scholarly journals Natural Extracts That Stimulate Adipocyte Browning and Their Underlying Mechanisms

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 308
Author(s):  
Min-Kyeong Lee ◽  
Bonggi Lee ◽  
Choon Young Kim
Keyword(s):  
Adipose Tissue ◽  
Synthetic Drugs ◽  
Natural Extracts ◽  
Current Review ◽  
Food Components ◽  
Beige Adipocytes ◽  
Marine Products ◽  
Underlying Mechanisms ◽  
Tissue Browning

Despite progress in understanding the developmental lineage and transcriptional factors regulating brown and beige adipocytes, the role of environmental modifiers, such as food components and natural extracts, remains to be elucidated. Furthermore, the undesirable pleiotropic effects produced by synthetic drugs targeting adipose tissue browning and thermogenesis necessitate research into alternative natural sources to combat obesity and related metabolic disorders. The current review, therefore, focused on the effects of various extracts from foods, plants, and marine products on adipose tissue browning and obesity. In particular, the recent findings of food components and marine products on adipose tissue browning will be discussed here.

Inter-Tissue and Intra-Tissue Co-Expression Networks in Human Metabolism: Morphological Evaluation of the Link Between Transcription Factors ERβ and NFAT in Morbid Obesity

2020 ◽  
Vol 17 (1) ◽  
pp. 63-80
Author(s):  
Athina Chasapi ◽  
Kostas Balampanis ◽  
Eleni Kourea ◽  
Fotios Kalfaretzos ◽  
Vaia Lambadiari ◽  
...  
Keyword(s):  
Morbid Obesity ◽  
Adipose Tissue ◽  
Clinicopathological Parameters ◽  
Morbidly Obese ◽  
Human Metabolism ◽  
Activated T Cells ◽  
Alcoholic Fatty Liver ◽  
Morphological Evaluation ◽  
Underlying Mechanisms

Background: Estrogen receptor β (ERβ) plays an important role in human metabolism and some of its metabolic actions are mediated by a positive “cross-talk” with Nuclear Factor of Activated T cells (NFAT) and the key metabolic transcriptional coregulator Transcriptional Intermediary Factor 2 (TIF2). Introduction: Our study is an “in situ” morphological evaluation of the communication between ERβ, NFAT and TIF2 in morbid obesity. Potential correlations with clinicopathological parameters and with the presence of diabetes and non-alcoholic fatty liver disease (NAFLD) were also explored. The aim of the present study was to determine the role of ERβ and NFAT in the underlying pathophysiology of obesity and related comorbidities. We have investigated the expression of specific proteins using immunochemistry methodologies. Methods: Our population consists of 50 morbidly obese patients undergoing planned bariatric surgery, during which biopsies were taken from visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT), skeletal muscle (SM), extramyocellular adipose tissue (EMAT) and liver and the differential protein expression was evaluated by immunohistochemistry. Results: We demonstrated an extensive intra- and inter-tissue co-expression network, which confirms the tissue-specific and integral role of each one of the investigated proteins in morbid obesity. Moreover, a beneficial role of ERβ and NFATc1 against NAFLD is implicated, whereas the distinct roles of TIF2 still remain an enigma. Conclusions: We believe that our findings will shed light on the complex underlying mechanisms and that the investigated biomarkers could represent future targets for the prevention and therapy of obesity and its comorbidities.

Cytoplasmic p16 Is Expressed in Normal Brown Fat and Hibernomas

2020 ◽  
Vol 28 (5) ◽  
pp. 496-501
Author(s):  
Georgia Karpathiou ◽  
Jean Marc Dumollard ◽  
Zoe Evangelou ◽  
Anna Batistatou ◽  
Michel Peoc’h ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Brown Fat ◽  
Fat Tissue ◽  
P16 Expression ◽  
Tissue Browning

White adipose tissue browning has emerged as a putative therapy of obesity, and studies in mice have shown that Cdkn2a is implicated in white-to-brown transition. However, the role of Cdkn2a product p16 has been never studied in human brown fat tissue. The aim of the study is to investigate the expression of p16 in normal brown fat and in hibernoma, a lipoma containing brown fat-like adipocytes. Ten normal brown fat tissues and 5 hibernomas were immunohistochemically studied for p16 expression. Nearby white adipose tissue was used for comparison. All brown fat and hibernomas specimens express p16 in a cytoplasmic manner. Neighboring white adipose tissue is negative for p16 expression. Thus, cytoplasmic p16 may be associated with fat tissue browning.

