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- W2003277720 abstract "Gravidas with obesity and diabetes (“diabesity”) may transmit this syndrome to their children through genetic and nongenetic mechanisms. Here, we used the Lepr db/+ diabese mouse to examine the magnitude of these transmission modes, focusing on adipose tissue (AT). We compared the following six groups: wild-type (+/+) offspring from +/+ or db/+ dams (different early life environment) and db/+ offspring from db/+ dams, fed a standard or high-fat diet. Weight gain (0–8 wk) was higher in +/+ offspring from db/+ vs. +/+ mothers, and even higher in db/+ vs. +/+ offspring from db/+ mothers. In addition, we observed a stepwise increase in AT and adipocyte size in +/+ from +/+ mice, +/+ from db/+ mice, and db/+ mice at 8 wk. Differences in weight and adiposity between +/+ offspring from db/+ vs. +/+ dams were more pronounced in males than in females. Leptin and apelin mRNA levels in white and brown AT were higher in +/+ offspring from db/+ vs. +/+ dams; however, leptin, apelin, and tumor necrosis factor-α expression were boosted more robustly in db/+ offspring. The high-fat diet amplified AT differences between db/+ vs. +/+ offspring from db/+ dams, but not between +/+ offspring from db/+ vs. +/+ dams. Moreover, db/+ but not +/+ offspring from db/+ mothers were insulin-resistant and hyperinsulinemic after a glucose challenge. In conclusion, the genetic transmission of the diabesity phenotype clearly prevailed, but the early-life diabesity environment had discernible effects on postnatal weight gain as well as on adipocyte size and adipokine expression at a postpubertal age." @default.
- W2003277720 created "2016-06-24" @default.
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- W2003277720 date "2007-01-01" @default.
- W2003277720 modified "2023-10-03" @default.
- W2003277720 title "Adipose tissue in offspring of<i>Lepr<sup>db/+</sup></i>mice: early-life environment vs. genotype" @default.
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- W2003277720 doi "https://doi.org/10.1152/ajpendo.00308.2006" @default.
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