scholarly journals A Distinctive NAFLD Signature in Adipose Tissue from Women with Severe Obesity

2021 ◽  
Vol 22 (19) ◽  
pp. 10541
Author(s):  
Óscar Osorio-Conles ◽  
Arturo Vega-Beyhart ◽  
Ainitze Ibarzabal ◽  
José María Balibrea ◽  
Isabel Graupera ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Severe Obesity ◽  
Matrix Remodeling ◽  
Cell Area ◽  
Obese Women ◽  
Fat Cell ◽  
Nonalcoholic Fatty Liver ◽  
Multinomial Logistic Model ◽  
Fat Depots ◽  
Group A

Development and severity of nonalcoholic fatty liver disease (NAFLD) have been linked to obesity and white adipose tissue (WAT) dysfunction plays a key role in this relation. We compared the main features of subcutaneous (SAT) and visceral WAT (VAT) tissue dysfunction in 48 obese women without (Ob) and with NAFLD (Ob-NAFLD) undergoing bariatric surgery and matched for age, BMI and T2D status. Fat cell area, adipocyte size distribution, the degree of histological fibrosis and the mRNA expression of adipokines and genes implicated in inflammation, adipogenesis, angiogenesis, metabolism and extracellular matrix remodeling were measured by RT-qPCR in both fat depots. Ob-NAFLD group showed higher TG and lower HDL circulating levels, increased VAT fat cell area and similar WAT fibrosis in comparison with Ob group. A sPLS-DA was performed in order to identify the set of genes that better characterize the presence of NAFLD. Finally, we build a multinomial logistic model including seven genes that explained 100% of the variance in NAFLD and correctly predicted 100% of cases. Our data support the existence of distinctive NAFLD signatures in WAT from women with severe obesity. A better understanding of these pathways may help in future strategies for the prevention and treatment of NAFLD.

Glycerokinase in mammalian adipose tissue: stimulation by lipogenic substances

1975 ◽  
Vol 228 (6) ◽  
pp. 1868-1874 ◽  
Author(s):  
PA Persico ◽  
M Cerchio ◽  
H Jeffay
Keyword(s):  
Adipose Tissue ◽  
Fat Metabolism ◽  
Main Function ◽  
Fat Pad ◽  
Fat Cell ◽  
Fat Depots ◽  
Anabolic Action ◽  
Brown Adipose ◽  
Gradual Accumulation

A connecting link between carbohydrate and fat metabolism in adipose tissue is theconcentration of alpha-glycerophosphate derived predominantly from the glycolysis ofglucose entering the fat cell. However, several investigators have reported the presence of a glycerol specific kinase in the epidiymal fat-pad of the rat and obob mouse.This enzyme's presence in other mammalian adipose tissue could contribute to the alpha-glycerophosphate pool and thus affect both carbohydrate and fat metabolism within the fat cell. Glycerokinase was demonstrated in isolated fat cells obtained from the subcutaneous, perirenal, epididymal, and dorsal intrascapular brown fat depots of the adultmale rat. It was found to be particularly sensitive to in vivo lipogenic stimuli in both the subcutaneous and the brown adipose tissue and concluded that insulin is involved in adipose glycerokinase stimulation. Therefore, the main function of glycerokinase in normal adipose tissue may be to augment the anabolic action of insulin. It isfurther suggested that deviation from the normal control of this lipogenic enzyme couldlead to a gradual accumulation of fat and eventual obesity.

scholarly journals Changes in adipose tissue of the rat due to early undernutrition followed by rehabilitation

1980 ◽  
Vol 43 (1) ◽  
pp. 27-31 ◽  
Author(s):  
Patricia M. Harris
Keyword(s):  
Adipose Tissue ◽  
Wistar Rats ◽  
Cell Number ◽  
Fat Cells ◽  
Stock Diet ◽  
Fat Cell ◽  
Black And White ◽  
Fat Depots ◽  
Male Wistar Rats ◽  
Number Of Cells

1. Male Wistar rats were allocated at birth to foster mothers in litters of three, nine or sixteen. At weaning animals from each litter size were ad lib.-fed on a stock diet. Further animals from litters of nine and sixteen were fed on the stock diet in restricted amounts until 12 weeks of age and then rehabilitated by being allowed ad lib. access to the stock diet.2. Five animals from each group were killed at 24 weeks of age and the size and number of cells determined in four specific fat depots.3. Animals reared in litters of sixteen and further undernourished from 3 to 12 weeks (group L16/U) had significantly fewer fat cells at all sites studied than animals reared in litters of three and ad lib.-fed. Group L16/U animals also had significantly fewer observable fat cells at the epididymal site than ad lib.-fed animals reared in litters of nine. These results differ from those found in the Black and White Hooded rat where, after similar treatments, no significant differences in observable fat cell number were found.

