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Review
. 2021 Apr 24;10(5):1004.
doi: 10.3390/cells10051004.

Adipocyte, Immune Cells, and miRNA Crosstalk: A Novel Regulator of Metabolic Dysfunction and Obesity

Sonia Kiran  1 , Vijay Kumar  1 , Santosh Kumar  1 , Robert L Price  2 , Udai P Singh  1
Affiliations
Review

Adipocyte, Immune Cells, and miRNA Crosstalk: A Novel Regulator of Metabolic Dysfunction and Obesity

Sonia Kiran et al. Cells. .

Abstract

Obesity is characterized as a complex and multifactorial excess accretion of adipose tissue (AT) accompanied with alterations in the immune response that affects virtually all age and socioeconomic groups around the globe. The abnormal accumulation of AT leads to several metabolic diseases, including nonalcoholic fatty liver disorder (NAFLD), low-grade inflammation, type 2 diabetes mellitus (T2DM), cardiovascular disorders (CVDs), and cancer. AT is an endocrine organ composed of adipocytes and immune cells, including B-Cells, T-cells and macrophages. These immune cells secrete various cytokines and chemokines and crosstalk with adipokines to maintain metabolic homeostasis and low-grade chronic inflammation. A novel form of adipokines, microRNA (miRs), is expressed in many developing peripheral tissues, including ATs, T-cells, and macrophages, and modulates the immune response. miRs are essential for insulin resistance, maintaining the tumor microenvironment, and obesity-associated inflammation (OAI). The abnormal regulation of AT, T-cells, and macrophage miRs may change the function of different organs including the pancreas, heart, liver, and skeletal muscle. Since obesity and inflammation are closely associated, the dysregulated expression of miRs in inflammatory adipocytes, T-cells, and macrophages suggest the importance of miRs in OAI. Therefore, in this review article, we have elaborated the role of miRs as epigenetic regulators affecting adipocyte differentiation, immune response, AT browning, adipogenesis, lipid metabolism, insulin resistance (IR), glucose homeostasis, obesity, and metabolic disorders. Further, we will discuss a set of altered miRs as novel biomarkers for metabolic disease progression and therapeutic targets for obesity.

Keywords: adipocyte; immune cells; inflammation; metabolic dysfunction; miRs.

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Conflict of interest statement

The author declares no conflict of interests.

Figures

Figure 1
Figure 1
The schematic illustration of miRNA biogenesis and mechanism of action: in the nucleus of cells pri-miRNA are transcripted from DNA with help of RNA polymerase. The pri-miRNA is then cleaved by Drosha enzyme to pre-miRNA and moved into the cytoplasm by exportin-5 activity. The pre-miRNA is matured to miRNA via DICER. The mature strand of miRNA is integrated into the RNA-induced silencing complex (RISC) which inhibits the translation of the complementary mRNA.
Figure 2
Figure 2
ROS and Obesity: In obese individuals, access supply of free fatty acid (FFA) toward mitochondria results in an increase in the production of ROS and OS, which leads toward inflammation; adipokines and miRs are also associated with OS and inflammation.
Figure 3
Figure 3
Crosstalk between AT-derived miRs and metabolic organs: microvesicles and exosomes loaded with miRs are secreted from AT into blood stream and distributed to different organs including liver, pancreas, muscles, and cardiovascular system to play their functions.
See this image and copyright information in PMC

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