Genetic contributors to obesity

McPherson, Ruth

doi:10.1016/s0828-282x(07)71002-4

Cited by 37 publications

(23 citation statements)

References 57 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Obesity has been thought to be caused by personal habits, primarily excess calorie intake and lack of exercise. Furthermore, genetic components such as hereditary deficiency and genetic variations including leptin gene mutations could also have a strong effect on the development of excess weight gain and obesity [2][3][4]. Leptin is a hormone, primarily secreted by the adipose tissue, and affects the hypothalamus, regulates appetite and energy balance, and consequently, body weight gain [5,6].…”

Section: Introductionmentioning

confidence: 99%

Antrodia cinnamomea Confers Obesity Resistance and Restores Intestinal Barrier Integrity in Leptin-deficient Obese Mice

et al. 2020

View full text Add to dashboard Cite

Obesity is associated with metabolic disorders. Thus, obesity prevention and treatment are essential for health. Antrodia cinnamomea (AC) is a multifunctional medicinal fungus used for the treatment of various diseases and for preventing diet-induced obesity. Leptin deficiency causes over-eating and spontaneous obesity. The concomitant metabolic symptoms are more severe than diet-induced obesity. Here, we used leptin-deficient (ob/ob) mice as an animal model for over-feeding to study the effect of AC on obesity. We fed C57BL/6 mice (WT, ob+/+) and ob/ob mice with AC for four weeks before performing qRT-PCR and immunoblot analysis to elaborate AC-modulated mechanisms. Further, we used Caco-2 cells as a human intestinal epithelial barrier model to examine the effect of AC on intestinal permeability. Our results suggested that AC reduces lipid deposits of the liver and epididymal white adipose tissue (EWAT) by promoting lipid metabolism and inhibiting lipogenesis-associated genes and proteins in ob/ob mice. Moreover, AC effectively repaired intestinal-barrier injury caused by leptin deficiency and enhanced intestinal barrier integrity in Caco-2 cells. Interestingly, AC significantly reduced body weight and EWAT with no compromise on food intake in ob/ob mice. Thus, AC effectively reduced obesity caused by leptin-deficiency and can potentially be used as a nutraceutical for treating obesity.

show abstract

Section: Introductionmentioning

confidence: 99%

Antrodia cinnamomea Confers Obesity Resistance and Restores Intestinal Barrier Integrity in Leptin-deficient Obese Mice

et al. 2020

View full text Add to dashboard Cite

show abstract

“…The increase in adipose tissue corresponds to increase in size and number of adipocytes ( 3 ), i.e., lipogenesis and differentiation. Factors that regulate fat tissue differentiation such as insulin, growth hormone, and glucocorticoids promote differentiation of pre-adipocytes ( 4 , 5 ) and genetic and transcriptional regulation ( 6 , 7 ). Among regulatory factors, transcription factors (TFs) play a critical role in the regulation of adipocyte differentiation.…”

Section: Introductionmentioning

confidence: 99%

Mechanistic Insights Into the Interaction Between Transcription Factors and Epigenetic Modifications and the Contribution to the Development of Obesity

Huang

Chen

et al. 2018

Front. Endocrinol.

View full text Add to dashboard Cite

Objective: The development of obesity is inseparable from genetic and epigenetic factors, and transcription factors (TFs) play an essential role in these two mechanisms. This review analyzes the interaction of TFs with epigenetic modifications and the epigenetic mechanisms underlying peroxisome proliferator-activated receptor (PPAR)γ, an important transcription factor, in the development of obesity.Methods: We describe the relationship between TFs and different epigenetic modifications and illustrate the several mechanisms described. Next, we summarize the epigenetic mechanisms of PPARs, an important class of transcription factors involved in obesity, that induce obesity with different triggering factors. Finally, we discuss the mechanisms of epigenetic modification of PPAR-related ligands in lipid metabolism and propose future avenues of research.Results: TFs participate in epigenetic modifications in different forms, causing changes in gene expression. The interactions between the different epigenetic modifications and PPARs are important biological developments that affect fat tissue differentiation, lipogenesis, and lipid metabolism, thereby inducing or inhibiting the development of obesity. We then highlight the need for more research to understand the role of epigenetic modifications and PPARs.Conclusions: Epigenetic mechanisms involved in the regulation of PPARs may be excellent therapeutic targets for obesity treatment. However, there is a need for a deeper understanding of how PPARs and other obesity-related transcription factors interact with epigenetic modifications.

