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Identification of Four Mouse Diabetes Candidate Genes Altering β-Cell Proliferation

Fig 1

Diabetes resistance of B6-ob/ob mice is conferred by an adaptive islet hyperplasia.

(A) Representative pictures of total pancreas slices from NZO and B6-ob/ob mice stained for insulin (digital red-colouring) before carbohydrate feeding (-CH) at day 0 and after 32 days of carbohydrate (+CH) feeding (upper panel). Morphometric analysis of insulin staining from 3–5 animals per time point performed in 3 cutting planes with regard to islet size (left panel), islet number per slice (middle panel), and islet area as percentage of total pancreatic area (right panel). Data are mean ± s.e.m.; *P≤0.05 (lower panel). (B) Representative immunohistochemical staining of Ki-67 in pancreatic slices from B6-ob/ob and NZO mice at the indicated time points of carbohydrate-free (-CH) or carbohydrate (+CH) feeding (upper panel). Quantification of Ki-67 positive islet cells from B6-ob/ob and NZO mice fed-CH or +CH at the indicated time points. Data represent mean ± s.e.m. of 4–6 animals, calculated from mean values of 3 cutting planes per pancreas; *P<0.05 (lower panel).

Fig 1