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. 2016 Dec;65(12):1720-1730.
doi: 10.1016/j.metabol.2016.09.003. Epub 2016 Sep 22.

Adiponectin Administration Prevents Weight Gain and Glycemic Profile Changes in Diet-Induced Obese Immune Deficient Rag1-/- Mice Lacking Mature Lymphocytes

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Adiponectin Administration Prevents Weight Gain and Glycemic Profile Changes in Diet-Induced Obese Immune Deficient Rag1-/- Mice Lacking Mature Lymphocytes

Xiaowen Liu et al. Metabolism. .
Free PMC article

Abstract

Background: Obesity is associated with chronic low-grade inflammation leading to insulin resistance and diabetes. Adiponectin is an adipokine that regulates inflammatory responses. The aim of our study was to investigate whether any effects of adiponectin against obesity and insulin-resistance may depend on the adaptive immune system.

Methods: We treated high-fat-diet fed Rag1-/- mice lacking mature lymphocytes with adiponectin over 7weeks and investigated alterations in their metabolic outcome and inflammatory state.

Results: Adiponectin protects from weight gain despite a small compensatory stimulation of energy intake in mice lacking an adaptive immune system. Additionally, adiponectin protects from dysglycemia. Minor alterations in the macrophage phenotype, but not in the circulating cytokine levels, may contribute to the protective role of adiponectin against hyperglycemia and diabetes.

Conclusion: Adiponectin or agents increasing adiponectin may be a promising therapeutic option against obesity and hyperglycemia in immune-deficient populations.

Keywords: Adiponectin; Diabetes; Immunity; Lymphocyte; Obesity.

Figures

Figure 1
Figure 1
Experimental timeline (A), body weight (B) and energy intake (C) in Rag1−/− mice maintained on low fat diet (LFD) or high fat diet (HFD) and treated either with adiponectin or placebo for 14 weeks. LFD= Rag1−/− mice maintained with LDF. HFD-PL= Rag1−/− mice maintained with HFD treated with placebo. HFD-AP= Rag1−/− mice maintained with HFD treated with adiponectin. P treatment (Trt) was considered the p-overall. Post hoc tests for body weight: HFD-AP vs HFD-PL p=0.039, HFD-AP vs LFD p<0.0001, HFD-PL vs LFD p<0.0001. For energy intake: HFD-AP vs HFD-PL p=0.001, HFD-AP vs LFD p<0.0001, HFD-PL vs LFD p<0.0001. Values are means ± SE; n= 7 for LFD, 8 HFD-PL and 6 HFD-APN.
Figure 2
Figure 2
Plasma concentration of leptin (A) and blood glucose (B) in Rag1−/− mice maintained on low fat diet (LFD) or high fat diet (HFD) and treated either with adiponectin or placebo for 14 weeks, ipGTT (C), and ipITT (D) in all groups of Rag1−/− mice at week 12 and week 13 respectively. LFD= Rag1−/− mice maintained with LFD. HFD-PL= Rag1−/− mice maintained with HFD treated with placebo. HFD-AP= Rag1−/− mice maintained with HFD treated with adiponectin. P treatment (Trt) was considered p overall. Post-hoc tests for leptin (A): HFD-AP vs HFD-PL p<0.0001, HFD-AP vs LFD p<0.0001, HFD-PL vs LFD p<0.0001. For Glucose levels (B) : HFD-AP vs HFD-PL p<0.0001, HFD-AP vs LFD p<0.0001, HFD-PL vs LFD p<0.0001. For ipGTT (C): HFD-AP vs HFD-PL p<0.0001, HFD-AP vs LFD p<0.006, HFD-PL vs LFD p<0.0001. After adjustment for baseline glucose (0 min), p treatment = 0.091. ipITT comparisons among the three groups, p treatment p = 0.652. After adjustment for baseline glucose (0 min), p treatment <0.0001, Post-hoc: HFD-AP vs HFD-PL, p=1, HFD-AP vs LFD p <0.0001, HFD-PL vs LFD p <0.0001. Values are means ± SE

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