scholarly journals The Influence of Epigenetic Modifications on Metabolic Changes in White Adipose Tissue and Liver and Their Potential Impact in Exercise

2021 ◽  
Vol 12 ◽  
Author(s):  
Jessie E. Axsom ◽  
Heath D. Schmidt ◽  
Lea Ann Matura ◽  
Joseph R. Libonati
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
De Novo ◽  
Epigenetic Modifications ◽  
Epigenetic Changes ◽  
Transcriptional Responses ◽  
Epigenetic Marks ◽  
Environmental Stimuli ◽  
Metabolic Substrates ◽  
Potential Impact

Background: Epigenetic marks are responsive to a wide variety of environmental stimuli and serve as important mediators for gene transcription. A number of chromatin modifying enzymes orchestrate epigenetic responses to environmental stimuli, with a growing body of research examining how changes in metabolic substrates or co-factors alter epigenetic modifications.Scope of Review: Here, we provide a systematic review of existing evidence of metabolism-related epigenetic changes in white adipose tissue (WAT) and the liver and generate secondary hypotheses on how exercise may impact metabolism-related epigenetic marks in these tissues.Major Conclusions: Epigenetic changes contribute to the complex transcriptional responses associated with WAT lipolysis, hepatic de novo lipogenesis, and hepatic gluconeogenesis. While these metabolic responses may hypothetically be altered with acute and chronic exercise, direct testing is needed.

Effects of pregnancy and ovarian steroids on fatty acid synthesis and uptake in Syrian hamsters

1991 ◽  
Vol 260 (1) ◽  
pp. R153-R158 ◽  
Author(s):  
A. J. Bhatia ◽  
G. N. Wade
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
White Adipose Tissue ◽  
Fatty Acid Synthesis ◽  
De Novo ◽  
Acid Synthesis ◽  
De Novo Lipogenesis ◽  
Ovarian Steroids ◽  
Syrian Hamsters

The effects of pregnancy and ovarian steroids on the in vivo distribution of newly synthesized fatty acids (incorporation of tritium from 3H2O into fatty acid) in Syrian hamsters (Mesocricetus auratus) were examined. During late, but not early, gestation hamsters had reduced levels of newly synthesized fatty acids in heart, liver, uterus, and white adipose tissues (parametrial and inguinal fat pads). Treatment of ovariectomized hamsters with estradiol + progesterone significantly decreased fatty acid synthesis-uptake in heart, liver, and inguinal white adipose tissue. Treatment with either estradiol or progesterone alone was without significant effect in any tissue. Pretreatment of hamsters with Triton WR-1339 (tyloxapol), an inhibitor of lipoprotein lipase activity and tissue triglyceride uptake, abolished the effects of estradiol + progesterone in white adipose tissue and heart but not in liver. Thus hamsters lose body fat during pregnancy in part because of decreased de novo lipogenesis. The effect of pregnancy on lipogenesis is mimicked by treatment with estradiol + progesterone but not by either hormone alone. Furthermore, it appears that the liver is the principal site of estradiol + progesterone action on lipogenesis in Syrian hamsters.

scholarly journals Adipogenic role of alternatively activated macrophages in β-adrenergic remodeling of white adipose tissue

2016 ◽  
Vol 310 (1) ◽  
pp. R55-R65 ◽  
Author(s):  
Yun-Hee Lee ◽  
Sang-Nam Kim ◽  
Hyun-Jung Kwon ◽  
Krishna Rao Maddipati ◽  
James G. Granneman
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
De Novo ◽  
Flow Cytometric Analysis ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Physical Relationship ◽  
Alternatively Activated Macrophages

