Biophysics

The Biology of the Pancreatic β-Cell by E. Edward Bittar and Simon L. Howell (Eds.)

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By E. Edward Bittar and Simon L. Howell (Eds.)

Because of the key advances made greater than 30 years in the past, particularly the facility to isolate islets of Langerhans from the pancreas, the power to degree insulin effectively via immunoasay, and the advance of microchemical strategies for learning cells and their elements, many study volumes, symposium experiences, and unique papers were produced. This explosion of curiosity has most likely had a minimum of 3 stimuli:

1. the inherent medical curiosity in knowing secretion of the pancreatic ß-cell
2. the ß-cells relevance to a truly universal illness
3. the provision of investment from particular assets concerning diabetes learn, for example, Juvenile Diabetes starting place foreign and the British Diabetic Association.

As as a result of all this task, certain medical literature together with examine reports are available.
Surprisingly sufficient, there are rather few makes an attempt to summarize this nice bulk of information in a fashion that's obtainable to the newcomer to this box and this ebook is meant to bridge this hole.

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The AtT-20ins cells contain glucokinase; stable transfection with GLUT-2 cDNA resulted in increased insulin content, indicative of increased biosynthetic activity, and glucose stimulated a significant increase in insulin secretion from these cells. , 1992). This left-shifted responsiveness to glucose probably occurred because AtT-20ins cells express more hexokinase than glucokinase, thus making them maximally responsive to glucose at subphysiological levels. Another problem with AtT20ins cells is that they still express large amounts of their native hormone, adrenocorticotropic hormone (ACTH), which is co-localized with insulin in the secretory granules.

47 . . . . . . 48 Cytokines . . . . . . . . . . . . . . . . . . . . . . . . . . 48 11. Inflammatory and Metabolic Agents Inducing P-Cell Dysfunction A. B. Reactive Nitrogen and Oxygen Species . . . . . . . . . . . . . . C. Chronic Hyperglycemia. 111. P-Cell Defense and Repair Mechanisms. . . . . . . . . . . . . . . . IV. P-Cell Outcome Following Damage . . . . . . . A. Functional Recovery or Permanent Dysfunction B.

Chronic Hyperglycemia. 111. P-Cell Defense and Repair Mechanisms. . . . . . . . . . . . . . . . IV. P-Cell Outcome Following Damage . . . . . . . A. Functional Recovery or Permanent Dysfunction B. P-Cell Death-The Role for Apoptosis 1. 50 52 53 INTRODUCTION The different forms of diabetes mellitus are characterized by deficient insulin release in relation to the insulin demand. This can be caused either by immune-, toxin-, or viral-mediated p-cell damage or by a site-specific defect in p-cell substrate metabolism.

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