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Metformin prevents liver tumorigenesis induced by high-fat diet in C57Bl/6 mice. Am J Physiol Endocrinol Metab 305: E987-

The derangement of endoplasmic reticulum (ER) homeostasis triggers β-cell apoptosis, leading to diabetes. Glucokinase upregulates insulin receptor substrate 2 (IRS-2) expression in β-cells, but the role of glucokinase and IRS-2 in ER stress has been unclear. In this study, we investigated the impact of glucokinase activation by glucokinase activator (GKA) on ER stress in β-cells. GKA administration improved β-cell apoptosis in Akita mice, a model of ER stress–mediated diabetes. GKA increased the expression of IRS-2 in β-cells, even under ER stress. Both glucokinase-deficient Akita mice and IRS-2–deficient Akita mice exhibited an increase in β-cell apoptosis, compared with Akita mice. β-cell–specific IRS-2–overexpressing (βIRS-2-Tg) Akita mice showed less β-cell apoptosis than Akita mice. IRS-2–deficient islets were vulnerable, but βIRS-2-Tg islets were resistant to ER stress–induced apoptosis. Meanwhile, GKA regulated the expressions of C/EBP homologous protein (CHOP) and other ER stress–related genes in an IRS-2–independent fashion in islets. GKA suppressed the expressions of CHOP and Bcl2-associated X protein (Bax) and protected against β-cell apoptosis under ER stress in an ERK1/2-dependent, IRS-2–independent manner. Taken together, GKA ameliorated ER stress–mediated apoptosis by harmonizing IRS-2 upregulation and the IRS-2–independent control of apoptosis in β-cells.

The silverleaf whitefly, Bemisia argentifolii Bellows et Perring (Bellows et al., 1994), also known as B-biotype of B. tabaci (Gennadius) (Byrne and Miller, 1990), has become one of the most serious agricultural pests in the world. This whitefly is polyphagous and infests a broad range of crops, including eggplant, cucumber, squash, tomato and sweet potato . Damage by B. argentifolii consists of direct feeding damage, deposition of large quantities of honeydew, plant physiological disorders, such as squash silverleaf disorder in pumpkin and irregular ripening of tomato fruit, and transmission of several plant viruses (Matsui, 1995).In Japan, B. argentifolii was first found to infest poinsettia (Ohto, 1990) and since has infested many plants, including cucumber, eggplant, sweet pepper and tomato. The biology of B. argentifolii has been studied extensively (Bethke et al., 1991;Enkegaard, 1993;Simmons, 1994;Wagner, 1995;Tsai and Wang, 1996;Wang and Tsai, 1996;Yee and Toscano, 1996;Nava-Camberos et al., 2001), although, with the exception of a study by Tsueda and Tsuchida (1998), the biology of the Japanese B. argentifolii population has not been investigated.To develop a successful integrated pest management (IPM) program for its host crops, it is critical to understand the life-history parameters of B. ar- Appl. Entomol. Zool. 42 (1): 63-70 (2007)

The glucokinase-induced up-regulation of insulin receptor substrate 2 (IRS-2) plays an important role in β-cell adaptive proliferation in response to high-fat diet-induced insulin resistance. This study aimed to investigate the role of IRS-2 in the proliferation of β-cells after a 60% partial pancreatectomy. IRS-2-deficient (IRS-2(-/-)) mice or wild-type mice were subjected to a pancreatectomy (60% partial pancreatectomy) or a sham operation (Sham). The β-cell proliferation and gene expression profiles of the islets were then assessed. Gene expression in islets from pancreatectomized and Sham C57BL/6J male mice was analyzed using a cDNA microarray analysis. To compare with β-cell proliferation induced by a high-fat diet, Gck(+/-) mice subjected to a pancreatectomy were also analyzed. The IRS-2(-/-) mice exhibited β-cell expansion and a significant increase in β-cell proliferation after the pancreatectomy, compared with the Sham group. Although glucose-stimulated insulin secretion from islets was not impaired, IRS-2(-/-) mice manifested severe hyperglycemia after the pancreatectomy. The expression levels of Aurora kinase B, Cyclin A, and Cyclin B1 in the pancreatectomized islets were also enhanced in the IRS-2(-/-) mice. A gene set enrichment analysis suggested an association between the genes that were up-regulated in the pancreatectomized islets and those involved in M phase progression in the cell cycle. β-Cell proliferation after a pancreatectomy was observed even in the Gck(+/-) mice. In conclusion, IRS-2 was not required for β-cell proliferation but might be needed for functional β-cell mass, after a pancreatectomy. A partial pancreatectomy in mice may be an attractive model for the development of new strategy for exploring the unique nature of β-cell proliferation.