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Review
. 2022 Jul 5:13:908868.
doi: 10.3389/fendo.2022.908868. eCollection 2022.

Cross-Talk Between Gut Microbiota and Adipose Tissues in Obesity and Related Metabolic Diseases

Affiliations
Review

Cross-Talk Between Gut Microbiota and Adipose Tissues in Obesity and Related Metabolic Diseases

Dan Wu et al. Front Endocrinol (Lausanne). .

Abstract

The rapid increase of obesity and associated diseases has become a major global health problem. Adipose tissues are critical for whole-body homeostasis. The gut microbiota has been recognized as a significant environmental factor in the maintenance of energy homeostasis and host immunity. A growing body of evidence suggests that the gut microbiota regulates host metabolism through a close cross-talk with adipose tissues. It modulates energy expenditure and alleviates obesity by promoting energy expenditure, but it also produces specific metabolites and structural components that may act as the central factors in the pathogenesis of inflammation, insulin resistance, and obesity. Understanding the relationship between gut microbiota and adipose tissues may provide potential intervention strategies to treat obesity and associated diseases. In this review, we focus on recent advances in the gut microbiota and its actions on adipose tissues and highlight the joint actions of the gut microbiota and adipose tissue with each other in the regulation of energy metabolism.

Keywords: adipose tissues; energy metabolism; gut microbiota; inflammation; obesity.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
The crosstalk between gut microbiota and adipose tissues. On the one hand, the gut microbiota and microbial-derived metabolites may mediate the external factors, such as dietary foods, to regulate white adipose tissue (WAT) expansion, inflammation, and insulin resistance in obesity. Different diets may have different effects on the gut microbiota, such as low carbohydrate diet (LCD) (22) can increase Bacteroidaceae Bacteroides and reduce body weight effectively; whereas western diet (WD) (24) or high-fat diet (HFD) (43, 76) can increase dysbiosis of gut microbiota and inflammation of adipose tissues; and ketogenic diet (KD) (117) can increase A. muciniphila, Lactobacillus and regulate lipid metabolism through PPARα/FGF21 pathway. On the other hand, the gut microbiota and its metabolites may mediate environmental temperature, intermittent fasting (IF), or caloric restriction (CR) in the process of energy expenditure by promoting browning and thermogenesis of beige and brown adipose tissue (BAT). In the meantime, some adipokines, including leptin, adiponectin, FGF21, and apelin, produced by adipose tissues can act on the gut microbiota to modulate its composition.

References

    1. Gadde KM, Martin CK, Berthoud HR, Heymsfield SB. Obesity: Pathophysiology and Management. J Am Coll Cardiol (2018) 71(1):69–84. doi: 10.1016/j.jacc.2017.11.011 - DOI - PMC - PubMed
    1. Rohm TV, Meier DT, Olefsky JM, Donath MY. Inflammation in Obesity, Diabetes, and Related Disorders. Immunity (2022) 55(1):31–55. doi: 10.1016/j.immuni.2021.12.013 - DOI - PMC - PubMed
    1. Loos RJ, Yeo GS. The Bigger Picture of FTO: The First GWAS-Identified Obesity Gene. Nat Rev Endocrinol (2014) 10(1):51–61. doi: 10.1038/nrendo.2013.227 - DOI - PMC - PubMed
    1. Yupanqui-Lozno H, Bastarrachea RA, Yupanqui-Velazco ME, Alvarez-Jaramillo M, Medina-Méndez E, Giraldo-Peña AP, et al. . Congenital Leptin Deficiency and Leptin Gene Missense Mutation Found in Two Colombian Sisters With Severe Obesity. Genes (Basel) (2019) 10(5):342. doi: 10.3390/genes10050342 - DOI - PMC - PubMed
    1. Kleinendorst L, Abawi O, van der Kamp HJ, Alders M, Meijers-Heijboer HEJ, van Rossum EFC, et al. . Leptin Receptor Deficiency: A Systematic Literature Review and Prevalence Estimation Based on Population Genetics. Eur J Endocrinol (2020) 182(1):47–56. doi: 10.1530/EJE-19-0678 - DOI - PubMed

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