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. Author manuscript; available in PMC: 2012 Oct 27.
Published in final edited form as: Neuroscience. 2011 Aug 5;194:36–52. doi: 10.1016/j.neuroscience.2011.07.079

Table 7.

Serum metabolic indices at pre- and post-intervention time points.

High fat diet Control diet
H I L
aCSF BDNF aCSF BDNF aCSF BDNF aCSF
Glucose (mg/dl) Pre-treatment 145.4 ± 7.7 135.4 ± 6.4 121.1 ± 15.4 109.4 ± 4.1 113.6 ± 6.9 106.1 ± 8.3 106.7 ± 5.5
Post-treatment 81.7 ± 8.2# 80.1 ± 6.8# 108.0 ± 7.4 85.7 ± 9.7# 81.4 ± 10.2 85.6 ± 8.2# 68.2 ± 9.1#
Insulin (ng/ml) Pre-treatment 10.02 ± 1.14 6.11 ± 0.91* 4.82 ± 0.74 5.45 ± 0.75 2.33 ± 0.50 3.57 ± 0.74 4.65 ± 0.77
Post-treatment 10.22 ± 2.87 3.74 ± 1.35* 9.41 ± 2.19# 7.65 ± 1.74 5.10 ± 0.88# 3.26 ± 0.74¥ 5.42 ± 0.95
Leptin (pg/ml) Pre-treatment 3.39 ± 0.22 3.17 ± 0.24 2.24 ± 0.20 2.34 ± 0.13 1.37 ± 0.11¥ 1.16 ± 0.14 1.65 ± 0.20
Post-treatment 3.17 ± 0.64 1.36 ± 0.24*,# 2.44 ± 0.23 0.92 ± 0.14*# 1.46 ± 0.28 0.49 ± 0.14*#,Δ 1.27 ± 0.22Δ

Glucose: Three-factor ANOVA (phenotype, time and treatment) showed a significant main effect of time (P < 0.0001) and interaction between phenotype and time (P= 0.008), with a weak effect of treatment (P = 0.1501). HC and H-BDNF rats had similar glucose at post-treatment, but both had decreased (P < 0.01) glucose compared to pre-treatment. I-BDNF rats had reduced glucose compared with IC and pre-treatment, but did not reach the significant levels (P = 0.1206 and P = 0.06133, respectively). L-BDNF rats had significantly reduced glucose compared to pre-treatment (P = 0.0348), but had no difference from LC rats.

Insulin: There were significant main effects of treatment (P < 0.0242), phenotype (P = 0.0011) and interactions between the two (P = 0.0435). In the H group, BDNF reduced insulin compared to aCSF (P = 0.02335) and pre-treatment (P = 0.08305). In I and L groups, IC and LC rats, but not I-BDNF and L-BDNF rats, had significantly elevated insulin compared with pre-intervention (P = 0.0484 and P = 0.03881, respectively).

Leptin: Three-factor ANOVA (phenotype, time and treatment) showed main effects of treatment (P < 0.0001), time (p = 0.0002), phenotype (P < 0.0001), and interactions between time and treatment (P < 0.0001). BDNF significantly decreased leptin compared to aCSF treatment and pre-treatment in the H (P = 0.029766 and P = 0.0012, respectively), I (P = 0.00045 and P = 0.00041, respectively) and L (P = 0.01516 and p = 0.0003, respectively) groups.

There were no significant differences in glucose (P = 0.0616) or insulin (P = 0.2253) between the CD-C and the HC, IC and LC post-treatment. CD-C rats had lower serum leptin than that of HC (P = 0.0043, with P = 0.0165 for main effect) at post-treatment. CD-C rats had comparable glucose, insulin and leptin with LC rats at post-treatment. Compared with pre-treatment, CD-C rats at post-treatment had similar levels of insulin and leptin, but significantly lower glucose (P = 0.0052).

H: high body fat; I: intermediate body fat; L: low body fat. Please refer to the detailed statistical analysis described in the method and results sections.

*

P < 0.05, comparison between BDNF- and aCSF-treated rats in same phenotype group;

#

P < 0.05, comparison between pre- and post- intervention in each phenotype;

Δ

P < 0.05, compared to aCSF-treated rats in H (HC) or BDNF-treated rats in H (H-BDNF);

¥

P < 0.05, compared to aCSF-treated rats in I (IC) or BDNF-treated rats in I (I-BDNF).