show abstract

“…MicroRNA (miRNA) is an endogenous small RNA that posttranscriptionally regulates gene expression. Recent evidence has demonstrated that miRNA is one of the key regulator molecules of gene expression, which may affect the differentiation of preadipocytes or fat storage capability of adipocytes (McPherson, ). The miR‐30 family, an important factor for adipogenesis, is strongly upregulated during the adipogenesis of human cells (Zaragosi et al, ).…”

Section: Introductionmentioning

confidence: 99%

Transcriptome Analysis of Potential miRNA Involved in Adipogenic Differentiation of C2C12 Myoblasts

Hou

et al. 2018

Lipids

View full text Add to dashboard Cite

>Emerging evidence indicates that microRNA (miRNA) plays an important role in adipogenesis and disease pathogenesis. To investigate the miRNA involved in regulating different periods of adipogenesis, we performed a comprehensive study on microRNAome during the stimulation of adipogenesis by an adipogenic differentiation cocktail in C2C12 myoblasts at 0, 2, 4, and 7 days using the Solexa sequencing technology. In this study, we identified 52 differentially expressed (DE) miRNA. Functional annotation indicated that the target genes of DE miRNA were mostly enriched in adipogenic transdifferentiation and fat metabolism-related pathways, including Wnt, mitogen-activated protein kinase (MAPK), and insulin signaling. The insulin signaling pathway was further analyzed for its close connections to Wnt and MAPK signaling pathways as well as for the containing of thymoma viral proto-oncogene-3 (Akt3) and glycogen synthase kinase-3 beta (Gsk3b), which were both target genes predicted by most DE miRNA. CLIP-seq (crosslinking-immunprecipitation and high-throughput sequencing) data showed that Akt3 was targeted by seven DE miRNA, including five upregulated (miR-203-3p, miR-181c-5p, miR-322-5p, miR-351-5p, and miR-181a-5p) and two downregulated (miR-15b-5p and miR-17-5p) ones. Likewise, Gsk3b was targeted by six DE miRNA, including four upregulated (miR-199a-3p, miR-126-5p, miR-26a-5p, and miR-101a-3p) and two downregulated (miR-150-5p and miR-140-3p) ones. Moreover, Akt3 could regulate the key transcription factor (TF) Foxo1, targeted by two downregulated miRNA (miR-96-5p and miR-183-5p). The expression levels of Akt3 and Gsk3b were downregulated, and TF Foxo1, which worked on the transcription axis of Pgc1a-Pparα-Rxrg-Pparγ to regulate adipogenesis, was upregulated. In conclusion, DE miRNA stimulated the adipogenesis of C2C12 myoblasts through the targeted insulin signaling pathway involving the genes Akt3, Gsk3b, and TF Foxo1.

show abstract

Genetic contributors to obesity

Cited by 37 publications

References 57 publications

Antrodia cinnamomea Confers Obesity Resistance and Restores Intestinal Barrier Integrity in Leptin-deficient Obese Mice

Antrodia cinnamomea Confers Obesity Resistance and Restores Intestinal Barrier Integrity in Leptin-deficient Obese Mice

Mechanistic Insights Into the Interaction Between Transcription Factors and Epigenetic Modifications and the Contribution to the Development of Obesity

Transcriptome Analysis of Potential miRNA Involved in Adipogenic Differentiation of C2C12 Myoblasts

Contact Info

Product

Resources

About