BTB and CNC homology 1 (Bach1) is a transcriptional repressor of antioxidative 
enzymes, such as heme oxygenase-1 (HO-1). Oxidative stress is reportedly 
involved in insulin secretion impairment and obesity-associated insulin 
resistance. However, the role of Bach1 in the development of diabetes is 
unclear. HO-1 expression in the liver, white adipose tissue, and pancreatic 
islets was markedly upregulated in Bach1-deficient mice. Unexpectedly, glucose 
and insulin tolerance tests showed no differences in obese wild-type (WT) and 
obese Bach1-deficient mice after high-fat diet loading for 6 wk, suggesting 
minimal roles of Bach1 in the development of insulin resistance. In contrast, 
Bach1 deficiency significantly suppressed alloxan-induced pancreatic insulin 
content reduction and the resultant glucose elevation. Furthermore, 
TUNEL-positive cells in pancreatic islets of Bach1-deficient mice were markedly 
decreased, by 60%, compared with those in WT mice. HO-1 expression in islets was 
significantly upregulated in alloxan-injected Bach1-deficient mice, whereas 
expression of other antioxidative enzymes, e.g., catalase, superoxide dismutase, 
and glutathione peroxidase, was not changed by either alloxan administration or 
Bach1 deficiency. Our results suggest that Bach1 deficiency protects pancreatic 
β-cells from oxidative stress-induced apoptosis and that the enhancement of HO-1 
expression plays an important role in this protection.