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PEDF Expression Is Inhibited by Insulin Treatment in Adipose Tissue via Suppressing 11β-HSD1  [PDF]
Yinli Zhou, Fen Xu, Hongrong Deng, Yan Bi, Weiping Sun, Yi Zhao, Zonglan Chen, Jianping Weng
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0084016
Abstract: Early intensive insulin therapy improves insulin sensitivity in type 2 diabetic patients; while the underlying mechanism remains largely unknown. Pigment epithelium-derived factor (PEDF), an anti-angiogenic factor, is believed to be involved in the pathogenesis of insulin resistance. Here, we hypothesize that PEDF might be down regulated by insulin and then lead to the improved insulin resistance in type 2 diabetic patients during insulin therapy. We addressed this issue by investigating insulin regulation of PEDF expression in diabetic conditions. The results showed that serum PEDF was reduced by 15% in newly diagnosed type 2 diabetic patients after insulin therapy. In adipose tissue of diabetic Sprague-Dawley rats, PEDF expression was associated with TNF-α elevation and it could be decreased both in serum and in adipose tissue by insulin treatment. In adipocytes, PEDF was induced by TNF-α through activation of NF-κB. The response was inhibited by knockdown and enhanced by over expression of NF-κB p65. However, PEDF expression was indirectly, not directly, induced by NF-κB which promoted 11β-hydroxysteroid dehydrogenase 1 (11β-HSD1) expression in adipocytes. 11β-HSD1 is likely to stimulate PEDF expression through production of active form of glucocorticoids as dexamethasone induced PEDF expression in adipose tissue. Insulin inhibited PEDF by down-regulating 11β-HSD1 expression. The results suggest that PEDF activity is induced by inflammation and decreased by insulin through targeting 11β-HSD1/glucocorticoid pathway in adipose tissue of diabetic patients.
Consumption of resistant starch decreases postprandial lipogenesis in white adipose tissue of the rat
Janine A Higgins, Marc A Brown, Leonard H Storlien
Nutrition Journal , 2006, DOI: 10.1186/1475-2891-5-25
Abstract: It has been reported that chronic resistant starch (RS) feeding in rats causes a decrease in adipocyte cell size, a decrease in fatty acid synthase expression, and reduced whole-body weight gain relative to digestible starch (DS) feeding [1,2]. Additionally, in healthy adults, a single RS meal caused a substantial elevation in total and meal fat oxidation compared to a DS meal [3]. These data suggest that RS intake may influence postprandial lipid metabolism. The aim of the present study was to examine the rate of lipogenesis in key lipogenic organs acutely following a RS or DS meal.Male Wistar rats (Rattus norvegicus) were obtained from the Animal Resource Center (Murdoch, Western Australia) and were housed in groups of three at the University of Wollongong, Animal House. The rats were maintained at 22°C on a 12-h light/dark cycle (light cycle from 0700–1900 h), with free access to a standard laboratory chow (Young Stock Feed, Young, Australia) and water. The study was conducted according to the National Health and Medical Research Council (NH&MRC; Australia) code of practice for the care and use of animals for scientific purposes. Test Diets were prepared as previously described [5]. As a percentage of total energy, all diets contained 67% carbohydrate (57% starch; 10% sucrose), 22% protein, and 11% fat. All diets were identical in composition except for the percentage of RS and DS included in the starch component. For the RS diet, the starch used was a natural high amylose starch, Hi-Maize 957? (National Starch and Chemical Co), which is 60% amylose/40% amylopectin, versus waxy cornstarch, which is 0% amylose/100% amylopectin, for the DS diet. Diets were presented to the animals in an unprocessed, unpelleted form so the starches were not subjected to cooking or extrusion. The dietary fiber level of the starches was determined using the Association of Analytical Chemistry (AOAC) enzymatic-gravimetric method. Total dietary fiber (dry solids) was lower (approximatel
De Novo Lipogenesis in Adipose Tissue Is Associated with Course of Morbid Obesity after Bariatric Surgery  [PDF]
Lourdes Garrido-Sánchez, Joan Vendrell, Diego Fernández-García, Victoria Ceperuelo-Mallafré, Matilde R. Chacón, Luis Oca?a-Wilhelmi, Juan Alcaide, Francisco J. Tinahones, Eduardo García-Fuentes
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0031280
