MicroRNAs in adipocyte formation and obesity

Scheideler, Marcel

doi:10.1016/j.beem.2016.11.009

Cited by 22 publications

(12 citation statements)

References 98 publications

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“…Adipose tissue, besides being an endocrine organ, acts as a caloric reservoir, which under excessive conditions of food intake stores excess in the form of neutral lipids [ 35 ]. In situations of obesity, a disordered remodeling of this tissue occurs [ 36 ].…”

Section: Discussionmentioning

confidence: 99%

Adipocytes and intestinal epithelium dysfunctions linking obesity to inflammation induced by high glycemic index pellet-diet in Wistar rats

et al. 2018

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We investigated the inflammatory effect of a pellet-diet with high glycemic index and load (HGLI) on the histological organization of adipocytes, intestinal epithelium, and fat in liver and pancreas in adult male Wistar rats. Two groups (n=10) received for 17 weeks: (1) HGLI diet or (2) Standard diet (Labina®). Histological analyses of adipose tissue, jejunum, liver, and pancreas were performed. Stereology analysis, visceral adiposity index, gene expression, and immunohistochemistry of tumor necrosis factor-α (TNF-α) in visceral adipose tissue and plasma TNF-α were also assessed. The HGLI diet-induced hypertrophy of adipocytes with adipocyte volume density equal to 97.0%, cross-sectional area of adipocytes equivalent to 1387 µm² and a total volume of adipocytes of 6.97 cm³ an elevation of 8%, 25%, and 58%, respectively. Furthermore, the HGLI diet increased liver and pancreatic fat deposition, altered and inflamed the intestinal epithelia, and increased TNF-α gene expression (P=0.014) with a positive immunostaining in visceral adipose tissue and high plasma TNF-α in comparison with standard diet. The results suggest that this diet was able to generate changes commonly caused to solid diets with high fat or fructose-rich beverages. To the best of our knowledge, this is the first report in the literature concerning the properties of low-cost, sucrose-rich pellet-diet presenting high glycemic index and high glycemic load efficient on the development of obesity complications in Wistar rats that were subjected to diet-induced obesity. Therefore, the HGLI pellet-diet may be considered an effective tool to be used by the scientific community in experimental research.

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Section: Discussionmentioning

confidence: 99%

Adipocytes and intestinal epithelium dysfunctions linking obesity to inflammation induced by high glycemic index pellet-diet in Wistar rats

et al. 2018

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“…Upon induction of adipogenic factors, C/EBP β and δ activate C/EBPα and PPARγ to coordinate the expression of adipogenic genes characteristic of terminally differentiated adipocytes like aP2 (Kang & Hata 2015). Moreover, emerging evidences suggest that miRNAs also regulate fate decisions of BMSCs to influence adipocyte differentiation (Scheideler 2016). In our previous report, we have shown that miR-20a-5p was upregulated in BMSCs and adipogenic cell lines 3T3-L1 and C3H10T1/2 3 days after adipogenic treatment (Zhou et al 2015).…”

Section: Discussionmentioning

confidence: 99%

miR-20a-5p promotes adipogenic differentiation of murine bone marrow stromal cells via targeting Kruppel-like factor 3

Zhu¹,

Zhang²,

Zhou³

et al. 2018

Journal of Molecular Endocrinology

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miR-20a-5p has recently been identified to induce adipogenesis of established adipogenic cell lines in our previous study. However, its role and molecular mechanisms in the regulation of adipocyte lineage commitment of bone marrow-derived stromal cells (BMSCs) still need to be explored. In this report, we demonstrated the expression of miR-20a-5p was promoted gradually during adipogenic differentiation in BMSCs. We also confirmed that miR-20a-5p has a positive function in the adipogenic differentiation of BMSCs by gain-of-function study with overexpression lentivirus or synthetic mimics of miR-20a-5p, and loss-of-function study with sponge lentivirus or synthetic inhibitor of miR-20a-5p. Dual luciferase reporter assay, GFP repression assay and Western blotting suggested Kruppel-like factor 3 () was a direct target of miR-20a-5p. Furthermore, siRNA-mediated silencing of recapitulated the potentiation of adipogenesis induced by miR-20a-5p overexpression, whereas enhanced expression of attenuated the effect of miR-20a-5p. As was reported to play an inhibitory role in adipogenesis at the initial stage of differentiation, the findings we present here indicate that miR-20a-5p promotes adipocyte differentiation from BMSCs by targeting and negatively regulating in the early phase during the procedure of adipogenesis.

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“…The enhancement of brown and brite adipocyte activity increases energy expenditure and is thought to counteract adipose tissue dysfunction and the development of obesity [23][24][25]. However, the amount of detectable BAT declines with increasing age [26], just like the adrenergic agonist-dependent inductive ability of brite adipocytes in WAT [27].…”

Section: Adipose Metabolism and Lifespanmentioning

confidence: 99%

Age-Induced Changes in White, Brite, and Brown Adipose Depots: A Mini-Review

Schosserer

Grillari²,

Wolfrum

et al. 2017

Gerontology

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Aging is a time-related process of functional decline at organelle, cellular, tissue, and organismal level that ultimately limits life. Cellular senescence is a state of permanent growth arrest in response to stress and one of the major drivers of aging and age-related disorders. Senescent cells accumulate with age, and removal of these cells delays age-related disorders in different tissues and prolongs healthy lifespan. One of the most studied aging mechanisms is the accumulation of reactive oxygen species damage in cells, organs, and organisms over time. Elevated oxidative stress is also found in metabolic diseases such as obesity, metabolic syndrome and associated disorders. Moreover, dysregulation of the energy homeostasis is also associated with aging, and many age-related genes also control energy metabolism, with the adipose organ, comprising white, brite, and brown adipocytes, as an important metabolic player in the regulation of whole-body energy homeostasis. This review summarizes transformations in the adipose organ upon aging and cellular senescence and sheds light on the reallocation of fat mass between adipose depots, on the metabolism of white and brown adipose tissue, on the regenerative potential and adipogenic differentiation capacity of preadipocytes, and on alterations in mitochondria and bioenergetics. In conclusion, the aging process is a lifelong, creeping process with gradual decline in (pre-)adipocyte function over time. Thus, slowing down the accumulation of (pre-)adipocyte damage and dysfunction, removal of senescent preadipocytes as well as blocking deleterious compounds of the senescent secretome are protective measures to maintain a lasting state of health at old age.

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MicroRNAs in adipocyte formation and obesity

Cited by 22 publications

References 98 publications

Adipocytes and intestinal epithelium dysfunctions linking obesity to inflammation induced by high glycemic index pellet-diet in Wistar rats

Adipocytes and intestinal epithelium dysfunctions linking obesity to inflammation induced by high glycemic index pellet-diet in Wistar rats

miR-20a-5p promotes adipogenic differentiation of murine bone marrow stromal cells via targeting Kruppel-like factor 3

Age-Induced Changes in White, Brite, and Brown Adipose Depots: A Mini-Review

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