CIDE Proteins in Human Health and Disease

Slayton, Mark; Gupta, Abhishek; Balakrishnan, Bijinu; Puri, Vishwajeet

doi:10.3390/cells8030238

Cited by 38 publications

(29 citation statements)

References 81 publications

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“…Adipocytes' Cidea expression increases in conditions that favor triglycerides deposition [32], an opposite phenomenon compared to what happens during BAT activation. According to some studies, in fact, it antagonizes UCP1 expression [33]. CIDEA lower expression in the PBMC of our cold-exposed group compared to controls could reflect similar differences in this marker's BAT expression, whose levels reduced following exposure to low temperatures in animal models [19,34].…”

Section: Discussionsupporting

confidence: 48%

Biomarkers of Browning in Cold Exposed Siberian Adults

Efremova¹,

Colleluori

Thomsky³

et al. 2020

Nutrients

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Cold-exposure promotes energy expenditure by inducing brown adipose tissue (BAT) thermogenesis, which over time, is also sustained by browning, the appearance, or increase, of brown-like cells into white fat depots. Identification of circulating markers reflecting BAT activity and browning is crucial to study this phenomenon and its triggers, also holding possible implications for the therapy of obesity and metabolic diseases. Using RT-qPCR, we evaluated the peripheral blood mononuclear cells (PBMC) expression profile of regulators of BAT activity (CIDEA, PRDM16), white adipocytes browning (HOXC9 and SLC27A1), and fatty acid β-oxidation (CPT1A) in 150 Siberian healthy miners living at extremely cold temperatures compared to 29 healthy subjects living in thermoneutral conditions. Anthropometric parameters, glucose, and lipid profiles were also assessed. The cold-exposed group showed significantly lower weight, BMI, hip circumference, and PBMC expression of CIDEA, but higher expression of HOXC9 and higher circulating glucose compared to controls. Within the cold-exposed group, BMI, total cholesterol, and the atherogenic coefficient were lower in individuals exposed to low temperatures for a longer time. In conclusion, human PBMC expresses the brown adipocytes marker CIDEA and the browning marker HOXC9, which, varying according to cold-exposure, possibly reflect changes in BAT activation and white fat browning.

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Section: Discussionsupporting

confidence: 48%

Biomarkers of Browning in Cold Exposed Siberian Adults

Efremova¹,

Colleluori

Thomsky³

et al. 2020

Nutrients

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“…In this work, we carried out experiments in human volunteers, mouse models and cultured cells to demonstrate that GH suppresses the expression of FSP27 at both the mRNA and protein level 54,55 (Figure 1). Of note, FSP27 levels are associated with insulin sensitivity in humans with obesity 26,85,91 , and nonsense mutation of FSP27 in humans leads to increased lipolysis, hypertriglyceridemia and insulin resistant diabetes mellitus. 92 .…”

Section: Mechanisms Of Gh-induced Lipolysismentioning

confidence: 99%

The effects of growth hormone on adipose tissue: old observations, new mechanisms

et al. 2019

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The ability of growth hormone (GH) to induce adipose tissue lipolysis has been known for over five decades; however, the molecular mechanisms that mediate this effect, as well as the ability of GH to inhibit insulin-stimulated glucose uptake, have been scarcely documented. In this same timeframe, our understanding of adipose tissue has evolved to reveal a complex structure with distinct types of adipocytes, depot-specific differences, a biologically significant extracellular matrix and important endocrine properties mediated by adipokines. All of these aforementioned features, in turn, can influence lipolysis. In this Review, we provide a historical and current overview of the lipolytic effect of GH in humans, mice and cultured cells. More globally, we explain lipolysis in terms of GH-induced intracellular signaling and its effect on obesity, insulin resistance and lipotoxicity. In this regard, findings that define molecular mechanisms by which GH induces lipolysis are described. Finally, data are presented for the differential effect of GH on specific adipose tissue depots and on distinct classes of metabolically active adipocytes. Together, these cellular, animal and human studies reveal novel cellular phenotypes and molecular pathways regulating the metabolic effects of GH on adipose tissue.

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“…in accordance with previous studies, the results of the present study revealed that the expression levels of Cidea, Cidec, Fabp4 and Plin4 were significantly higher in the livers of NASH model mice fed a high aGe diet compared with those in the livers of mice in the nd group. cidea, cidec and Plin4 localize to lipid droplets to promote lipid droplet fusion and hepatic lipid storage under high caloric intake, thus promoting liver steatosis (42,44). FaBP4 is highly upregulated by fatty acids and inflammatory activation, and further promotes lipid infusion and inflammation in hepatocytes (45).…”

Section: Discussionmentioning

confidence: 99%

Identification of hub genes and key pathways of dietary advanced glycation end products‑induced non‑alcoholic fatty liver disease by bioinformatics analysis and animal experiments

et al. 2019

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non-alcoholic fatty liver disease (naFld) is a common chronic liver disease. advanced glycation end products (aGes) negatively affect the liver and accelerate naFld progression; however, the underlying mechanisms remain unclear. The present study aimed to examine the effect and mechanism of dietary aGes on the mouse liver using bioinformatics and in vivo experimental approaches. Gene expression datasets associated with naFld were obtained from the Gene expression omnibus and differentially expressed genes (DEGs) were identified using GEO2R. Functional enrichment analyses were performed using the database for annotation, Visualization and integrated discovery and a protein-protein interaction network for the deGs was constructed using the Search Tool for the retrieval of interacting Genes database. Mcode, a cytoscape plugin, was subsequently used to identify the most significant module. The key genes involved were verified in a dietary AGE-induced non-alcoholic steatohepatitis (naSH) mouse model using reverse transcription-quantitative Pcr (rT-qPcr). The 462 deGs associated with naFld in the two datasets, of which 34 overlapping genes were found in two microarray datasets. Functional analysis demonstrated that the 34 deGs were enriched in the 'PPar signaling pathway', 'central carbon metabolism in cancer', and 'cell adhesion molecules (caMs)'. Moreover, four hub genes (cell death-inducing dFFa-like effector a, cell death-inducing dFFa-like effector c, fatty acid-binding protein 4 and perilipin 4) were identified from a protein-protein interaction network and were verified using RT-qPCR in a mouse model of NASH. The results suggested that aGes and their receptor axis may be involved in naFld onset and/or progression. This integrative analysis identified candidate genes and pathways in NAFLD, as well as deGs and hub genes related to naFld progression in silico and in vivo.

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CIDE Proteins in Human Health and Disease

Cited by 38 publications

References 81 publications

Biomarkers of Browning in Cold Exposed Siberian Adults

Biomarkers of Browning in Cold Exposed Siberian Adults

The effects of growth hormone on adipose tissue: old observations, new mechanisms

Identification of hub genes and key pathways of dietary advanced glycation end products‑induced non‑alcoholic fatty liver disease by bioinformatics analysis and animal experiments

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