2013 Volume 66 Issue 1 Pages 17-24
Previously, we have demonstrated that administration of 2.5％ trehalose in drinking water for 8 weeks to mice fed a high-fat diet (HFD) suppresses adipocyte hypertrophy and mitigates insulin resistance, in comparison with other saccharides (glucose, maltose, high-fructose corn syrup, or fructose). Therefore, we hypothesized that the hypoinsulinemic effect of trehalose would also be effective for protecting the islets of Langerhans in mice with HFD-induced obesity. Sections of the pancreas from these mice were double-stained with antibodies against insulin and glucagon, and the mean area of islets of Langerhans, the insulin-stained area of β-cells, and glucagon-stained area of α-cells were analyzed on digital images using Scion Image software. In islets, trehalose significantly suppressed HFD-induced hypertrophy in comparison with those from mice fed water, maltose or fructose. Interestingly, trehalose significantly suppressed hypertrophy in the α-cell area in comparison with other saccharide/HFD groups and the DW/HFD group. It is known that α-cells increase in number along with aggravation of type 2 diabetes, and secrete glucagon, which raises the level of blood glucose. Moreover, intake of trehalose for 15 weeks with a HFD suppressed the increase in the circulating level of glucagon at 30 min after glucose administration in an oral glucose tolerance test (OGTT), compared with maltose/HFD. Our findings suggest that trehalose suppresses the compensatory hypertrophy of islets of Langerhans and elevation of the glucagon level in HFD-induced obese mice by suppressing the proliferation of α-cells. Therefore, trehalose would be an excellent food for protection of pancreatic islets in patients with metabolic syndrome.
