scholarly journals Estrogen Metabolism in Abdominal Subcutaneous and Visceral Adipose Tissue in Postmenopausal Women

2017 ◽  
Vol 102 (12) ◽  
pp. 4588-4595 ◽  
Author(s):  
Natalia Hetemäki ◽  
Hanna Savolainen-Peltonen ◽  
Matti J Tikkanen ◽  
Feng Wang ◽  
Hanna Paatela ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Mrna Expression ◽  
Postmenopausal Women ◽  
Messenger Rna ◽  
Metabolic Diseases ◽  
Quantitative Polymerase Chain Reaction ◽  
Subcutaneous Fat ◽  
Estrogen Metabolism ◽  
Serum Samples ◽  
Estrogen Exposure

Abstract Context In postmenopausal women, adipose tissue (AT) levels of estrogens exceed circulating concentrations. Although increased visceral AT after menopause is related to metabolic diseases, little is known about differences in estrogen metabolism between different AT depots. Objective We compared concentrations of and metabolic pathways producing estrone and estradiol in abdominal subcutaneous and visceral AT in postmenopausal women. Design, Setting, Patients, and Interventions AT and serum samples were obtained from 37 postmenopausal women undergoing surgery for nonmalignant gynecological reasons. Serum and AT estrone, estradiol, and serum estrone sulfate (E1S) concentrations were quantitated using liquid chromatography-tandem mass spectrometry. Activity of steroid sulfatase and reductive 17β-hydroxysteroid dehydrogenase enzymes was measured using radiolabeled precursors. Messenger RNA (mRNA) expression of estrogen-converting enzymes was analyzed by real-time reverse transcription quantitative polymerase chain reaction. Results Estrone concentration was higher in visceral than subcutaneous AT (median, 928 vs 706 pmol/kg; P = 0.002) and correlated positively with body mass index (r = 0.46; P = 0.011). Both AT depots hydrolyzed E1S to estrone, and visceral AT estrone and estradiol concentrations correlated positively with serum E1S. Compared with visceral AT, subcutaneous AT produced more estradiol from estrone (median rate of estradiol production, 1.02 vs 0.57 nmol/kg AT/h; P = 0.004). In visceral AT, the conversion of estrone to estradiol increased with waist circumference (r = 0.65; P = 0.022), and estradiol concentration correlated positively with mRNA expression of HSD17B7 (r = 0.76; P = 0.005). Conclusions Both estrone and estradiol production in visceral AT increased with adiposity, but estradiol was produced more effectively in subcutaneous fat. Both AT depots produced estrone from E1S. Increasing visceral adiposity could increase overall estrogen exposure in postmenopausal women.

Unusual increase of Scd1 and Elovl6 expression in rat inguinal adipose tissue

2012 ◽  
Vol 7 (2) ◽  
pp. 192-200
Author(s):  
Jacek Turyn ◽  
Adriana Mika ◽  
Piotr Stepnowski ◽  
Julian Swierczynski
Keyword(s):  
Adipose Tissue ◽  
Food Restriction ◽  
Metabolic Diseases ◽  
Quantitative Polymerase Chain Reaction ◽  
Mrna Levels ◽  
Gene Expressions ◽  
Tissue Mass ◽  
Expression Of Genes ◽  
Fat Deposits ◽  
Rat Adipose Tissue

AbstractIt is generally accepted that the location of body fat deposits may play an important role in the risk of developing some endocrine and metabolic diseases. We have studied the effect of food restriction and food restriction/refeeding, often practiced by individuals trying to lose body weight, on the expression of genes which are associated with obesity and certain metabolic disorders in inguinal, epididymal, and perirenal rat white adipose tissues. Gene expression was analyzed by real time semi-quantitative polymerase chain reaction and by Western blot. We found that prolonged food restriction caused a significant decrease of body and adipose tissue mass as well as the increase of Scd1 and Elovl6 gene expressions in all main rat adipose tissue deposits. Food restriction/refeeding caused increases of: a) Scd1 and Elovl6 mRNA levels in adipose tissue, b) Scd1 protein level and c) desaturation index in adipose tissue. The increased expression of both genes was unusually high in inguinal adipose tissue. The results suggest that the increase of Scd1 and Elovl6 gene expressions in white adipose tissue by prolonged food restriction and prolonged food restriction/refeeding may contribute to accelerated fat recovery that often occurs in individuals after food restriction/refeeding.