Abstract: Objective De novo lipogenesis is involved in fatty acid biosynthesis and could be involved in the regulation of the triglyceride storage capacity of adipose tissue. However, the association between lipogenic and lipolytic genes and the evolution of morbidly obese subjects after bariatric surgery remains unknown. In this prospective study we analyze the association between the improvement in the morbidly obese patients as a result of bariatric surgery and the basal expression of lipogenic and lipolytic genes. Methods We study 23 non diabetic morbidly obese patients who were studied before and 7 months after bariatric surgery. Also, we analyze the relative basal mRNA expression levels of lipogenic and lipolytic genes in epiploic visceral adipose tissue (VAT) and abdominal subcutaneous adipose tissue (SAT). Results When the basal acetyl-CoA carboxylase 1 (ACC1), acetyl-CoA synthetase 2 (ACSS2) and ATP citrate lyase (ACL) expression in SAT was below percentile-50, there was a greater decrease in weight (P = 0.006, P = 0.034, P = 0.026), body mass index (P = 0.008, P = 0.033, P = 0.034) and hip circumference (P = 0.033, P = 0.021, P = 0.083) after bariatric surgery. In VAT, when the basal ACSS2 expression was below percentile-50, there was a greater decrease in hip circumference (P = 0.006). After adjusting for confounding variables in logistic regression models, only the morbidly obese patients with SAT or VAT ACSS2 expression≥P50 before bariatric surgery had a lower percentage hip circumference loss (
Insulin action in adipose tissue in type 1 diabetes  [cached]
F Arrieta-Blanco,JI Botella-Carretero,P Iglesias,et al
International Journal of General Medicine , 2011,
Abstract: F Arrieta-Blanco1, JI Botella-Carretero1, P Iglesias1, JA Balsa1, I Zamarrón1, C De la Puerta1, JJ Arrieta2, F Ramos3, C Vázquez1, A Rovira21Unit of Clinical Nutrition and Dietetics, Department of Endocrinology and Nutrition, Hospital Ramóny, Cajal, Madrid, Spain, Irycis, Ciberobn; 2Fundación Jimenez Díaz. Madrid, Spain; 3Hospital Sureste de ArgandaBackground: Insulin action has been reported to be normal in type 1 diabetic patients. However, some studies have reported an insulin resistance state in these patients. The aim of this study was to investigate insulin resistance in a group of type 1 diabetic patients. We studied the insulin action in adipose tissue and analyzed the effects of duration of disease, body mass index (BMI), and glycosylated hemoglobin on insulin action at the receptor and postreceptor levels in adipocytes.Methods: Nine female type 1 diabetic patients with different durations of disease and eight nondiabetic female patients of comparable age and BMI were studied. 125I-insulin binding and U-[14C]-D-glucose transport was measured in a sample of subcutaneous gluteus adipose tissue obtained by open surgical biopsy from each subject.Results: The duration of disease was negatively correlated with both 125I-insulin binding capacity (r = -0.70, P < 0.05) and basal and maximum insulin-stimulated glucose transport (r = -0.87, P < 0.01, and r = -0.88, P < 0.01, respectively). Maximum specific 125I-insulin binding to the receptors in adipocytes was higher in the group of patients with a shorter duration of disease (P < 0.01). Basal and maximum insulin-stimulated glucose transport was significantly higher in the group with less than 5 years of disease (P < 0.01). No correlation was found between BMI and insulin action.Conclusion: Female type 1 diabetic patients have normal insulin action. There is a high glucose uptake in the early phase of the disease, although a longer duration of disease appears to be a contributing factor to a decrease in insulin action in these patients, and involving both receptor and postreceptor mechanisms.Keywords: type 1 diabetes, insulin action, insulin resistance, adipose tissue
Role of Subcutaneous Adipose Tissue in the Pathogenesis of Insulin Resistance  [PDF]
Pavankumar Patel,Nicola Abate
Journal of Obesity , 2013, DOI: 10.1155/2013/489187