scholarly journals Diversity of lipid mediators in human adipose tissue depots

2013 ◽  
Vol 304 (12) ◽  
pp. C1141-C1149 ◽  
Author(s):  
Joan Clària ◽  
Binh T. Nguyen ◽  
Arin L. Madenci ◽  
C. Keith Ozaki ◽  
Charles N. Serhan
Keyword(s):  
Adipose Tissue ◽  
Cell Metabolism ◽  
Human Adipose Tissue ◽  
Lipid Mediators ◽  
Anatomical Location ◽  
Fat Cell ◽  
Perivascular Adipose Tissue ◽  
Fat Depots ◽  
Fat Depot ◽  
Marked Deficit

Adipose tissue is a heterogeneous organ with remarkable variations in fat cell metabolism depending on the anatomical location. However, the pattern and distribution of bioactive lipid mediators between different fat depots and their relationships in complex diseases have not been investigated. Using LC-MS/MS-based metabolo-lipidomics, here we report that human subcutaneous (SC) adipose tissues possess a range of specialized proresolving mediators (SPM) including resolvin (Rv) D1, RvD2, protectin (PD) 1, lipoxin (LX) A4, and the monohydroxy biosynthetic pathway markers of RvD1 and PD1 (17-HDHA), RvE1 (18-HEPE), and maresin 1 (14-HDHA). The “classic” eicosanoids prostaglandin (PG) E2, PGD2, PGF2α, leukotriene (LT) B4, 5-hydroxyeicosatetraenoic acid (5-HETE), 12-HETE, and 15-HETE were also identified in SC fat. SC fat from patients with peripheral vascular disease (PVD) exhibited a marked deficit in PD1 and 17-HDHA levels. Compared with SC, perivascular adipose tissue displayed higher SPM levels, suggesting an enhanced resolution capacity in this fat depot. In addition, augmented levels of eicosanoids and SPM were observed in SC fat surrounding foot wounds. Notably, the profile of SC PGF2αdiffered significantly when patients were grouped by body mass index (BMI). In the case of peri-wound SC fat, BMI negatively correlated with PGE2.In this tissue, proresolving mediators RvD2 and LXA4were identified in lower levels than the proinflammatory LTB4. Collectively, these findings demonstrate a diverse distribution of bioactive lipid mediators depending on the localization of human fat depots and uncover a specific SPM pattern closely associated with PVD.

Fibrogenesis marker PRO-C3 is higher in advanced liver fibrosis and improves in patients undergoing bariatric surgery

2021 ◽  
Author(s):  
Pierre Bel Lassen ◽  
Nicole Nori ◽  
Pierre Bedossa ◽  
Laurent Genser ◽  
Judith Aron-Wisnewsky ◽  
...  
Keyword(s):  
Bariatric Surgery ◽  
Adipose Tissue ◽  
Liver Fibrosis ◽  
Severe Obesity ◽  
Liver Enzymes ◽  
Nonalcoholic Fatty Liver ◽  
Omental Adipose Tissue ◽  
Advanced Liver Fibrosis ◽  
Liver Parameters

Abstract Objectives Serum propeptides of type III and type VI collagen (PRO-C3 and PRO-C6) are elevated in advanced nonalcoholic fatty liver disease, but their value in patients with severe obesity and their evolution after bariatric surgery (BS) is unknown. It is unclear if these markers of fibrogenesis are affected by adipose tissue fibrosis (ATF). We studied the association of PRO-C3 and PRO-C6 with liver fibrosis before BS, examined their evolution after BS and how much patients’ ATF contribute to their levels. Methods Serum PRO-C3 and PRO-C6 were measured in 158 BS patients and compared with liver, subcutaneous and omental adipose tissue histology obtained during surgery. PRO-C3 and PRO-C6 levels of 63 patients were determined in follow-up at 3 and 12 months post BS. Results Patients in the highest quartile of PRO-C3 had a higher risk of advanced liver fibrosis (stage F3-4; odds ratio 5.8; 95% CI [1.5-29.9]; p=0.017) compared to the lowest quartile (adjustment for age, gender and BMI). PRO-C3 was positively correlated with markers of insulin resistance and liver enzymes. After BS, PRO-C3 levels decreased in patients with high baseline liver fibrosis. This decrease correlated with improvement of metabolic and liver parameters. PRO-C6 was not related to stage of liver fibrosis. ATF did not correlate with PRO-C3 or PRO-C6 levels at baseline or after BS. Conclusions PRO-C3 was associated with advanced liver fibrosis in patients with severe obesity, and decreased after BS, without being affected by ATF. These data suggest that BS prominently eliminates drivers of hepatic fibrogenesis in NAFLD.

