Decrease of stimulated amylin release precedes impairment of insulin secretion in type II diabetes.

Area of Science:

• Endocrinology
• Metabolic Research
• Diabetes Pathogenesis

Background:

• Amylin, a pancreatic polypeptide, is a key component of amyloid deposits in type II diabetes.
• Amylin is co-stored and co-released with insulin, suggesting a role in diabetes pathogenesis.
• Understanding amylin's secretion patterns is crucial for diabetes research.

Purpose of the Study:

• To compare amylin release and its ratio to insulin secretion across different metabolic states.
• To investigate the impact of obesity and glucose tolerance on amylin secretion.
• To elucidate amylin's role in the progression of type II diabetes.

Main Methods:

• Oral and intravenous glucose tolerance tests (OGTT and IVGTT) were conducted.
• Participants included lean controls, obese individuals with normal glucose tolerance (NGT), impaired glucose tolerance (IGT), and type II diabetes.
• Amylin and insulin levels were measured during glucose challenges.

Main Results:

• Basal and stimulated amylin secretion during OGTT was higher in obese NGT and IGT groups compared to controls.
• The amylin-insulin ratio decreased in obese subjects and significantly in type II diabetic patients.
• Amylin secretion was stimulated by IVGTT in controls and obese NGT/IGT groups, but not in type II diabetes.

Conclusions:

• Amylin is physiologically released by pancreatic beta-cells proportionally to insulin in non-diabetic individuals.
• Obesity is associated with increased glucose-stimulated amylin secretion in non-diabetic states.
• Type II diabetes is characterized by reduced amylin secretion relative to insulin and a lack of glucose-stimulated amylin release.