Abstract: Burden of obesity has increased significantly in the United States over last few decades. Association of obesity with insulin resistance and related cardiometabolic problems is well established. Traditionally, adipose tissue in visceral fat depot has been considered a major culprit in development of insulin resistance. However, growing body of the literature has suggested that adipose tissue in subcutaneous fat depot, not only due to larger volume but also due to inherent functional characteristics, can have significant impact on development of insulin resistance. There are significant differences in functional characteristics of subcutaneous abdominal/truncal versus gluteofemoral depots. Decreased capacity for adipocyte differentiation and angiogenesis along with adipocyte hypertrophy can trigger vicious cycle of inflammation in subcutaneous adipose tissue and subsequent ectopic fat deposition. It is important to shift focus from fat content to functional heterogeneity in adipose tissue depots to better understand the relative role of subcutaneous adipose tissue in metabolic complications of obesity. Therapeutic lifestyle change continues to be the most important intervention in clinical practice at any level of increased adiposity. Future pharmaceutical interventions aimed at improving adipose tissue function in various subcutaneous depots have potential to help maintain adequate insulin sensitivity and reduce risk for development of insulin resistance complications. Prevalence of obesity has been increasing in the US. In 1960s, prevalence of obesity was approximately 13% [1]. The most recent analyses of National Health and Nutrition Examination Survey (NHANES) reported that 33.8% of adults (age 20 years or more) and 16.8% of children and adolescents (age 2–19 years) are obese [2, 3]. Obesity is associated with increased morbidity and mortality and decreased life expectancy. Obesity is associated with increased risk for cardiovascular diseases. These include coronary heart disease, heart failure, and sudden death [4, 5]. In fact heart disease is the leading cause of death (1 in every 4 deaths) for both men and women in the USA [6]. In addition to cardiovascular diseases, obesity is associated with numerous other medical conditions including type 2 diabetes, dyslipidemia, hypertension, nonalcoholic fatty liver disease, cancers, and sleep apnea [4]. Insulin resistance is the key underlying pathophysiologic process for development of many of these comorbidities. Medical costs associated with obesity have increased and were estimated at 147 billion
Insulin action in adipose tissue in type 1 diabetes
F Arrieta-Blanco, JI Botella-Carretero, P Iglesias, et al
International Journal of General Medicine , 2011, DOI: http://dx.doi.org/10.2147/IJGM.S15809
Abstract: sulin action in adipose tissue in type 1 diabetes Original Research (3573) Total Article Views Authors: F Arrieta-Blanco, JI Botella-Carretero, P Iglesias, et al Published Date February 2011 Volume 2011:4 Pages 153 - 157 DOI: http://dx.doi.org/10.2147/IJGM.S15809 F Arrieta-Blanco1, JI Botella-Carretero1, P Iglesias1, JA Balsa1, I Zamarrón1, C De la Puerta1, JJ Arrieta2, F Ramos3, C Vázquez1, A Rovira2 1Unit of Clinical Nutrition and Dietetics, Department of Endocrinology and Nutrition, Hospital Ramóny, Cajal, Madrid, Spain, Irycis, Ciberobn; 2Fundación Jimenez Díaz. Madrid, Spain; 3Hospital Sureste de Arganda Background: Insulin action has been reported to be normal in type 1 diabetic patients. However, some studies have reported an insulin resistance state in these patients. The aim of this study was to investigate insulin resistance in a group of type 1 diabetic patients. We studied the insulin action in adipose tissue and analyzed the effects of duration of disease, body mass index (BMI), and glycosylated hemoglobin on insulin action at the receptor and postreceptor levels in adipocytes. Methods: Nine female type 1 diabetic patients with different durations of disease and eight nondiabetic female patients of comparable age and BMI were studied. 125I-insulin binding and U-[14C]-D-glucose transport was measured in a sample of subcutaneous gluteus adipose tissue obtained by open surgical biopsy from each subject. Results: The duration of disease was negatively correlated with both 125I-insulin binding capacity (r = -0.70, P < 0.05) and basal and maximum insulin-stimulated glucose transport (r = -0.87, P < 0.01, and r = -0.88, P < 0.01, respectively). Maximum specific 125I-insulin binding to the receptors in adipocytes was higher in the group of patients with a shorter duration of disease (P < 0.01). Basal and maximum insulin-stimulated glucose transport was significantly higher in the group with less than 5 years of disease (P < 0.01). No correlation was found between BMI and insulin action. Conclusion: Female type 1 diabetic patients have normal insulin action. There is a high glucose uptake in the early phase of the disease, although a longer duration of disease appears to be a contributing factor to a decrease in insulin action in these patients, and involving both receptor and postreceptor mechanisms.
