A difference between the inheritance of classical juvenile-onset and maturity-onset type diabetes of young people

Tattersall, R. B.; Fajans, Stefan S.

doi:10.2337/diabetes.24.1.44

Cited by 214 publications

(135 citation statements)

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“…This is in accord with a previous Japanese report which revealed a higher frequency of positive family histories for diabetes in Type 2 than in Type 1 diabetic patients when the onset of diabetes was before the age of 25 years [7]. Our data also agree with some reports from Western countries [2,3], despite the fact that there are certain differences between Type 1 diabetes in Japanese and Caucasoid people. Typical juvenileonset Type 1 diabetes is less frequent in Japan than in Western countries [8] and is associated with different HLA antigens from those seen in Caucasoid patients [9,10].…”

Section: Discussionsupporting

confidence: 93%

“…It was reported that a family history of diabetes was significantly more prevalent in early-onset Type 2 diabetes than in Type 1 diabetes [2], and the concordance of diabetes in monozygotic twins was signficantly higher in Type 2 than in Type 1 diabetes [3]. These data were obtained mainly in Caucasoid diabetic patients.…”

Section: Summary Family Histories Of Diabetes Mellitus Inmentioning

confidence: 97%

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Family histories of diabetes among Japanese patients with Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetes

Kuzuya

Matsuda

1982

Diabetologia

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Summary. Family histories of diabetes mellitus infirst-degree relatives were compared in Japanese patients with Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetes. The frequency of positive family histories for diabetes in first-degree relatives was 24% (13/55) in Type 1, 44% (281/631) in Type 2 (p < 0.01 versus Type 1) and 47% (16/34) when the type of diabetes could not be classified. The prevalence of diabetes in siblings of Type 2 patients was higher than in Type I diabetic patients (p < 0.01). Patients with Type 2 diabetes and definite obesity in the past had a lower frequency of a family history of diabetes (p < 0.01) and a lower prevalence of diabetes in their parents (p < 0.01) than did Type 2 patients without obesity. The highest rate of family history for diabetes was observed in non-obese Type 2 diabetic patients of early onset. Our data agree with the previously known higher frequency of familial diabetes in Type 2 compared with Type 1 diabetes, despite the fact that there are significant dissimilarities between Type 1 diabetes in Japanese and Caucasoid populations.

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Section: Discussionsupporting

confidence: 93%

Section: Summary Family Histories Of Diabetes Mellitus Inmentioning

confidence: 97%

Family histories of diabetes among Japanese patients with Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetes

Kuzuya

Matsuda

1982

Diabetologia

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“…Thus MacDonald (1974) compared the ancestors of patients with type 1 with a control group and found an equal incidence of diabetes mellitus, surprising as this may be for several reasons. Separate groups of JOD and MOD (of the young) were studied by Tattersall and Fajans (1975b Isolated growth hormone deficiency Cudworth and Woodrow (1974 Optdiatrophy elapsing pancretitis not in rubella by Menser et al (1974Menser et al ( , 1978. In Photomyoclonus, diabetes, deafness, nephropathy, and cerebral Sardinia, Contu et al (1976) (1976) suggested an increased risk to siblings of the propositus, while Koivisto et al (1977) found it at its a family possessing diabetic relatives, picks out this greatest when JOD coexisted with coeliac disease.…”

Section: Parents and Ancestorssupporting

confidence: 41%

Juvenile diabetes mellitus: possibility of prevention.

Farquhar¹

1979

Archives of Disease in Childhood

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“…Maturity-onset diabetes of the young (MODY) is a monogenic, autosomal dominant, early onset form of Type II diabetes which was first described by Stefan Fajans in 1975 [71]. It could account for 2 to 5 % of Type II diabetic patients [72].…”

Section: Maturity-onset Diabetes Of the Youngmentioning

confidence: 99%

Beta-cell mitochondria in the regulation of insulin secretion: a new culprit in Type II diabetes

Wollheim¹

2000

Diabetologia

176

149

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In previous lectures, Claude Bernard's many scientific contributions have been highlighted. Among others he suggested in 1850 that the liver stores glucose and 7 years later, in 1857, he finally isolated glycogen [2]. Before that, in 1849, Claude Bernard reported his ªPiqßre sucrØeº to the SociØtØ de Biologie, Paris [3]. In analogy to his experiments in which stimulation of the fifth cranial nerve caused saliva secretion, he assumed that stimulation of the vagus nerve would elicit glucose secretion from the liver. In unanaesthetised rabbits and dogs, the pricking of the bottom of the fourth ventricle resulted in pronounced hyperglycaemia and glucosuria within 20 min. The ªdiabetesº was transient and disappeared after a few hours. He later showed that this effect was mediated, not by the vagus, but by sympathetic nerves. His discovery of glycogen made Claude Bernard the true father of Diabetologia (2000) AbstractInsulin is stored in secretory granules in the beta-cell and is secreted by exocytosis. This process is precisely controlled to achieve blood glucose homeostasis. Many forms of diabetes mellitus display impaired glucose-induced insulin secretion. This has been shown to be the primary cause of the disease in the various forms of maturity-onset diabetes of the young (MODY) and has also been implicated in adult-onset Type II (non-insulin-dependent) diabetes mellitus. Glucose generates ATP and other metabolic coupling factors in the beta-cell mitochondria. By plasma membrane depolarisation ATP promotes Ca 2+ influx, which raises cytosolic Ca 2+ and triggers insulin exocytosis. Through hyperpolarisation of the mitochondrial membrane glucose also increases the Ca 2+ concentration in the mitochondrial matrix activating Ca 2+ -sensitive dehydrogenases in the tricarboxylic acid cycle. The resulting generation of glutamate participates in Ca 2+ -stimulated exocytosis. Mitochondrial DNA (mtDNA) encodes some of the polypeptides of the respiratory chain enzyme complexes. Mutations in mtDNA lead to maternally inherited diabetes mellitus characterised by impaired insulin secretion. The impact of altered mtDNA on insulin secretion has been shown in mtDNA-deficient beta-cell lines which have lost glucose-stimulated insulin secretion but retain a Ca 2+ -induced insulin secretion. A cellular model of MODY3 expressing dominant-negative hepatocyte nuclear factor-1a (HNF-1a) also displayed deletion of glucose-induced but not Ca 2+ -induced insulin secretion. Reduced mitochondrial metabolism explains this secretory pattern. Thus, genetically manipulated beta-cell lines are essential tools in the investigation of the molecular basis of beta-cell dysfunction in diabetes and should explain the role of other transcription factors in the disease. [Diabetologia (2000) 43: 265±277]

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A difference between the inheritance of classical juvenile-onset and maturity-onset type diabetes of young people

Cited by 214 publications

References 0 publications

Family histories of diabetes among Japanese patients with Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetes

Family histories of diabetes among Japanese patients with Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetes

Juvenile diabetes mellitus: possibility of prevention.

Beta-cell mitochondria in the regulation of insulin secretion: a new culprit in Type II diabetes

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