scholarly journals Polysaccharides fromEnteromorpha proliferaImprove Glucose Metabolism in Diabetic Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Wenting Lin ◽  
Wenxiang Wang ◽  
Dongdong Liao ◽  
Damiao Chen ◽  
Pingping Zhu ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Glucose Metabolism ◽  
Mrna Expression ◽  
Glucose Transporter ◽  
Fasting Blood Glucose ◽  
Diabetic Rats ◽  
High Dose ◽  
Sensitivity Index ◽  
Serum Samples ◽  
Glut 4

This study investigated the effects of polysaccharides fromEnteromorpha prolifera(PEP) on glucose metabolism in a rat model of diabetes mellitus (DM). PEP (0, 150, 300, and 600 mg/kg) was administered intragastrically to rats for four weeks. After treatment, fasting blood glucose (FBG) and insulin (INS) levels were measured, and the insulin sensitivity index (ISI) was calculated. The morphopathological changes in the pancreas were observed. Serum samples were collected to measure the oxidant-antioxidant status. The mRNA expression levels of glucokinase (GCK) and insulin receptor (InsR) in liver tissue and glucose transporter type 4 (GLUT-4) and adiponectin (APN) in adipose tissue were determined. Compared with the model group, the FBG and INS levels were lower, the ISI was higher, and the number of isletβ-cells was significantly increased in all the PEP groups. In the medium- and high-dose PEP groups, MDA levels decreased, and the enzymatic activities of SOD and GSH-Px increased. The mRNA expression of InsR and GCK increased in all the PEP groups; APN mRNA expression increased in the high-dose PEP group, and GLUT-4 mRNA expression increased in adipose tissue. These findings suggest that PEP is a potential therapeutic agent that can be utilized to treat DM.

scholarly journals Increase of E3 ubiquitin ligase NEDD4 expression leads to degradation of its target proteins PTEN/IGF1R during the formation of goose fatty liver

2020 ◽  
Vol 98 (9) ◽  
Author(s):  
Chunchi Yan ◽  
Minmeng Zhao ◽  
Shuo Li ◽  
Tongjun Liu ◽  
Cheng Xu ◽  
...  
Keyword(s):  
Fatty Liver ◽  
Mrna Expression ◽  
Messenger Rna ◽  
Quantitative Polymerase Chain Reaction ◽  
Normal Liver ◽  
Protective Mechanism ◽  
Nonalcoholic Fatty Liver ◽  
Target Proteins ◽  
Protein Levels ◽  
Gene 4

Abstract Goose fatty liver may have a unique protective mechanism as it does not show a pathological injury even in the case of severe steatosis. Although neural precursor cell-expressed developmentally downregulated gene 4 (NEDD4) participates in repair and regeneration of injured liver through its target proteins, its role in nonalcoholic fatty liver disease remains unknown. Using quantitative polymerase chain reaction (PCR) and immunoblot analyses, here, we found that the messenger RNA (mRNA) and protein expressions of NEDD4 were induced in goose fatty liver compared with normal liver. The mRNA expression of the gene of phosphate and tension homology deleted on chromosome ten (PTEN) and insulin-like growth factor 1 receptor (IGF1R) was also induced in goose fatty liver; however, their protein expression was or tended to be suppressed. Moreover, the co-immunoprecipitation analysis indicated that there was a physical association between NEDD4 and PTEN in goose liver, which was consistent with the ubiquitination of PTEN in goose fatty liver. Furthermore, NEDD4 overexpression in goose primary hepatocytes suppressed the PTEN and IGF1R protein levels without a significant effect on their mRNA expression. In conclusion, the increased expression of NEDD4 leads to the degradation of PTEN and IGF1R proteins through ubiquitination in goose fatty liver, suggesting that NEDD4 may protect goose fatty liver from severe steatosis-associated injury via its target proteins during the development of goose fatty liver.

scholarly journals Cardiac Hepcidin Expression Associates with Injury Independent of Iron

2016 ◽  
Vol 44 (5) ◽  
pp. 368-378 ◽  
Author(s):  
G. Fenna van Breda ◽  
Lennart G. Bongartz ◽  
Wenqing Zhuang ◽  
Rachel P.L. van Swelm ◽  
Jeanne Pertijs ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mrna Expression ◽  
Messenger Rna ◽  
Iron Homeostasis ◽  
Quantitative Polymerase Chain Reaction ◽  
Cardiac Injury ◽  
Tissue Growth ◽  
Hepcidin Expression ◽  
Sham Surgery ◽  
Hepcidin Gene

