NIDDM is characterized by both insulin resistance and defective insuli
n secretion, Although significant advances in our understanding of the
regulation of both insulin action and secretion have been achieved, w
e have yet to define the underlying pathophysiology or genetic basis o
f the most common types of NIDDM. Transgenic technology, which permits
the introduction of genes into the germ line of mice, and homologous
recombinant gene knockout, which allows elimination of endogenous gene
expression, are powerful new tools for exploring the complex pathogen
esis of NIDDM. In this review we briefly summarize principal methods u
sed to create genetically altered animals and highlight results from t
hose models that have contributed to our understanding of the role of
specific candidate genes and the overall pathophysiology of NIDDM.