Differential circulating and visceral fat microRNA expression of non-obese and obese subjects

Kim, Nan Hee; Ahn, Jiyun; Choi, Yong; Son, Hyo Jung; Choi, Won Hee; Cho, Hyun Joo; Yu, Ji Hee; Seo, Ji A; Jang, Young Jin; Jung, Chang Hwa; Ha, Tae Youl

doi:10.1016/j.clnu.2019.03.033

Cited by 27 publications

(16 citation statements)

References 34 publications

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“…The discovery of a role for miR-26 as a regulator of adult adipogenesis expands our understanding of the functions of this miRNA family in mammalian metabolic homeostasis. Previously, miR-26 was found to be down-regulated in the livers of obese humans and mice (Fu et al 2015;Kim et al 2019). Hepatic overexpression of miR-26a was demonstrated to improve, whereas miR-26 inhibition was shown to decrease insulin sensitivity (Fu et al 2015).…”

Section: Discussionmentioning

confidence: 99%

miR-26 suppresses adipocyte progenitor differentiation and fat production by targeting Fbxl19

et al. 2019

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Fat storage in adult mammals is a highly regulated process that involves the mobilization of adipocyte progenitor cells (APCs) that differentiate to produce new adipocytes. Here we report a role for the broadly conserved miR-26 family of microRNAs (miR-26a-1, miR-26a-2, and miR-26b) as major regulators of APC differentiation and adipose tissue mass. Deletion of all miR-26-encoding loci in mice resulted in a dramatic expansion of adipose tissue in adult animals fed normal chow. Conversely, transgenic overexpression of miR-26a protected mice from high-fat dietinduced obesity. These effects were attributable to a cell-autonomous function of miR-26 as a potent inhibitor of APC differentiation. miR-26 blocks adipogenesis, at least in part, by repressing expression of Fbxl19, a conserved miR-26 target without a previously known role in adipocyte biology that encodes a component of SCF-type E3 ubiquitin ligase complexes. These findings have therefore revealed a novel pathway that plays a critical role in regulating adipose tissue formation in vivo and suggest new potential therapeutic targets for obesity and related disorders.

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Section: Discussionmentioning

confidence: 99%

miR-26 suppresses adipocyte progenitor differentiation and fat production by targeting Fbxl19

et al. 2019

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“…The expression of IL-6 and TNFα in response to LPS was found to be augmented in PBMCs isolated from T2D patients compared to cells obtained from healthy controls [ 49 ], providing a possible mechanistic link to higher plasma levels of IL-6 in T2D [ 48 ]. Of note, miR-155 expression was also found to be altered in the adipose tissue [ 58 ].…”

Section: Dysregulation Of Mir-155 In Dm: Findings From Clinical Studiesmentioning

confidence: 99%

“…Profiling miRNAs expression in omental and subcutaneous adipose tissue revealed that miR-155 expression had a negative correlation with the mean adipocyte volume in omental fat and with macrophage infiltration in subcutaneous adipose tissue [ 57 ]. Obese non-diabetic patients displayed increased levels of miR-155 both in bloodstream and in adipose tissue, suggesting that miR-155 upregulation may play a beneficial role in maintaining adipose tissue health [ 58 ].…”

Section: Dysregulation Of Mir-155 In Dm: Findings From Clinical Studiesmentioning

confidence: 99%

Functional Role of miR-155 in the Pathogenesis of Diabetes Mellitus and Its Complications

Jankauskas

Gambardella

Sardu

et al. 2021

ncRNA

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Substantial evidence indicates that microRNA-155 (miR-155) plays a crucial role in the pathogenesis of diabetes mellitus (DM) and its complications. A number of clinical studies reported low serum levels of miR-155 in patients with type 2 diabetes (T2D). Preclinical studies revealed that miR-155 partakes in the phenotypic switch of cells within the islets of Langerhans under metabolic stress. Moreover, miR-155 was shown to regulate insulin sensitivity in liver, adipose tissue, and skeletal muscle. Dysregulation of miR-155 expression was also shown to predict the development of nephropathy, neuropathy, and retinopathy in DM. Here, we systematically describe the reports investigating the role of miR-155 in DM and its complications. We also discuss the recent results from in vivo and in vitro models of type 1 diabetes (T1D) and T2D, discussing the differences between clinical and preclinical studies and shedding light on the molecular pathways mediated by miR-155 in different tissues affected by DM.

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“…The global repression of miRNA maturation triggers cellular transformation and tumorigenesis [136]. Kim et al demonstrated that in subcutaneous and visceral adipose tissue depots of obese patients, miRNAs (miR-133a, miR-139-5-p, miR-26a, and miR-451) were downregulated, while miR-155 was upregulated [137]. Studies have shown that these miRNAs, which are downregulated in adipose tissue depots from obese patients, have a well-established tumor suppressive activity [138][139][140][141]; whereas miR-155, which was upregulated in the same depots, serves as an oncomir [142].…”

Section: Dual Roles Of At-evs In Tumor Cells: Mirnasmentioning

confidence: 99%

Adipose Tissue-Derived Extracellular Vesicles and the Tumor Microenvironment: Revisiting the Hallmarks of Cancer

Moraes

Encarnação

Franco

et al. 2021

Cancers

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Extracellular vesicles (EVs) are crucial elements that sustain the communication between tumor cells and their microenvironment, and have emerged as a widespread mechanism of tumor formation and metastasis. In obesity, the adipose tissue becomes hypertrophic and hyperplastic, triggering increased production of pro-inflammatory adipokines, such as tumor necrosis factor α, interleukin 6, interleukin 1, and leptin. Furthermore, obese adipose tissue undergoes dysregulation in the cargo content of the released EVs, resulting in an increased content of pro-inflammatory proteins, fatty acids, and oncogenic microRNAs. These alterations drive obesity-associated inflammatory responses both locally and systemically. After being ignored for a long time, adipose tissues have recently received considerable attention as a major player in tumor microenvironment-linked obesity and cancer. The role of adipose tissue in the establishment and progression of cancer is reinforced by its high plasticity and inflammatory content. Such a relationship may be established by direct contact between adipocytes and cancer cells within the microenvironment or systemically, via EV-mediated cell-to-cell communication. Here, we highlight cues evidencing the influence of adipose tissue-derived EVs on the hallmarks of cancer, which are critical for tumor malignancy.

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Differential circulating and visceral fat microRNA expression of non-obese and obese subjects

Cited by 27 publications

References 34 publications

miR-26 suppresses adipocyte progenitor differentiation and fat production by targeting Fbxl19

miR-26 suppresses adipocyte progenitor differentiation and fat production by targeting Fbxl19

Functional Role of miR-155 in the Pathogenesis of Diabetes Mellitus and Its Complications

Adipose Tissue-Derived Extracellular Vesicles and the Tumor Microenvironment: Revisiting the Hallmarks of Cancer

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