scholarly journals Relevance of Leptin and Other Adipokines in Obesity-Associated Cardiovascular Risk

Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2664 ◽  
Author(s):  
Manuel F. Landecho ◽  
Carlota Tuero ◽  
Víctor Valentí ◽  
Idoia Bilbao ◽  
Magdalena de la Higuera ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Adipose Tissue ◽  
The Body ◽  
Matrix Remodeling ◽  
Nonalcoholic Fatty Liver ◽  
Visceral Fat Accumulation ◽  
Vasoactive Factors ◽  
Increased Risk ◽  
Endocrine Organs ◽  
Adipocyte Hypertrophy

Obesity, which is a worldwide epidemic, confers increased risk for multiple serious conditions including type 2 diabetes, nonalcoholic fatty liver disease, and cardiovascular diseases. Adipose tissue is considered one of the largest endocrine organs in the body as well as an active tissue for cellular reactions and metabolic homeostasis rather than an inert tissue only for energy storage. The functional pleiotropism of adipose tissue relies on its ability to synthesize and release a large number of hormones, cytokines, extracellular matrix proteins, and growth and vasoactive factors, which are collectively called adipokines known to influence a variety of physiological and pathophysiological processes. In the obese state, excessive visceral fat accumulation causes adipose tissue dysfunctionality that strongly contributes to the onset of obesity-related comorbidities. The mechanisms underlying adipose tissue dysfunction include adipocyte hypertrophy and hyperplasia, increased inflammation, impaired extracellular matrix remodeling, and fibrosis together with an altered secretion of adipokines. This review describes the relevance of specific adipokines in the obesity-associated cardiovascular disease.

Adipose tissue blood flow and cellularity in the growing rabbit

1975 ◽  
Vol 229 (1) ◽  
pp. 107-112 ◽  
Author(s):  
M Digirolamo ◽  
J Esposito
Keyword(s):  
Blood Flow ◽  
Adipose Tissue ◽  
Cell Volume ◽  
Cell Number ◽  
Tissue Blood Flow ◽  
Tissue Composition ◽  
Fat Cell ◽  
Fat Depots ◽  
Wide Range ◽  
Definition Of

Resting blood flow was measured in isolated, innervated, epigastric fat-pads of 27 male rabbits during growth in the 1st yr of life and found to vary widely in range (7.6-28.1 ml/100 g tissue per min). Definition of adipose tissue composition and of fat-cell size and number made it possible to explain the wide range of flow and to identify two types of relationships between adipose blood flow and tissue constituents. Expressed in the usual manner (ml/100 g tissue per min), adipose blood flow declined with increasing adiposity of the fat depots, and a negative correlation was found between flow and fat-cell volume (r equals -.571, P less than .01). In contrast, when blood flow was expressed on the basis of fat-cell number (ml/108 fat cells/min), a positive and highly significant correlation was found between blood flow per fat cell and fat-cell volume (r equals .842, P less than .001). In the rabbit tissue the relationship of blood flow to fat-cell number and size was more predictable than the usual expression of flow in terms of tissue wet weight. Food deprivation for 18-24 h did not significantly alter these relationships. The results indicate that changes in adipose tissue composition and cellularity, resulting from growth and from accumulation of lipid in enlarging adipocytes, are important determinants of blood flow regulation to adipose tissue.

Qualitative regional differences in adipose tissue growth and cellularity in male Wistar rats fed ad libitum

1998 ◽  
Vol 274 (5) ◽  
pp. R1460-R1467 ◽  
Author(s):  
M. DiGirolamo ◽  
J. B. Fine ◽  
K. Tagra ◽  
R. Rossmanith
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Regional Differences ◽  
Wistar Rats ◽  
Cell Number ◽  
Tissue Growth ◽  
Fat Cell ◽  
Fat Depots ◽  
Male Wistar Rats ◽  
Ad Libitum

Adipose tissue grows primarily by a combination of increases in fat cell volume (hypertrophy) and in fat cell number (hyperplasia), but the regional growth pattern of white adipose tissue depots in animal species and in the human is still unclear. In this study we characterized fully the age-related changes in adipose tissue growth, composition, and cellularity of four fat depots of male Wistar rats that varied in age from 7 wk to 15 mo and in body weight from 178 to 808 g. Body weight and the weight of each of the four adipose depots studied (epididymal, mesenteric, subcutaneous inguinal, and retroperitoneal) increased progressively with age and ad libitum feeding. Comparison of the cellularity of the four adipose depots, however, showed remarkable and significant differences in the pattern of growth within the same animals. The cumulative growth of the two intra-abdominal fat depots (mesenteric and epididymal) was due mostly to hypertrophy (increases in cell volume of 83 and 64%, respectively), whereas the growth of the other two depots (retroperitoneal and inguinal) was due predominantly to hyperplasia (increases in cell number of 58 and 65%, respectively). These findings uncover major and unexpected regional differences in the modulation of adipose tissue growth within aging animals fed ad libitum and suggest local, region-specific regulatory controls of this growth.

