Adipokine, IGF-1, IGFBP-3, and insulin levels among CR, control, and DIO mice.

<p>Levels of <b>A</b>) IGF-1, <b>B</b>) IGFBP-3, <b>C</b>) insulin, <b>D</b>) leptin, <b>E</b>) resistin, and <b>F</b>) adiponectin were measured in the serum of the mice ten weeks after the last injection of AOM. Each boxplot represent the mean and range (n = 20). Overall differences among groups were determined using a one-way ANOVA. For <b>A</b>) IGF-1, p = 0.002; <b>B</b>) IGFBP-3, p<0.001; <b>C</b>) insulin, p = 0.002; <b>D</b>) leptin, p<0.0001; <b>E</b>) resistin, p = 0.001; and <b>F</b>) adiponectin, p = 0.14. <i>a</i>,<i>b</i>, and <i>c</i> represent dietary treatments that are significantly different (p<0.05) from one another as determined by a Bonferroni test.</p

Real time PCR of microRNAs to validate microarray.

<p>Ten miRs were validated using real-time PCR. They included miR-425, miR-196a, miR-155, miR-150, miR-351, miR-16, let-7f, miR-34c, miR-138a, and miR-21. Results were analyzed using the comparative C_T method and reported as fold differences compared to the control group. Each bar represents the mean of six animals.</p

A. Bodyweights in calorie restricted (CR), control, and diet-induced obesity (DIO) FVB mice.

<p>Bodyweight was measured weekly in all three dietary interventions. Each data point represents the mean of all the mice in that dietary group. B. Body fat in CR, control, and DIO dietary treatments. Dual-energy X-ray absorptiometer (DEXA) scans were conducted at the beginning of the study and after ten weeks of dietary treatment. Each bar represents the mean of ten mice per group. One-way analysis of variance (ANOVA) at the beginning of the study, p = 0.78. One-way ANOVA at ten weeks, p<0.001. <i>a</i>, <i>b</i>, and <i>c</i> represent dietary treatments that are significantly different from one another (p<0.05) as determined by Bonferroni test.</p

Obesity is associated with differences in microRNA expression.

<p>Obesity is associated with differences in microRNA expression.</p

Glucose tolerance testing in CR, control, and DIO mice after ten weeks on dietary treatment.

<p>Each data point represents the mean of ten mice per dietary treatment.</p

Diet composition.

<p>Diet composition.</p

Cellular proliferation and apoptosis in CR, control, and DIO mice 20 weeks after the last AOM injection.

<p><b>A</b>) Proliferation was assessed via immunohistochemistry for proliferating cell nuclear antigen (PCNA). A field of 1000 cells was counted for each animal and the proliferative index represents the percentage of cells that stained positive for PCNA. The bars represent the average proliferative index for each dietary group (n = 20). <b>B</b>) Apoptosis in the tumors of LID versus wildtype mice 20 weeks after the last AOM injection. Apoptosis was assessed via TUNEL staining. A field of 1000 cells was counted for each animal and the apoptotic index represents the percentage of cells that stained positive and also appeared apoptotic based on cell morphology. The bars represent the average apoptotic index for each dietary group (n = 20). <i>a</i>,<i>b</i>, and <i>c</i> represent dietary treatments that are significantly different (p<0.05) from one another as determined by a Bonferroni test.</p