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In this study we investigated the development of diet-induced T2DM in these two strains.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Methods and Results<\/jats:title>\n            <jats:p>When deficient in apolipoprotein E (apoE<jats:sup>-\/-<\/jats:sup>) and fed a Western diet for 12 weeks, atherosclerosis-susceptible B6 mice developed significant hyperglycemia. In contrast, atherosclerosis-resistant BALB apoE<jats:sup>-\/-<\/jats:sup> mice had much lower plasma glucose levels than B6.apoE<jats:sup>-\/-<\/jats:sup> mice on either chow or Western diet and during an intraperitoneal glucose tolerance test. In response to glucose BALB.apoE<jats:sup>-\/-<\/jats:sup> mice displayed both the first and second phases of insulin secretion but the second phase of insulin secretion was absent in B6.apoE<jats:sup>-\/-<\/jats:sup> mice. In response to insulin B6.apoE<jats:sup>-\/-<\/jats:sup> mice showed a deeper and longer-lasting fall in blood glucose levels while BALB.apoE<jats:sup>-\/-<\/jats:sup> mice showed little reduction in glucose levels. Pancreatic islet area of BALB.apoE<jats:sup>-\/-<\/jats:sup> mice on light microscopy nearly doubled the area of B6.apoE<jats:sup>-\/-<\/jats:sup> mice. Most circulating proinflammatory cytokines were lower in BALB.apoE<jats:sup>-\/-<\/jats:sup> than in B6.apoE<jats:sup>-\/-<\/jats:sup> mice on the Western diet, as determined by protein arrays. Increased macrophage infiltration in islets was observed in B6.apoE<jats:sup>-\/-<\/jats:sup> mice by immunostaining for Mac2 and also by flow cytometry.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusion<\/jats:title>\n            <jats:p>This study demonstrates that defects in insulin secretion rather than defects in insulin resistance explain the marketed difference in susceptibility to T2DM in the B6.apoE<jats:sup>-\/-<\/jats:sup> and BALB.apoE<jats:sup>-\/-<\/jats:sup> mouse model. A smaller islet mass and more prominent islet inflammation may explain the vulnerability of B6.apoE<jats:sup>-\/-<\/jats:sup> mice to diet-induced diabetes.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1186\/1475-2840-10-117","type":"journal-article","created":{"date-parts":[[2011,12,28]],"date-time":"2011-12-28T19:42:19Z","timestamp":1325101339000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":39,"title":["Hyperglycemia in apolipoprotein E-deficient mouse strains with different atherosclerosis susceptibility"],"prefix":"10.1186","volume":"10","author":[{"given":"Jing","family":"Li","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qian","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Weidong","family":"Chai","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mei-Hua","family":"Chen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhenqi","family":"Liu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Weibin","family":"Shi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2011,12,28]]},"reference":[{"issue":"4","key":"424_CR1","doi-asserted-by":"publisher","first-page":"229","DOI":"10.1056\/NEJM199807233390404","volume":"339","author":"SM Haffner","year":"1998","unstructured":"Haffner SM, Lehto S, Ronnemaa T, Pyorala K, Laakso M: Mortality from coronary heart disease in subjects with type 2 diabetes and in nondiabetic subjects with and without prior myocardial infarction. 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