De novo brown adipogenesis involves the proliferation and differentiation of progenitors, yet the mechanisms that guide these events in vivo are poorly understood. We previously demonstrated that treatment with a β3-adrenergic receptor (ADRB3) agonist triggers brown/beige adipogenesis in gonadal white adipose tissue following adipocyte death and clearance by tissue macrophages. The close physical relationship between adipocyte progenitors and tissue macrophages suggested that the macrophages that clear dying adipocytes might generate proadipogenic factors. Flow cytometric analysis of macrophages from mice treated with CL 316,243 identified a subpopulation that contained elevated lipid and expressed CD44. Lipidomic analysis of fluorescence-activated cell sorting-isolated macrophages demonstrated that CD44+ macrophages contained four- to five-fold higher levels of the endogenous peroxisome-proliferator activated receptor gamma (PPARγ) ligands 9-hydroxyoctadecadienoic acid (HODE), and 13-HODE compared with CD44− macrophages. Gene expression profiling and immunohistochemistry demonstrated that ADRB3 agonist treatment upregulated expression of ALOX15, the lipoxygenase responsible for generating 9-HODE and 13-HODE. Using an in vitro model of adipocyte efferocytosis, we found that IL-4-primed tissue macrophages accumulated lipid from dying fat cells and upregulated expression of Alox15. Furthermore, treatment of differentiating adipocytes with 9-HODE and 13-HODE potentiated brown/beige adipogenesis. Collectively, these data indicate that noninflammatory removal of adipocyte remnants and coordinated generation of PPARγ ligands by M2 macrophages provides localized adipogenic signals to support de novo brown/beige adipogenesis.

scholarly journals Bioinformatics challenges and perspectives when studying the effect of epigenetic modifications on alternative splicing

2018 ◽  
Vol 373 (1748) ◽  
pp. 20170073 ◽  
Author(s):  
Clare Pacini ◽  
Magdalena J. Koziol
Keyword(s):  
Alternative Splicing ◽  
Chemical Biology ◽  
Epigenetic Modifications ◽  
Mrna Splicing ◽  
Epigenetic Changes ◽  
Epigenetic Marks

It is widely known that epigenetic modifications are important in regulating transcription, but several have also been reported in alternative splicing. The regulation of pre-mRNA splicing is important to explain proteomic diversity and the misregulation of splicing has been implicated in many diseases. Here, we give a brief overview of the role of epigenetics in alternative splicing and disease. We then discuss the bioinformatics methods that can be used to model interactions between epigenetic marks and regulators of splicing. These models can be used to identify alternative splicing and epigenetic changes across different phenotypes. This article is part of a discussion meeting issue ‘Frontiers in epigenetic chemical biology’.

scholarly journals Hyperplasia, de novo lymphangiogenesis, and lymphatic regression in mice with tissue-specific, inducible overexpression of murine VEGF-D

2016 ◽  
Vol 311 (2) ◽  
pp. H384-H394 ◽  
Author(s):  
Gabriela M. Lammoglia ◽  
Carolynn E. Van Zandt ◽  
Daniel X. Galvan ◽  
Jose L. Orozco ◽  
Michael T. Dellinger ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
De Novo ◽  
Lymphatic Vessels ◽  
Secretory Protein ◽  
Clara Cell ◽  
Tissue Fluid ◽  
Specific Expression ◽  
Tissue Specific ◽  
Brown Adipose

Lymphatic vessels modulate tissue fluid balance and inflammation and provide a conduit for endocrine and lipid transport. The growth of new lymphatic vessels in the adult, lymphangiogenesis, is predominantly mediated through vascular endothelial growth factor receptor-3 (VEGFR-3) signaling. We took advantage of the unique binding of murine VEGF-D specifically to VEGFR-3 and generated mice capable of inducible, tissue-specific expression of murine VEGF-D under a tightly-controlled tetracycline response element (TRE) promoter to stimulate adult tissue lymphangiogenesis. With doxycycline-activated expression, TRE-VEGF-D mouse crossed to mice with tissue-specific promoters for the lung [Clara cell secretory protein-reverse tetracycline transactivator (rtTA)] developed pulmonary lymphangiectasia. In the kidney, (kidney-specific protein-rtTA × TRE-VEGF-D) mice exhibited rapid lymphatic hyperplasia on induction of VEGF-D expression. Crossed with adipocyte-specific adiponectin-rtTA mice [Adipo-VEGF-D (VD)], chronic VEGF-D overexpression was capable of inducing de novo lymphangiogenesis in white adipose tissue and a massive expansion of brown adipose tissue lymphatics. VEGF-D expression in white adipose tissue also increased macrophage infiltration and tissue fibrosis in the tissue. Expression did not, however, measurably affect peripheral fluid transport, the blood vasculature, or basal metabolic parameters. On removal of the doxycycline stimulus, VEGF-D expression returned to normal, and the expanded adipose tissue lymphatics regressed in Adipo-VD mice. The inducible TRE-VEGF-D mouse thus provides a novel murine platform to study the adult mechanisms and therapies of an array of disease- and tissue-specific models of lymphangiogenesis.