Munc18c in Adipose Tissue Is Downregulated in Obesity and Is Associated with Insulin  [PDF]
Lourdes Garrido-Sanchez, Xavier Escote, Leticia Coin-Aragüez, Jose Carlos Fernandez-Garcia, Rajaa El Bekay, Joan Vendrell, Eduardo Garcia-Fuentes, Francisco J. Tinahones
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0063937
Abstract: Objective Munc18c is associated with glucose metabolism and could play a relevant role in obesity. However, little is known about the regulation of Munc18c expression. We analyzed Munc18c gene expression in human visceral (VAT) and subcutaneous (SAT) adipose tissue and its relationship with obesity and insulin. Materials and Methods We evaluated 70 subjects distributed in 12 non-obese lean subjects, 23 overweight subjects, 12 obese subjects and 23 nondiabetic morbidly obese patients (11 with low insulin resistance and 12 with high insulin resistance). Results The lean, overweight and obese persons had a greater Munc18c gene expression in adipose tissue than the morbidly obese patients (p<0.001). VAT Munc18c gene expression was predicted by the body mass index (B = ?0.001, p = 0.009). In SAT, no associations were found by different multiple regression analysis models. SAT Munc18c gene expression was the main determinant of the improvement in the HOMA-IR index 15 days after bariatric surgery (B = ?2148.4, p = 0.038). SAT explant cultures showed that insulin produced a significant down-regulation of Munc18c gene expression (p = 0.048). This decrease was also obtained when explants were incubated with liver X receptor alpha (LXRα) agonist, either without (p = 0.038) or with insulin (p = 0.050). However, Munc18c gene expression was not affected when explants were incubated with insulin plus a sterol regulatory element-binding protein-1c (SREBP-1c) inhibitor (p = 0.504). Conclusions Munc18c gene expression in human adipose tissue is down-regulated in morbid obesity. Insulin may have an effect on the Munc18c expression, probably through LXRα and SREBP-1c.
Is the Adipose Tissue the Key Road to Inflammation?
Stéphanie Lucas, Claudie Verwaerde and Isabelle Wolowczuk
Immunology and Immunogenetics Insights , 2012,
Abstract: It is now broadly accepted that white adipose tissue disorders, such as obesity, are associated with a chronic low-grade inflammation predisposing to the development of insulin-resistance, type 2 diabetes and cardiovascular complications. In obesity, accumulation of visceral adipose tissue, rather than subcutaneous adipose tissue, is regarded as the most critical factor contributing to the pathogenesis of these metabolic diseases. Recently has emerged the notion that inflammatory response accompanying obesity corresponds to a cytokine-mediated activation of innate immunity. The purpose of this review is to provide an update on this emerging concept and to show the reader how innate immune metabolic pathways engaged within white adipose tissue could interfere with innate inflammatory immune defense. First, adipose tissue is reported as an important in vivo source of inflammatory cytokines and adipocytes express some receptors of the innate immune system (namely the Toll-like receptors). Second, both innate and adaptive immune cells (respectively, macrophages, dendritic-like cells and T-lymphocytes) appear more and more essential to the initiation and the development of adipose tissue inflammation. More specifically, adipose tissue macrophages have recently emerged as key players in the inflammatory process of obese adipose tissue. Their number and their phenotypic switch from a non inflammatory (i.e. M2) to an inflammatory (i.e. M1) state are likely crucial in the onset of obese adipose tissue inflammation and in the development of insulin-resistance. Finally, the hormonal regulation of adipose tissue inflammation is exemplified by recent data regarding the role of glucocorticoids, both at the level of adipose cells and macrophages. Altogether, adipose tissue might therefore be regarded as a true immune organ, at the crossroad between metabolism and immune system.