scholarly journals Paradoxical Increase of Insulin Sensitivity Despite Blunted Adipose Tissue Browning in Genetic Ablation of IRP1 (OR09-08-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Mikyoung You ◽  
Jin-Seon Yook ◽  
Soonkyu Chung
Keyword(s):  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Iron Metabolism ◽  
Core Body Temperature ◽  
Serum Levels ◽  
Genetic Ablation ◽  
Ucp1 Expression ◽  
Core Body ◽  
Tissue Browning

Abstract Objectives Iron regulatory protein 1 (IRP1) plays a key regulator of cellular iron metabolism, systemic oxygen sensing, and erythropoiesis. Deletion of IRP1 leads to profound HIF2a-dependent abnormalities in erythropoiesis and iron metabolism. Previously, we demonstrated that modulation of adipose tissue iron metabolism is necessary for adipose tissue browning. However, the role of IRP1 in adipose tissue browning and its metabolic consequences are uncertain. This study aimed to investigate the role of IRP1 in regulating adipose tissue browning in a mouse model of genetic ablation of IPR1 (IRP1−/−). Methods The IRP1−/− mice and wildtype (WT) controls were kept either at room (25°C) or cold (6°C) temperature for 7 days. Adipose tissue browning was evaluated by UCP1 expression and prevalence of beige-like structure in inguinal fat. Thermogenic heat release captured by infrared camera and core body temperature was measured by a rectal thermometer. The modulation of iron metabolism was assessed by serum levels of ferritin, hematocrit, and erythropoietin levels by ELISA. To investigate the role of IRP1 on energy metabolism, IRP1−/− and WT controls were fed a high-fat diet (45%) for 14 weeks. Insulin sensitivity was determined by glucose and insulin tolerance test and HOMA-IR score. [3H]-2-deoxyglucose (DOG) was injected to determine the distribution of 3H-radioactivity was quantified. Results IRP1−/− mice dramatically increased serum levels of erythropoietin but decreased hepcidin. IRP1−/− developed polycythemia and reticulocytosis, which was not affected by cold exposure. IRP1−/− were completely blunted in cold-induced browning in the inguinal fat showing no changes in UCP1 and adipocyte morphology. Unexpectedly, IRP1−/− showed higher core body temperature and heat release than control independent of UCP1 expression. Chronic intake of HF diet paradoxically increased the insulin sensitivity regardless of obesity. 2-DOG distribution was significantly increased in red blood cells, suggesting that red blood cell-dependent energy expenditure significantly contributed to rapid glucose disposal. Conclusions Disruption of IRP1 blunted adipose tissue browning. The paradoxical rise in insulin sensitivity in IRP1−/− is likely due to red blood cells-mediated energy expenditure. Funding Sources None.

scholarly journals Comparative analyses of chromatin landscape in white adipose tissue suggest humans may have less beigeing potential than other primates

2019 ◽  
Author(s):  
Devjanee Swain-Lenz ◽  
Alejandro Berrio ◽  
Alexias Safi ◽  
Gregory E. Crawford ◽  
Gregory A. Wray
Keyword(s):  
Adipose Tissue ◽  
Body Fat ◽  
White Adipose Tissue ◽  
Sequence Motif ◽  
Primary Role ◽  
Regulatory Regions ◽  
Comparative Analyses ◽  
White Adipocytes ◽  
Beige Adipocytes

AbstractHumans carry a much larger percentage of body fat than other primates. Despite the central role of adipose tissue in metabolism, little is known about the evolution of white adipose tissue in primates. Phenotypic divergence is often caused by genetic divergence in cis-regulatory regions. We examined the cis-regulatory landscape of fat during human origins by performing comparative analyses of chromatin accessibility in human and chimpanzee adipose tissue using macaque as an outgroup. We find that many cis-regulatory regions that are specifically closed in humans are under positive selection, located near genes involved with lipid metabolism, and contain a short sequence motif involved in the beigeing of fat, the process in which white adipocytes are transdifferentiated into beige adipocytes. While the primary role of white adipocytes is to store lipids, beige adipocytes are thermogeneic. The collective closing of many putative regulatory regions associated with beiging of fat suggests an adaptive mechanism that increases body fat in humans.