Effects of adipocyte lipoprotein lipase on de novo lipogenesis and white adipose tissue browning

2013 ◽  
Vol 1831 (5) ◽  
pp. 934-942 ◽  
Author(s):  
Alexander Bartelt ◽  
Clara Weigelt ◽  
M. Lisa Cherradi ◽  
Andreas Niemeier ◽  
Klaus Tödter ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Lipoprotein Lipase ◽  
White Adipose Tissue ◽  
De Novo ◽  
De Novo Lipogenesis ◽  
Tissue Browning

Involvement of miR-539-5p in the inhibition of de novo lipogenesis induced by resveratrol in white adipose tissue

2016 ◽  
Vol 7 (3) ◽  
pp. 1680-1688 ◽  
Author(s):  
Ana Gracia ◽  
Jonatan Miranda ◽  
Alfredo Fernández-Quintela ◽  
Itziar Eseberri ◽  
Marcos Garcia-Lacarte ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
De Novo ◽  
Mechanisms Of Action ◽  
De Novo Lipogenesis ◽  
Triacylglycerol Metabolism

Proposed miRNA mechanisms of action of resveratrol in triacylglycerol metabolism changes in adipose tissue.

scholarly journals Taurine (2-Aminoethanesulfonic Acid) Deficiency Creates a Vicious Circle Promoting Obesity

Endocrinology ◽  
2006 ◽  
Vol 147 (7) ◽  
pp. 3276-3284 ◽  
Author(s):  
Nobuyo Tsuboyama-Kasaoka ◽  
Chikako Shozawa ◽  
Kayo Sano ◽  
Yasutomi Kamei ◽  
Seiichi Kasaoka ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
High Fat Diet ◽  
De Novo ◽  
Resting Energy Expenditure ◽  
The Body ◽  
Vicious Circle ◽  
High Fat ◽  
Taurine Supplementation ◽  
Taurine Deficiency

The relation between blood taurine (2-aminoethanesulfonic acid) concentrations and obesity was investigated. Taurine is supplied to the body by dietary ingestion as well as by de novo synthesis; it is anabolized by cysteine dioxygenase (CDO), which is abundantly expressed in liver and white adipose tissue. Overexpression of CDO in 3T3-L1 preadipocytes caused a decrease in the level of cysteine (precursor of taurine) and an increase in the level of taurine in the culture medium, suggesting that CDO is involved in biosynthesis and secretion of taurine in white adipose tissue. In high-fat diet-induced and/or genetically obese mice, a decrease in the blood taurine concentration was observed along with a decrease in CDO expression in adipose tissue but not in liver. Dietary taurine supplementation prevented high-fat diet-induced obesity with increased resting energy expenditure. Thus, taurine deficiency observed in association with obesity may create a vicious circle promoting obesity. Dietary taurine supplementation interrupts this vicious circle and may prevent obesity.

scholarly journals Effects of Angiopoietin-Like 3 on Triglyceride Regulation, Glucose Homeostasis, and Diabetes

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Eliza Christopoulou ◽  
Moses Elisaf ◽  
Theodosios Filippatos
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
White Adipose Tissue ◽  
De Novo ◽  
Glucose Production ◽  
De Novo Lipogenesis ◽  
Metabolic Effects ◽  
Hepatic Insulin Resistance ◽  
Model Assessment ◽  
Loss Of Function