scholarly journals Mitogen-Activated Protein Kinases, Inhibitory-κB Kinase, and Insulin Signaling in Human Omental Versus Subcutaneous Adipose Tissue in Obesity

Endocrinology ◽  
2007 ◽  
Vol 148 (6) ◽  
pp. 2955-2962 ◽  
Author(s):  
Nava Bashan ◽  
Karina Dorfman ◽  
Tanya Tarnovscki ◽  
Ilana Harman-Boehm ◽  
Idit F. Liberty ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Adipose Tissue ◽  
Body Mass ◽  
Obese Women ◽  
Fat Depots ◽  
Jun Kinase ◽  
Mitogen Activated Protein ◽  
Severely Obese ◽  
Fat Depot ◽  
Omental Fat

MAPKs and inhibitory-κB kinase (IKK) were suggested to link various conditions thought to develop in adipose tissue in obesity (oxidative, endoplasmic reticulum stress, inflammation) with insulin resistance. Yet whether in obesity these kinases are affected in a fat-depot-differential manner is unknown. We assessed the expression and phosphorylation of these kinases in paired omental and abdominal-sc fat biopsies from 48 severely obese women (body mass index > 32 kg/m2). Protein and mRNAs of p38MAPK, ERK, c-Jun kinase-1, and IKKβ were increased 1.5–2.5-fold in omental vs. sc fat. The phosphorylated (activated) forms of these kinases were also increased to similar magnitudes as the total expression. However, phosphorylation of insulin receptor substrate-1 on Ser312 (equivalent of murine Ser307) was not increased in omental, compared with sc, fat. Consistently, fat tissue fragments stimulated with insulin demonstrated that tyrosine phosphorylation and signal transduction to Akt/protein kinase B in omental fat was not inferior to that observable in sc fat. Comparison with lean women (body mass index 23.2 ± 2.9 kg/m2) revealed similar ERK2 and IKKβ expression and phosphorylation in both fat depots. However, as compared with lean controls, obese women exhibited 480 and 270% higher amount of the phosphorylated forms of p38MAPK and c-Jun kinase, respectively, in omental, but not sc, fat, and this expression level correlated with clinical parameters of glycemia and insulin sensitivity. Increased expression of stress-activated kinases and IKK and their phosphorylated forms in omental fat occurs in obesity, potentially contributing to differential roles of omental and sc fat in the pathophysiology of obesity.

Revisiting the adipocyte: a model for integration of cytokine signaling in the regulation of energy metabolism

2015 ◽  
Vol 309 (8) ◽  
pp. E691-E714 ◽  
Author(s):  
Amaia Rodríguez ◽  
Silvia Ezquerro ◽  
Leire Méndez-Giménez ◽  
Sara Becerril ◽  
Gema Frühbeck
Keyword(s):  
Extracellular Matrix ◽  
Adipose Tissue ◽  
Metabolic Diseases ◽  
Glucose Disposal ◽  
Cytokine Signaling ◽  
Matrix Remodeling ◽  
Nonalcoholic Fatty Liver ◽  
Brown Adipose ◽  
Wide Range ◽  
Beige Fat

Adipose tissue constitutes an extremely active endocrine organ with a network of signaling pathways enabling the organism to adapt to a wide range of different metabolic challenges, such as starvation, stress, infection, and short periods of gross energy excess. The functional pleiotropism of adipose tissue relies on its ability to synthesize and release a huge variety of hormones, cytokines, complement and growth factors, extracellular matrix proteins, and vasoactive factors, collectively termed adipokines. Obesity is associated with adipose tissue dysfunction leading to the onset of several pathologies including type 2 diabetes, dyslipidemia, nonalcoholic fatty liver, or hypertension, among others. The mechanisms underlying the development of obesity and its associated comorbidities include the hypertrophy and/or hyperplasia of adipocytes, adipose tissue inflammation, impaired extracellular matrix remodeling, and fibrosis together with an altered secretion of adipokines. Recently, the potential role of brown and beige adipose tissue in the protection against obesity has been also recognized. In contrast to white adipocytes, which store energy in the form of fat, brown and beige fat cells display energy-dissipating capacity through the promotion of triacylglycerol clearance, glucose disposal, and generation of heat for thermogenesis. Identification of the morphological and molecular changes in white, beige, and brown adipose tissue during weight gain is of utmost relevance for the identification of pharmacological targets for the treatment of obesity and its associated metabolic diseases.

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