The incidence of end-stage renal disease (ESRD) has risen considerably in t
he past two decades. This trend is partly due to the alarming rise in the i
ncidence of type 2 diabetes over the same period, which in turn might be li
nked to the staggering increase in overweight and obesity. If these trends
continue, ESRD can be expected not only to cause suffering of ever growing
numbers of patients, but also to become an increasing financial as well as
logistical burden on the health care system. Therefore, it is imperative no
t only to gain a better understanding of the molecular, cellular and metabo
lic mechanisms involved in renal pathology, but also to uncover treatment m
odalities, including lifestyle changes, that can help prevent and/or slow t
he progression of kidney pathogenesis. Insights into both of these aspects
are provided by animal models of obesity and diabetes. It has long been kno
wn that food restriction, more so than restriction of any particular dietar
y component, can greatly enhance longevity in laboratory rodents. These fin
dings are being extended into a variety of other mammals, including nonhuma
n primates. These studies have indicated that caloric restriction in nonobe
se laboratory animals does not primarily affect specific disease processes
but rather nonspecifically slows the aging process. In contrast, a growing
body of evidence suggests that in genetically obese animals, food restricti
on can prevent or greatly delay the onset of specific degenerative lesions,
in particular glomerulonephritis associated with obesity and diabetes.