Angiopoietin-like 3 (ANGPTL3) is a regulator of plasma triglyceride (TRG) levels due to its inhibitory action on the activity of lipoprotein lipase (LPL). ANGPTL3 is proteolytically cleaved by proprotein convertases to generate an active N-terminal domain, which forms a complex with ANGPTL8 orchestrating LPL inhibition. ANGPTL3-4-8 mouse model studies indicate that these three ANGPTL family members play a significant role in partitioning the circulating TRG to specific tissues according to nutritional states. Recent data indicate a positive correlation of ANGPTL3 with plasma glucose, insulin, and homeostatic model assessment of insulin resistance (HOMA-IR) in insulin-resistant states. The aim of this review is to critically present the metabolic effects of ANGPTL3, focusing on the possible mechanisms involved in the dysregulation of carbohydrate homeostasis by this protein. Heterozygous and homozygous carriers of ANGPTL3 loss-of-function mutations have reduced risk for type 2 diabetes mellitus. Suggested mechanisms for the implication of ANGPTL3 in carbohydrate metabolism include the (i) increment of free fatty acids (FFAs) owing to the enhancement of lipolysis in adipose tissue, which can induce peripheral as well as hepatic insulin resistance; (ii) promotion of FFA flux to white adipose tissue during feeding, leading to the attenuation of de novo lipogenesis and decreased glucose uptake and insulin sensitivity; (iii) induction of hypothalamic LPL activity in mice, which is highly expressed throughout the brain and is associated with enhanced brain lipid sensing, reduction of food intake, and inhibition of glucose production (however, the effects of ANGPTL3 on hypothalamic LPL in humans need more clarification); and (iv) upregulation of ANGPTL4 expression (owing to the plasma FFA increase), which possibly enhances insulin resistance due to the selective inhibition of LPL in white adipose tissue leading to ectopic lipid accumulation and insulin resistance. Future trials will reveal if ANGPTL3 inhibition could be considered an alternative therapeutic target for dyslipidemia and dysglycemia.

scholarly journals DNA Methylation Changes are Associated with the Programming of White Adipose Tissue Browning Features by Resveratrol and Nicotinamide Riboside Neonatal Supplementations in Mice

Nutrients ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 461
Author(s):  
Alba Serrano ◽  
Madhu Asnani-Kishnani ◽  
Charlene Couturier ◽  
Julien Astier ◽  
Andreu Palou ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Adipose Tissue ◽  
White Adipose Tissue ◽  
De Novo ◽  
Brown Adipocyte ◽  
Chow Diet ◽  
Male Mice ◽  
Nicotinamide Riboside ◽  
Epigenetic Effects

Neonatal supplementation with resveratrol (RSV) or nicotinamide riboside (NR) programs in male mice brown adipocyte-like features in white adipose tissue (WAT browning) together with improved metabolism in adulthood. We tested the involvement in this programming of long-term epigenetic changes in two browning-related genes that are overexpressed in WAT of supplemented mice, Slc27a1 and Prdm16. Suckling mice received orally the vehicle, RSV or NR from postnatal days 2-to-20. After weaning (d21) onto a chow diet, male mice were habituated to a normal-fat diet (NFD) starting d75, and split on d90 into continuation on the NFD or switching to a high-fat diet (HFD) until euthanization on d164. CpG methylation by bisulfite-sequencing was analyzed on inguinal WAT. Both treatments modified methylation marks in Slc27a1 and Prdm16 and the HFD-dependent dynamics of these marks in the adult WAT, with distinct and common effects. The treatments also affected gene expression of de novo DNA methylases in WAT of young animals (euthanized at d35 in independent experiments). Studies in 3T3-L1 adipocytes indicated the direct effects of RSV and NR on the DNA methylation machinery and favoring browning features. The results support epigenetic effects being involved in WAT programming by neonatal RSV or NR supplementation in male mice.

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