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Meta-Analysis
. 2020 Feb 17:2020:1508764.
doi: 10.1155/2020/1508764. eCollection 2020.

The Effects of Obesity on Outcome in Preclinical Animal Models of Infection and Sepsis: A Systematic Review and Meta-Analysis

Wanying Xu  1 , Dominique Pepper  1 , Junfeng Sun  1 , Judith Welsh  2 , Xizhong Cui  1 , Peter Q Eichacker  1
Affiliations
Meta-Analysis

The Effects of Obesity on Outcome in Preclinical Animal Models of Infection and Sepsis: A Systematic Review and Meta-Analysis

Wanying Xu et al. J Obes. .

Abstract

Background: Clinical studies suggest obesity paradoxically increases survival during bacterial infection and sepsis but decreases it with influenza, but these studies are observational. By contrast, animal studies of obesity in infection can prospectively compare obese versus nonobese controls. We performed a systematic review and meta-analysis of animal investigations to further examine obesity's survival effect in infection and sepsis.

Methods: Databases were searched for studies comparing survival in obese versus nonobese controls. We performed a systematic review and meta-analysis of animal investigations to further examine obesity's survival effect in infection and sepsis. Methods. Databases were searched for studies comparing survival in obese versus nonobese animals following bacteria, lipopolysaccharide, or influenza virus challenges.

Results: Twenty-one studies (761 obese and 603 control animals) met the inclusion criteria. Obesity reduced survival in 19 studies (11 significantly) and the odds ratio (95% CI) of survival (0.21(0.13, 0.35); I 2 = 64%, p < 0.01p < 0.01p < 0.01) but with high heterogeneity. Obesity reduced survival (1) consistently in both single-strain bacteria- and lipopolysaccharide-challenged studies (n = 6 studies, 0.21(0.13, 0.34); I 2 = 64%, p < 0.01p < 0.01) but with high heterogeneity. Obesity reduced survival (1) consistently in both single-strain bacteria- and lipopolysaccharide-challenged studies (n = 6 studies, 0.21(0.13, 0.34); I 2 = 64%, p < 0.01p < 0.01) but with high heterogeneity. Obesity reduced survival (1) consistently in both single-strain bacteria- and lipopolysaccharide-challenged studies (n = 6 studies, 0.21(0.13, 0.34); I 2 = 64%, p < 0.01p < 0.01) but with high heterogeneity. Obesity reduced survival (1) consistently in both single-strain bacteria- and lipopolysaccharide-challenged studies (n = 6 studies, 0.21(0.13, 0.34); I 2 = 64%, p < 0.01p < 0.01p < 0.01) but with high heterogeneity. Obesity reduced survival (1) consistently in both single-strain bacteria- and lipopolysaccharide-challenged studies (n = 6 studies, 0.21(0.13, 0.34); I 2 = 31%, p=0.20 and n = 5, 0.22(0.13, 0.36); I 2 = 0%, p=0.59, respectively), (2) not significantly with cecal ligation and puncture (n = 4, 0.72(0.08, 6.23); I 2 = 75%, p < 0.01), and (3) significantly with influenza but with high heterogeneity (n = 6, 0.12(0.04, 0.34); I 2 = 73%, p < 0.01). Obesity's survival effects did not differ significantly comparing the four challenge types (p=0.49). Animal models did not include antimicrobials or glycemic control and study quality was low.

Conclusions: Preclinical and clinical studies together emphasize the need for prospective studies in patients accurately assessing obesity's impact on survival during severe infection.

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Conflict of interest statement

The authors declare that they have no conflicts of interest.

Figures

Figure 1
Figure 1
Flow diagram that summarizes the results of the literature search.
Figure 2
Figure 2
The number of total and surviving animals in obese and control groups for each of the 21 analyzed studies and the effects of obesity on the odds ratios (OR (95% CI)) of survival for each study. Also shown is the OR (95% CI) for the 21 studies and the associated I2 and its level of significance.
Figure 3
Figure 3
The number of total and surviving animals in obese and control groups for studies employing either a diet-induced obesity model or genetic-induced obesity model and the effects of obesity on the odds ratios (OR (95% CI)) of survival for each study and the overall OR (95% CI) for each type of obesity model and the associated I2 and its level of significance. As described in the results, because four studies examined both diet and genetic obesity models, this figure presents 25 comparisons, 16 with diet and 9 with genetic obesity models. The effects of obesity did not differ statistically significantly comparing the two types of models (p=0.19).
Figure 4
Figure 4
The number of total and surviving animals in obese and control groups for studies examining obesity in either mouse (18 studies) or rat (3 studies) and the effects of obesity on the odds ratios (OR (95% CI)) of survival for each study and the overall OR (95% CI) for each of the two species and the associated I2 and its level of significance. The effects of obesity did not differ statistically significantly comparing the two species (p=0.99).
Figure 5
Figure 5
The number of total and surviving animals in obese and control groups for studies employing either a single strain bacterial infection model (n = 6 studies), a lipopolysaccharide model (n = 5 studies), a cecal ligation and puncture (polymicrobial infection) model (n = 4 studies), or a viral infection model (n = 6 studies) and the effects of obesity on the odds ratios (OR (95% CI)) of survival for each study and the overall OR (95% CI) for each type of infectious challenge model and the associated I2 and its level of significance. The effects of obesity did not differ significantly comparing the four model types (p=0.49).
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