Background: Hepcidin regulates systemic iron homeostasis by downregulating the iron exporter ferroportin. Circulating hepcidin is mainly derived from the liver but hepcidin is also produced in the heart. We studied the differential and local regulation of hepcidin gene expression in response to myocardial infarction (MI) and/or chronic kidney disease (CKD). We hypothesized that cardiac hepcidin gene expression is induced by and regulated to severity of cardiac injury, either through direct (MI) or remote (CKD) stimuli, as well as through increased local iron content. Methods: Nine weeks after subtotal nephrectomy (SNX) or sham surgery (CON), rats were subjected to coronary ligation (CL) or sham surgery to realize 4 groups: CON, SNX, CL and SNX + CL. In week 16, the gene expression of hepcidin, iron and damage markers in cardiac and liver tissues was assessed by quantitative polymerase chain reaction and ferritin protein expression was studied by immunohistochemistry. Results: Cardiac hepcidin messenger RNA (mRNA) expression was increased 2-fold in CL (p = 0.03) and 3-fold in SNX (p = 0.01). Cardiac ferritin staining was not different among groups. Cardiac hepcidin mRNA expression correlated with mRNA expression levels of brain natriuretic peptide (β = 0.734, p < 0.001) and connective tissue growth factor (β = 0.431, p = 0.02). In contrast, liver hepcidin expression was unaffected by SNX and CL alone, while it had decreased 50% in SNX + CL (p < 0.05). Hepatic ferritin immunostaining was not different among groups. Conclusions: Our data indicate differences in hepcidin regulation in liver and heart and suggest a role for injury rather than iron as the driving force for cardiac hepcidin expression in renocardiac failure.

scholarly journals Changes in Omentin Levels and Its mRNA Expression in Epicardial Adipose Tissue in Patients Undergoing Elective Cardiac Surgery: the Influence of Type 2 Diabetes and Coronary Heart Disease

2018 ◽  
pp. 881-890 ◽  
Author(s):  
Z. MATLOCH ◽  
H. KRATOCHVÍLOVÁ ◽  
A. CINKAJZLOVÁ ◽  
M. LIPŠ ◽  
P. KOPECKÝ ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Coronary Artery Disease ◽  
Adipose Tissue ◽  
Cardiac Surgery ◽  
Coronary Artery ◽  
Mrna Expression ◽  
Subcutaneous Fat ◽  
Elective Cardiac Surgery ◽  
Artery Disease

Omentin is a protein produced by numerous tissues including adipose tissue. Its concentrations are decreased in patients with obesity, type 2 diabetes mellitus (DM) and coronary artery disease (CAD). Experimental studies suggest that omentin may have anti-inflammatory and insulin-sensitizing properties. In the present study, we measured circulating omentin levels and its mRNA expression in epicardial and subcutaneous fat, intercostal and heart muscle before and after elective cardiac surgery in patients with CAD (CAD+, DM-, n=18), combination of CAD and DM (CAD+, DM+, n=9) or with none of these conditions (CAD-, DM-, n=11). The groups did not differ in baseline anthropometric and biochemical characteristics with the exception of higher blood glucose and HBA1c in CAD+, DM+ group. Baseline circulating omentin levels tended to be lower in CAD+, DM- and CAD+, DM+ groups as compared to CAD-, DM- group and cardiac surgery increased its concentration only in CAD-, DM- group. The change in serum omentin levels during surgery inversely correlated with epicardial fat thickness. While baseline omentin mRNA expression did not differ among the groups in any of the studied tissues, its increase after surgery was present only in subcutaneous fat in CAD-, DM- and CAD+, DM- groups, but not in CAD+, DM+ group. Intercostal muscle omentin mRNA expression increased after surgery only in CAD-, DM- group. In conclusion, cardiac surgery differentially affects omentin levels and subcutaneous fat and skeletal muscle mRNA expression in patients without coronary artery disease and diabetes as compared to patients with these conditions.