scholarly journals AMP-activated protein kinase (AMPK) contributes to the anti-obesity effects and adipose tissue browning of alpha-lipoic acid in ovariectomized rats

2021 ◽  
Author(s):  
Hsin-Hsueh Shen ◽  
Ming-Ting Chung ◽  
Shieh-Yang Huang ◽  
Ching-Wen Kung ◽  
Shu-Ying Chen ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Protein Kinase ◽  
Lipoic Acid ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Ampk Signaling ◽  
Ovx Rats ◽  
Beige Adipocytes ◽  
Amp Activated Protein Kinase ◽  
Tissue Browning

Abstract BackgroundBilateral ovariectomy is an experimental model used to analyze the conditions of menopause and develop strategies for alleviation of the deleterious effects during estrogen deficiency. Brown and beige adipocytes exert thermogenesis capacities and are promising therapeutic strategy for obesity. This study aims to investigate the adipose tissue browning potentials of antioxidant α-lipoic acid (ALA) and underlying mechanisms involved in ovariectomized (Ovx) rats.Methods:Eight weeks old female Wistar rats were randomly divided into Sham or Ovx groups. The Ovx rats were subjected to bilateral ovariectomy and administered with ALA 200 or ALA 300 mg/kg/day (gavage) for 8 weeks. Results:Ovx group significantly increased boy weight (BW) and fat pad mass as compared to Sham group, while ALA supplementation reversed these changes. Lipid profiles including serum triglycerides (TG), total (TC) and low-density lipoprotein cholesterol (LDL-C) levels were significantly elevated in the Ovx group, whereas the ALA treatment showed a significant decrease in these levels. Furthermore, high density lipoprotein cholesterol (HDL-C) and myokine irisin secretion were increased by ALA as well. Morphology results showed ALA treatment reduced Ovx-induced adipocyte hypertrophy and enhanced UCP1 expression by immunohistochemical staining in inguinal WAT. Protein expression of brown fat-specific markers UCP1, PRDM16 and CIDEA was markedly reduced in Ovx rats, whereas ALA treatment reversed these changes. ALA significantly increased liver kinase B1 (LKB1) and phosphorylation of AMP-activated protein kinase (AMPK) and the downstream acetyl-CoA carboxylase (ACC) that were decreased by Ovx, suggesting the browning effects were mediated by AMPK signaling. Conclusions:ALA ameliorates obesity caused by hormone deprivation in menopause via conversion of white to beige adipocytes concomitant with the activation of AMPK signaling.

scholarly journals The Impact of Ethologically Relevant Stressors on Adult Mammalian Neurogenesis

2019 ◽  
Vol 9 (7) ◽  
pp. 158 ◽  
Author(s):  
Claudia Jorgensen ◽  
James Taylor ◽  
Tyler Barton
Keyword(s):  
Social Interactions ◽  
Adult Neurogenesis ◽  
Psychosocial Stress ◽  
Environmental Enrichment ◽  
Functional Integration ◽  
Current Review ◽  
Induced Stress ◽  
Underlying Mechanisms ◽  
The Impact

Adult neurogenesis—the formation and functional integration of adult-generated neurons—remains a hot neuroscience topic. Decades of research have identified numerous endogenous (such as neurotransmitters and hormones) and exogenous (such as environmental enrichment and exercise) factors that regulate the various neurogenic stages. Stress, an exogenous factor, has received a lot of attention. Despite the large number of reviews discussing the impact of stress on adult neurogenesis, no systematic review on ethologically relevant stressors exists to date. The current review details the effects of conspecifically-induced psychosocial stress (specifically looking at the lack or disruption of social interactions and confrontation) as well as non-conspecifically-induced stress on mammalian adult neurogenesis. The underlying mechanisms, as well as the possible functional role of the altered neurogenesis level, are also discussed. The reviewed data suggest that ethologically relevant stressors reduce adult neurogenesis.

scholarly journals Novel role of autophagy-associated Pik3c3 gene in gonadal white adipose tissue browning in aged C57/Bl6 male mice

