β-Cell Failure in Type 2 Diabetes: A Case of Asking Too Much of
Too Few?    1. Peter C. Butler1   1. 1Division of Endocrinology,
Larry L. Hillblom Islet Research Center, David Geffen School of
Medicine, University of California, Los Angeles, Los Angeles,
California   2. 2Department of Biochemistry and Molecular
Biology, Keck School of Medicine, Zilkha Neurogenetic Institute,
University of Southern California, Los Angeles, California   1.
Corresponding author: Safia Costes, scostes{at}mednet.ucla.edu.
The islet in type 2 diabetes (T2DM) is characterized by a
deficit in β-cells, increased β-cell apoptosis, and
extracellular amyloid deposits derived from islet amyloid
polypeptide (IAPP). In the absence of longitudinal studies, it
is unknown if the low β-cell mass in T2DM precedes diabetes
onset (is a risk factor for diabetes) or develops as a
consequence of the disease process. Although insulin resistance
is a risk factor for T2DM, most individuals who are insulin
resistant do not develop diabetes. By inferenc