Lycopene-rich tomato oleoresin modulates plasma adiponectin concentration and mRNA levels of adiponectin, SIRT1, and FoxO1 in adipose tissue of obese rats

2015 ◽  
Vol 34 (6) ◽  
pp. 612-619 ◽  
Author(s):  
RAM Luvizotto ◽  
AF Nascimento ◽  
NCM Miranda ◽  
X-D Wang ◽  
ALA Ferreira
Keyword(s):  
Adipose Tissue ◽  
Messenger Rna ◽  
High Performance ◽  
Quantitative Polymerase Chain Reaction ◽  
Sirtuin 1 ◽  
Mrna Levels ◽  
Obese Rats ◽  
Male Wistar Rats ◽  
Foxo1 Gene ◽  
Cluster Of Differentiation

Aim: To investigate whether lycopene can modulate adiponectin levels and SIRT1 and FoxO1 gene expression in the adipose tissue of diet-induced obese rats. Methods: Male Wistar rats were first fed with hypercaloric diet (HD, n = 12) for 6 weeks, and afterward, these rats were randomly assigned to receive HD ( n = 6) or HD with lycopene-rich tomato oleoresin (equivalent to lycopene 10 mg/kg body weight (BW)/day, HD + L, n = 6) by gavage for additional 6 weeks. Plasma lycopene and adiponectin levels were analyzed by high-performance liquid chromatography and immunoassay, respectively. The messenger RNA (mRNA) expressions of adiponectin, Sirtuin 1 (SIRT1), Forkhead box O 1 (FoxO1), fatty acid translocase/cluster of differentiation 36 (FAT/CD36), and PPARγ in adipose tissues were determined by quantitative polymerase chain reaction. Results: Lycopene was detected in the plasma of rats in HD + L group but not in the HD group. Although both BW and adiposity were not different between the two groups, there was a significant increase in both plasma concentration and mRNA expression of adiponectin in the adipose tissue of the HD + L group. In addition, the lycopene supplementation upregulated mRNA expressions of SIRT1, FoxO1, and FAT/CD36 but downregulated PPARγ in adipose tissue of obese rats. Conclusion: These data suggest that lycopene, in the concentration used, is not toxic and also its health benefits in adipose tissue may play a role against obesity-related complications.

scholarly journals Three Months of Regular Aerobic Exercise in Patients With Obesity Improve Systemic Subclinical Inflammation Without Major Influence on Blood Pressure and Endocrine Production of Subcutaneous Fat

2014 ◽  
pp. S299-S308 ◽  
Author(s):  
P. TRACHTA ◽  
J. DRÁPALOVÁ ◽  
P. KAVÁLKOVÁ ◽  
V. TOUŠKOVÁ ◽  
A. CINKAJZLOVÁ ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Adipose Tissue ◽  
Aerobic Exercise ◽  
Mrna Expression ◽  
Subcutaneous Adipose Tissue ◽  
Subcutaneous Fat ◽  
Control Group ◽  
Regular Exercise ◽  
Subclinical Inflammation ◽  
Subcutaneous Adipose

The aim of our study was to explore the effects of regular aerobic exercise on anthropometric, biochemical and hormonal parameters and mRNA expression of selected factors involved in metabolic regulations in subcutaneous adipose tissue of patients with obesity. Fifteen obese women with arterial hypertension underwent a three-month exercise program consisting of 30 min of aerobic exercise 3 times a week. Fifteen healthy lean women with no intervention served as a control group. Obese group underwent anthropometric measurements, blood sampling, subcutaneous adipose tissue (SCAT) biopsy and 24-h blood pressure monitoring at baseline and after three months of exercise, while control group was examined only once. At baseline, obese group had increased SCAT expression of proinflammatory cytokines and adipokines relative to control group. Three months of regular exercise improved anthropometric parameters, decreased CRP, blood glucose and HOMA-IR, while having no significant effect on lipid profile and blood pressure. Gene expressions in SCAT were not affected by physical activity with the exception of increased aquaporin-3 mRNA expression. We conclude that three months of regular exercise decrease systemic subclinical inflammation with only minor influence on the blood pressure and the endocrine function of subcutaneous fat.

