The experimental model developed is all the more relevant since diabetes is first allowed to develop in adult rats as is the case with type 2 diabetes appearing in adult age. The recognized model of beta cell neogenesis in STZ-treated neonatal rats[18] has a drawback that damage to beta cells by STZ in new born is followed by a rapid remission from neonatal diabetes starting from nearly day 3 to 5 after birth.[19,32] Adult rats with STZ exhibit decreased beta cell mass and a chronic pathological pattern that presents functional similarities to type 2 diabetes.[19,20] Secondly, the model developed can be put to use by those who do not have the facilities for carrying out cytological studies involving immunochemical and morphometric methods.

The pancreatic beta cell responsible for maintenance of body’s glucose level within a narrow range, their number, and functioning can be said to be dynamic, i.e., undergoing both replication and apoptosis in a balanced way.[33] One determinant in the development of diabetes is inadequate mass of beta cells, either absolute in Type 1 diabetes or relative in Type 2 diabetes.[18] A better understanding of regeneration and factors responsible for stimulating regeneration and replication can lead to new therapeutic strategies for the treatment of diabetes. If beta cell neogenesis by AR is further confirmed by cytological evidence, it will provide a new dimension to the therapeutic intervention of diabetes mellitus. Beta cell neogenesis means the regeneration of new beta cells from precursor cells.

Neogenesis from duct epithelium is the most currently described and best documented process of differentiation of precursor cells into beta cells. This process contributes not only to beta cell mass expansion during fetal and neonatal life, but it is also involved in the maintenance of beta cell mass in adults and further a number of factors controlling the differentiation of precursor cells have been identified.[34�C36] Recently, the incretin hormone glucagon-like peptide (GLP-1) and its long-acting analogue exendin-4, known to enhance glucose-stimulated insulin release and glucose disposal in peripheral tissues, have been reported to stimulate the proliferation of INS-1 cells in vitro,[37] and increase beta cell mass in adult rodents in vivo.[38�C40] It is likely that D-pinitol present in AR is exerting both hypoglycemic and beta cell neogenesis by augmenting the release of GLP-1, as GLP-1 has been reported to mediate its action by promoting DNA synthesis, activation of phosphotidylinostol 3-kinase and by increasing transcription Anacetrapib factor.[37] Follow-up study for recording cytological evidence on beta cell neogenesis by AR or its active constituents is warranted.