Post-transcriptional regulation in metabolic diseases

Kim, Wook; Lee, Eun Kyung

doi:10.4161/rna.20091

Cited by 27 publications

(17 citation statements)

References 105 publications

(99 reference statements)

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“…It is possible that the role of STK11 in regulating the development of fat cells is different in different animal models due to the non-conserved nature of the untranslated region of STK11 gene and the phosphorylation sites of encoded protein in different species. In addition, recent work has shown that two posttranscriptional pathways of miRNAs and RBPs appear to be involved in glucose homeostasis and lipid metabolism (Kim and Kyung, 2012). Given this data and our current findings, it will be of great interest to determine the exact mechanism of such post-transcriptional upregulation of STK11 by miR-424.…”

Section: Discussionsupporting

confidence: 57%

miR-424 Promotes Bovine Adipogenesis Through an Unconventional Post-Transcriptional Regulation of STK11

Wang

Zhang

et al. 2020

Front. Genet.

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Adipose tissue is the largest energy reservoir and secretory organ in the animal body, and is essential for maintaining normal physiological functions and metabolic balance. MicroRNAs regulate the process of adipogenic differentiation through posttranscriptional regulatory mechanisms. In the present study, miR-424 was upregulated during bovine adipocyte differentiation both in vivo and in vitro. The overexpression and interference of miR-424 exhibited the positive regulatory role in the differentiation of bovine adipocytes. Furthermore, miR-424 directly binds to the three prime untranslated region (3' UTR) of serine/threonine kinase 11 (STK11, also called LKB1), a master upstream gene in the AMP-activated protein kinase (AMPK) cascade, and up-regulates its expression. Functional studies showed that the knockdown of STK11 attenuated the pro-adipogenic effect of miR-424. Post-transcriptional regulation of STK11 by miR-424 was mediated potentially in an RNA binding protein (RBP) binding site-dependent manner. In conclusion, our study shows that miR-424 promotes bovine adipogenesis through an unconventional post-transcriptional regulation of STK11, which may serve as a potential target for the regulation of bovine adipogenesis and the improvement of livestock breeding efficiency.

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Section: Discussionsupporting

confidence: 57%

miR-424 Promotes Bovine Adipogenesis Through an Unconventional Post-Transcriptional Regulation of STK11

Wang

Zhang

et al. 2020

Front. Genet.

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“…Multiple mechanisms contribute to the regulation of enzymatic activity but rapid cessation of an enzymatic process requires inactivation (by post-translational modification or thorugh endogenous inhibitors (Kim and Kyung Lee, 2012; Xiong and Guan, 2012)) or elimination of the active enzyme already present in the cell. Elimination of enzymes by proteolysis, as described in this work by CMA, allows for a more global effect on the composition of the subproteome directly involved in several metabolic pathways.…”

Section: Discussionmentioning

confidence: 99%

Deficient Chaperone-Mediated Autophagy in Liver Leads to Metabolic Dysregulation

2014

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Summary The activity of chaperone-mediated autophagy (CMA), a catabolic pathway for selective degradation of cytosolic proteins in lysosomes, decreases with age, but the consequences of this functional decline in vivo remain unknown. In this work, we have generated a conditional knockout mouse to selectively block CMA in liver. We have found that blockage of CMA causes hepatic glycogen depletion and hepatosteatosis. The liver phenotype is accompanied by reduced peripheral adiposity, increased energy expenditure, and altered glucose homeostasis. Comparative lysosomal proteomics revealed that key enzymes in carbohydrate and lipid metabolism are normally degraded by CMA and that impairment of their regulated degradation contributes to the metabolic abnormalities observed in CMA-defective animals. These findings highlight the involvement of CMA in regulating hepatic metabolism and suggest that the age-related decline in CMA may have a negative impact on the energetic balance in old organisms.

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“…Frost and Olson [2011] reported global over‐expression of let‐7 to impair glucose tolerance and reduce fat mass, while knockdown resulted in improvements in insulin sensitivity in muscle and liver of C57BL/6 mice. Also, miRNAs miR‐27, miR‐130, miR‐378/378*, and Hzf have been reported to target PPARγ and C/EBPα which were not analyzed in this study (see review: [Kim and Kyung Lee, 2012]). Furthermore, we cannot exclude PPARγ regulation by CML earlier in adipogenesis, as we analyzed gene and miRNA expression only on day 9 of differentiation, on which cells were considered mature adipocytes and previous reports of AGEs on adipogenesis reported increased protein levels on day 5 of differentiation [Yang et al, 2013].…”

Section: Discussionmentioning

confidence: 99%

N^ϵ‐Carboxymethyllysine Increases the Expression of miR‐103/143 and Enhances Lipid Accumulation in 3T3‐L1 Cells

Holik

Lieder

Kretschy

et al. 2016

J of Cellular Biochemistry

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Advanced glycation endproducts, formed in vivo, but also by the Maillard reaction upon thermal treatment of foods, have been associated with the progression of pathological conditions such as diabetes mellitus. In addition to the accumulation with age, exogenous AGEs are introduced into the circulation from dietary sources. In this study, we investigated the effects of addition of free Nϵ‐carboxymethyllysine (CML), a well‐characterized product of the Maillard reaction, on adipogenesis in 3T3‐L1 preadipocytes. Treatment with 5, 50, or 500 μM CML resulted in increased lipid accumulation to similar extents, by 11.5 ± 12.6%, 12.9 ± 8.6%, and 12.8 ± 8.5%, respectively. Long‐term treatment with 500 μM CML during adipogenesis resulted in increases in miR‐103 and miR‐143 levels, two miRNAs described to be involved in impaired glucose homeostasis and increased lipid accumulation. Furthermore, the expression of genes associated with these miRNAs, consisting of Akt1, PI3k, and Cav1 was regulated by CML. Short‐term treatment of mature 3T3‐L1 adipocytes with CML resulted in decreased basal glucose uptake. These results, indicate that the addition of protein‐free CML to 3T3‐L1 cells influence parameters associated with adipogenesis and glucose homeostasis at transcriptional, and functional level; this indicates that free CML derived from exogenous sources, in addition to protein‐bound CML may be relevant in this context. J. Cell. Biochem. 117: 2413–2422, 2016. © 2016 The Authors. Journal of Cellular Biochemistry Published by Wiley Periodicals, Inc.

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Post-transcriptional regulation in metabolic diseases

Cited by 27 publications

References 105 publications

miR-424 Promotes Bovine Adipogenesis Through an Unconventional Post-Transcriptional Regulation of STK11

miR-424 Promotes Bovine Adipogenesis Through an Unconventional Post-Transcriptional Regulation of STK11

Deficient Chaperone-Mediated Autophagy in Liver Leads to Metabolic Dysregulation

N^ϵ‐Carboxymethyllysine Increases the Expression of miR‐103/143 and Enhances Lipid Accumulation in 3T3‐L1 Cells

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Post-transcriptional regulation in metabolic diseases

Cited by 27 publications

References 105 publications

miR-424 Promotes Bovine Adipogenesis Through an Unconventional Post-Transcriptional Regulation of STK11

miR-424 Promotes Bovine Adipogenesis Through an Unconventional Post-Transcriptional Regulation of STK11

Deficient Chaperone-Mediated Autophagy in Liver Leads to Metabolic Dysregulation

Nϵ‐Carboxymethyllysine Increases the Expression of miR‐103/143 and Enhances Lipid Accumulation in 3T3‐L1 Cells

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N^ϵ‐Carboxymethyllysine Increases the Expression of miR‐103/143 and Enhances Lipid Accumulation in 3T3‐L1 Cells