Silymarin prevents lipid accumulation in the liver of rats with type 2 diabetes via sirtuin1 and SREBP-1c

2018 ◽  
Vol 29 (3) ◽  
pp. 301-308 ◽  
Author(s):  
Nejat Kheiripour ◽  
Jamshid Karimi ◽  
Iraj Khodadadi ◽  
Heidar Tavilani ◽  
Mohammad Taghi Goodarzi ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Messenger Rna ◽  
Glycogen Content ◽  
Regulatory Element ◽  
Quantitative Polymerase Chain Reaction ◽  
Diabetic Rat ◽  
Model Assessment ◽  
Control Groups ◽  
Protein Carbonyl Content

Abstract Background: In this study, we have investigated whether silymarin intake influences lipid and glycogen content in conjunction with sirtuin1 (SIRT1) and sterol regulatory element-binding protein 1c (SREBP-1c) expressions in liver of type 2 diabetic rat. Methods: Thirty-six male Wistar rats were randomly divided into six groups: control groups (C) and diabetic groups (D); the control groups received 60 or 120 mg/kg silymarin (C+S60 or C+S120), and the diabetic groups received 60 or 120 mg/kg silymarin (D+S60 or D+S120) daily for 8 weeks. Serum biochemical parameters, as well as glycogen, lipid and oxidative stress biomarkers, in the liver tissue were measured by spectrophotometric methods. Additionally, SIRT1 and SREBP-1c messenger RNA (mRNA) expressions were evaluated by quantitative polymerase chain reaction. Results: Diabetes caused a significantly increased fasting blood sugar, homeostasis model assessment for insulin resistance, liver total cholesterol and triglyceride (TG) content, which were attenuated after the administration of silymarin. Dietary silymarin caused the improvement of lipid content in the liver of diabetic rats. Moreover, silymarin administration promoted SIRT1, suppressed SREBP-1c mRNA expression, reduced liver nitric oxide and protein carbonyl content, and increased liver glycogen, catalase and glutathione peroxidase activity. Furthermore, histopathological changes were improved in the treated groups. Conclusions: Silymarin administration considerably restored hepatic changes induced by streptozotocin and nicotinamide. The upregulation of SIRT1 mRNA expression by silymarin may be associated with decreased lipid, increased glycogen content and downregulation of the SREBP-1c gene in the liver.

scholarly journals Breast Adipose Tissue Estrogen Metabolism in Postmenopausal Women With or Without Breast Cancer

2014 ◽  
Vol 99 (12) ◽  
pp. E2661-E2667 ◽  
Author(s):  
Hanna Savolainen-Peltonen ◽  
Veera Vihma ◽  
Marjut Leidenius ◽  
Feng Wang ◽  
Ursula Turpeinen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Adipose Tissue ◽  
Postmenopausal Women ◽  
Estrogen Metabolism ◽  
Breast Adipose Tissue ◽  
Breast Adipose

scholarly journals Secoisolariciresinol Diglucoside Regulates Adipose Tissue Metabolic Disorder in Obese Mice Induced by a Western Diet

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Shan Dong ◽  
Wenliang Bai ◽  
Jiaping Chen ◽  
Li Zhang ◽  
Wanli Sheng ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Mrna Expression ◽  
Metabolic Disorder ◽  
Metabolic Diseases ◽  
Western Diet ◽  
Obese Mice ◽  
Secoisolariciresinol Diglucoside ◽  
Reduced Body ◽  
Main Component ◽  
Lipid Metabolic Disorder

Secoisolariciresinol diglucoside (SDG) is the main component of flax lignans. Current studies have reported a positive effect of SDG on obesity and metabolic diseases. SDG has strong blood fat- and blood sugar-lowering, anti-inflammatory, and antioxidant effects and prevents heart disease and other chronic diseases. In this study, we explored the effects of SDG on Western diet-induced obesity and lipid metabolic disorder. Supplementing Western diet-induced obese mice with 40 mg kg1 d1, SDG for 12 weeks significantly reduced body and tissue weights. Increased adiponectin levels and decreased serum leptin and resistin levels were observed in obese mice orally administered SDG. Proliferation of adipose tissue was observed by hematoxylin and eosin staining, and cell size was quantitatively analyzed. As a result, SDG inhibited the proliferation of adipose tissue. In addition, SDG suppressed the mRNA expression of lipid synthetic genes and upregulated the mRNA expression of lipolytic genes. Overall, these results indicate that SDG inhibits obesity induced by a Western diet and regulates adipose tissue metabolic disorder. These results provide a theoretical basis for further study on the regulation of obesity and lipid metabolic disorder caused by SDG.

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