Apoptosis and the β-Cell in Type 1 and Type 2 Diabetes

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Abstract
Type 2 diabetes is characterized by both insulin resistance and impaired insulin secretion. The defect in insulin secretion clearly involves β-cell dysfunction. Until recently there has been controversy surrounding a possible defect in β-cell mass. In this presentation data will be given which affirm that there is a defect in β-cell mass which precedes the development of type 2 diabetes (hyperglycemia). After a threshold of 60% decrease in β-cell mass there is a marked increase in fasting blood glucose for each further decrement in β-cell mass. Data will also be presented to support the notion that the mechanism subserving this defect is an increased frequency of β-cell apoptosis which leads to the loss of β-cell mass despite ongoing new β-cell input, predominantly from new islet formation (islet neogenesis). Finally, potential causes of the increased frequency of β-cell apoptosis will be reviewed.

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