October 9 - 12, 2012
Building 10 & Natcher Conference Center
- General Schedule of Events
- Opening Plenary Session
- Concurrent Symposia Sessions
- Poster Sessions
- National Graduate Student Research Conference
- FARE Award Ceremony
- Special Exhibits on Resources for Intramural Research
- TSA Research Festival Exhibit Show
- Clinical Center Tours
- Research Festival Committees
- Past Research Festivals
Beta-cell Compensation: Form Follows Function
| Friday, November 08, 2013 — Poster Session IV | |||
|---|---|---|---|
2:00 p.m. – 4:00 p.m. |
FAES Academic Center (Upper-Level Terrace) |
NIDDK |
COMPBIO-4 |
Authors
- Joon Ha
- Les Satin
- A. Sherman
Abstract
It is generally accepted that type 2 diabetes results when insulin secretion fai ls to compensate for the increased demand imposed by insulin resistance. Howeve r, the mechanism of compensation has been mysterious. Thus, it is not clear whe ther compensation consists of increased beta-cell function (secretion per cell), increased beta cell mass or both. In addition, overt hyperglycemia, the most ob vious putative trigger for compensation, is not typically observed. Acutely, beta cells dose dependently increase their in sulin release according to the prevailing glucose concentration. However, persistent post-prandial hyperglycemia, which constitutes a small increase in avera ge daily glucose but a large increase in average daily workload, shifts the beta-cell dose response curve to the left. If high workload persists for an exten ded period, beta-cell mass in diabetes-resistant individuals slowly expands, allowing workload and post-prandial glucose to return to normal. If insulin resi stance is extreme, or accompanied by an impaired ability to increase mass, chronic hyperglycemia results. We show that a mathematical model based on these c ore principles can account for a variety of observed scenarios for the progression from euglycemia to diabetes or its reversal in patients.