Is the Adipose Tissue the Key Road to Inflammation?
Stéphanie Lucas,Claudie Verwaerde,Isabelle Wolowczuk
Immunology and Immunogenetics Insights , 2009,
Abstract: It is now broadly accepted that white adipose tissue disorders, such as obesity, are associated with a chronic low-grade inflammation predisposing to the development of insulin-resistance, type 2 diabetes and cardiovascular complications. In obesity, accumulation of visceral adipose tissue, rather than subcutaneous adipose tissue, is regarded as the most critical factor contributing to the pathogenesis of these metabolic diseases. Recently has emerged the notion that inflammatory response accompanying obesity corresponds to a cytokine-mediated activation of innate immunity. The purpose of this review is to provide an update on this emerging concept and to show the reader how innate immune metabolic pathways engaged within white adipose tissue could interfere with innate inflammatory immune defense. First, adipose tissue is reported as an important in vivo source of inflammatory cytokines and adipocytes express some receptors of the innate immune system (namely the Toll-like receptors). Second, both innate and adaptive immune cells (respectively, macrophages, dendritic-like cells and T-lymphocytes) appear more and more essential to the initiation and the development of adipose tissue inflammation. More specifically, adipose tissue macrophages have recently emerged as key players in the inflammatory process of obese adipose tissue. Their number and their phenotypic switch from a non inflammatory (i.e. M2) to an inflammatory (i.e. M1) state are likely crucial in the onset of obese adipose tissue inflammation and in the development of insulin-resistance. Finally, the hormonal regulation of adipose tissue inflammation is exemplified by recent data regarding the role of glucocorticoids, both at the level of adipose cells and macrophages. Altogether, adipose tissue might therefore be regarded as a true immune organ, at the crossroad between metabolism and immune system.
Breast Cancer 1 (BrCa1) May Be behind Decreased Lipogenesis in Adipose Tissue from Obese Subjects  [PDF]
Francisco J. Ortega, José M. Moreno-Navarrete, Dolores Mayas, Eva García-Santos, María Gómez-Serrano, José I. Rodriguez-Hermosa, Bartomeu Ruiz, Wifredo Ricart, Francisco J. Tinahones, Gema Frühbeck, Belen Peral, José M. Fernández-Real
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0033233
Abstract: Context Expression and activity of the main lipogenic enzymes is paradoxically decreased in obesity, but the mechanisms behind these findings are poorly known. Breast Cancer 1 (BrCa1) interacts with acetyl-CoA carboxylase (ACC) reducing the rate of fatty acid biosynthesis. In this study, we aimed to evaluate BrCa1 in human adipose tissue according to obesity and insulin resistance, and in vitro cultured adipocytes. Research Design and Methods BrCa1 gene expression, total and phosphorylated (P-) BrCa1, and ACC were analyzed in adipose tissue samples obtained from a total sample of 133 subjects. BrCa1 expression was also evaluated during in vitro differentiation of human adipocytes and 3T3-L1 cells. Results BrCa1 gene expression was significantly up-regulated in both omental (OM; 1.36-fold, p = 0.002) and subcutaneous (SC; 1.49-fold, p = 0.001) adipose tissue from obese subjects. In parallel with increased BrCa1 mRNA, P-ACC was also up-regulated in SC (p = 0.007) as well as in OM (p = 0.010) fat from obese subjects. Consistent with its role limiting fatty acid biosynthesis, both BrCa1 mRNA (3.5-fold, p<0.0001) and protein (1.2-fold, p = 0.001) were increased in pre-adipocytes, and decreased during in vitro adipogenesis, while P-ACC decreased during differentiation of human adipocytes (p = 0.005) allowing lipid biosynthesis. Interestingly, BrCa1 gene expression in mature adipocytes was restored by inflammatory stimuli (macrophage conditioned medium), whereas lipogenic genes significantly decreased. Conclusions The specular findings of BrCa1 and lipogenic enzymes in adipose tissue and adipocytes reported here suggest that BrCa1 might help to control fatty acid biosynthesis in adipocytes and adipose tissue from obese subjects.
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