity and diversity of biological systems, it seems increasingly likely that the mechanistic approach will need to be supplemented by a more ecological concept of balanced competition between complex biological processes, a dynamic interaction with more than one possible outcome.…”

Section: Discussionmentioning

confidence: 99%

The Rise of Childhood Type 1 Diabetes in the 20th Century

2002

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The incidence of childhood type 1 diabetes increased worldwide in the closing decades of the 20th century, but the origins of this increase are poorly documented. A search through the early literature revealed a number of useful but neglected sources, particularly in Scandinavia. While these do not meet the exacting standards of more recent surveys, tentative conclusions can be drawn concerning long-term changes in the demography of the disease. Childhood type 1 diabetes was rare but well recognized before the introduction of insulin. Low incidence and prevalence rates were recorded in several countries over the period 1920 -1950, and one carefully performed study showed no change in childhood incidence over the period 1925-1955. An almost simultaneous upturn was documented in several countries around the mid-century. The overall pattern since then is one of linear increase, with evidence of a plateau in some high-incidence populations and of a catch-up phenomenon in some low-incidence areas. Steep rises in the age-group under 5 years have been recorded recently. The disease process underlying type 1 diabetes has changed over time and continues to evolve. Understanding why and how this produced the pandemic of childhood diabetes would be an important step toward reversing it. Diabetes 51:3353-3361, 2002

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Section: Discussionmentioning

confidence: 99%

The Rise of Childhood Type 1 Diabetes in the 20th Century

2002

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“…Type 1 diabetes is believed to be due to immune-mediated beta cell loss, leading to insufficient insulin secretion [1][2][3]. It has long been recognised that a few beta cells can still be identified in pancreas tissue from people with longstanding type 1 diabetes [4][5][6].…”

Section: Introductionmentioning

confidence: 99%

Direct evidence of attempted beta cell regeneration in an 89-year-old patient with recent-onset type 1 diabetes

Meier¹,

Lin

Butler³

et al. 2006

Diabetologia

169

113

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Aims/hypothesis We investigated whether there was evidence of attempted beta cell regeneration in the pancreas obtained from a patient with recent-onset type 1 diabetes, and if so by what mechanism this occurred. Subjects, materials and methods We examined pancreas tissue from a lean 89-year-old patient (BMI 18.0 kg/m 2 ) with recent-onset type 1 diabetes who had had a distal pancreatectomy to remove a low-grade pancreatic intraepithelial neoplasia. Results In the tumour-free tissue, the fractional beta cell area was 0.54±0.2% of pancreas area (about one-third of that in non-diabetic humans). CD3-positive T lymphocytes and macrophages had infiltrated the majority of the islets. Subclassification of the T cell population revealed a predominance of CD8-positive cells over CD4-positive cells. Beta cell apoptosis (terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labelling [TUNEL] staining) was greatly increased, consistent with ongoing immune-mediated beta cell destruction. There was also a marked increase (more than ∼100-fold) in the frequency of beta cell replication (0.69±0.15% Ki67-positive beta cells) in all blocks examined. Conclusions/interpretationThe present report provides direct evidence of attempted beta cell regeneration through the mechanism of beta cell replication in a case of newly diagnosed type 1 diabetes, and affirms that beta cell apoptosis is an important mechanism for beta cell loss in type 1 diabetes.

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“…Idiopathic diabetes was long considered a single disease, despite mounting evidence of heterogeneity. Once formulated, however, the concept of two major disorders with distinct phenotypes, genetic determinants and aetiology won almost immediate acceptance [2] and now rules our thinking, just as the one-disease concept did in the past. For this reason it is rarely acknowledged that the methods we use are of limited value in telling the two conditions apart [3].…”

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confidence: 99%