Aging ◽  
2018 ◽  
Vol 10 (4) ◽  
pp. 764-774 ◽  
Author(s):  
Amiya Kumar Ghosh ◽  
Theresa Mau ◽  
Martin O’Brien ◽  
Raymond Yung
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Male Mice ◽  
Tissue Browning

scholarly journals Additive Effects of Omega-3 Fatty Acids and Thiazolidinediones in Mice Fed a High-Fat Diet: Triacylglycerol/Fatty Acid Cycling in Adipose Tissue

Nutrients ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3737
Author(s):  
Kristina Bardova ◽  
Jiri Funda ◽  
Radek Pohl ◽  
Tomas Cajka ◽  
Michal Hensler ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Additive Effects ◽  
Omega 3 ◽  
High Fat ◽  
Futile Cycle ◽  
Dietary Obesity ◽  
Underlying Mechanisms ◽  
Metabolic Dysfunctions

Long-chain n-3 polyunsaturated fatty acids (Omega-3) and anti-diabetic drugs thiazolidinediones (TZDs) exhibit additive effects in counteraction of dietary obesity and associated metabolic dysfunctions in mice. The underlying mechanisms need to be clarified. Here, we aimed to learn whether the futile cycle based on the hydrolysis of triacylglycerol and re-esterification of fatty acids (TAG/FA cycling) in white adipose tissue (WAT) could be involved. We compared Omega-3 (30 mg/g diet) and two different TZDs—pioglitazone (50 mg/g diet) and a second-generation TZD, MSDC-0602K (330 mg/g diet)—regarding their effects in C57BL/6N mice fed an obesogenic high-fat (HF) diet for 8 weeks. The diet was supplemented or not by the tested compound alone or with the two TZDs combined individually with Omega-3. Activity of TAG/FA cycle in WAT was suppressed by the obesogenic HF diet. Additive effects in partial rescue of TAG/FA cycling in WAT were observed with both combined interventions, with a stronger effect of Omega-3 and MSDC-0602K. Our results (i) supported the role of TAG/FA cycling in WAT in the beneficial additive effects of Omega-3 and TZDs on metabolism of diet-induced obese mice, and (ii) showed differential modulation of WAT gene expression and metabolism by the two TZDs, depending also on Omega-3.

scholarly journals TFEB drives PGC-1α expression in adipocytes to protect against diet-induced metabolic dysfunction

2019 ◽  
Vol 12 (606) ◽  
pp. eaau2281 ◽  
Author(s):  
Trent D. Evans ◽  
Xiangyu Zhang ◽  
Se-Jin Jeong ◽  
Anyuan He ◽  
Eric Song ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Metabolic Diseases ◽  
Therapeutic Potential ◽  
Metabolic Effects ◽  
Metabolic Dysfunction ◽  
Helix Loop Helix ◽  
Downstream Effects ◽  
Brown Adipose ◽  
Tissue Browning

TFEB is a basic helix-loop-helix transcription factor that confers protection against metabolic diseases such as atherosclerosis by targeting a network of genes involved in autophagy-lysosomal biogenesis and lipid catabolism. In this study, we sought to characterize the role of TFEB in adipocyte and adipose tissue physiology and evaluate the therapeutic potential of adipocyte-specific TFEB overexpression in obesity. We demonstrated that mice with adipocyte-specific TFEB overexpression (Adipo-TFEB) were protected from diet-induced obesity, insulin resistance, and metabolic sequelae. Adipo-TFEB mice were lean primarily through increased metabolic rate, suggesting a role for adipose tissue browning and enhanced nonshivering thermogenesis in fat. Transcriptional characterization revealed that TFEB targeted genes involved in adipose tissue browning rather than those involved in autophagy. One such gene encoded PGC-1α, an established target of TFEB that promotes adipocyte browning. To dissect the role of PGC-1α in mediating the downstream effects of TFEB overexpression, we generated mice with adipocyte-specific PGC-1α deficiency and TFEB overexpression. Without PGC-1α, the ability of TFEB overexpression to brown adipose tissue and to elicit beneficial metabolic effects was blunted. Overall, these data implicate TFEB as a PGC-1α–dependent regulator of adipocyte browning and suggest its therapeutic potential in treating metabolic disease.

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