Plasma and Pancreatic Tissue Levels of Islet Amyloid Polypeptide in Type 1 and Type 2Diabetes: A Review
Journal Title: Journal of Endocrinology and Diabetes - Year 2016, Vol 3, Issue 6
Abstract
The etiology of type 2 diabetes includes obesity-associated insulin resistance, defective insulin secretion and loss of β-cell mass. Islets remodel at a delicate balance between regeneration and apoptosis. Ample amyloid deposit is a characteristic finding for type 2 diabetic islets and islet amyloid polypeptide (IAPP) is a chief component of amyloid deposits. It is concomitantly co-secreted with insulin from β-cells in response to glucose-induced insulin secretion. In insulinrequiring subjects with type 1 and type 2 diabetes, synthetic IAPP, Pramlintide28-30 works synergistically with insulin for a better glycemic control. A loss of soluble IAPP in β-cells coincides with dying β-cells by toxic small molecular weight IAPP oligomers. There is markedly reduced immunostaining for insulin and IAPP in type 1 diabetic islets whereas there is moderately reduced immunostaining with extracellular amyloid deposits in type 2 diabetic islets. Type 2 diabetic islets show variable amount of amyloid deposits from small to massive deposits with less insulin and IAPP immunostaining with disproportionally increased α- and δ- cells. Insulin-deficient β-cells contribute to initial hyperglycemia and massive amyloid sheets in islets contribute to sustained insulin and IAPP deficiency. Amyloid sheets surround remaining β-cells and mechanically obstruct insulin secretion and transport into the blood.
Authors and Affiliations
Tatsuo Tomita
Keywords
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- EP ID EP333699
- DOI 10.15226/2374-6890/3/6/00156
- Views 90
- Downloads 0
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