Protective effect of BCH

Pancreatic β-cells produce the hormone insulin, which helps maintain glucose homeostasis. The mitochondrial matrix enzyme glutamate dehydrogenase (GDH), which catalyzes the interconversion of glutamate and the tricarboxylic acid (TCA) cycle intermediate α-ketoglutarate, is an important regulator of insulin secretion in pancreatic β-cells. Research has shown that 2-aminobicyclo-(2,2,1)-heptane-2-carboxylic acid (BCH) is an activator of GDH.

Han et al. investigated the effect of BCH on high-glucose (HG)-induced reduction in glucose-stimulated insulin secretion (GSIS), the HG/palmitate (PA)-induced reduction in insulin gene expression, and HG/PA-induced β-cell death. They also studied whether long-term treatment with BCH lowers blood glucose and improves β-cell integrity in db/db mice, a type 2 diabetes animal model.

In summary, they demonstrated that treatment with BCH improved glucose tolerance in db/db mice. Improved glycemic control was associated with improved insulin secretion, increased insulin-positive β-cell area as a percentage of total islet area, restoration of normal islet architecture, and reduced β-cell apoptosis. These results suggest that pharmacological activation of GDH may represent a novel therapy for type 2 diabetes. Han et al. (2012) Journal of Endocrinology 212 307-315.

Read the full article at DOI:10.1530/JOE-11-0340.