Dead adipocytes, detected as crown-like structures, are prevalent in visceral fat depots of genetically obese mice

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Abstract

Accumulation of visceral fat is a key phenomenon in the onset of obesity-associated metabolic disorders. Macrophage infiltration induces chronic mild inflammation widely considered as a causative factor for insulin resistance and eventually diabetes. We previously showed that >90% of macrophages infiltrating the adipose tissue of obese animals and humans are arranged around dead adipocytes, forming characteristic crown-like structures (CLS). In this study we quantified CLS in visceral and subcutaneous depots from two strains of genetically obese mice, db/db and ob/ob. In both strains, CLS were prevalent in visceral compared with subcutaneous fat. Adipocyte size and CLS density exhibited a positive correlation both in visceral and in subcutaneous depots; however, the finding that adipocyte size was smallest and CLS density highest in visceral fat suggests a different susceptibility of visceral and subcutaneous adipocytes to death. Visceral fat CLS density was 3.4-fold greater in db/db than in ob/ob animals, which at the age at which our experimental strain was used are more prone to glucose metabolic disorders. Accumulation of visceral fat is a key phenomenon in the onset of obesity-associated metabolic disorders. Macrophage infiltration induces chronic mild inflammation widely considered as a causative factor for insulin resistance and eventually diabetes. We previously showed that >90% of macrophages infiltrating the adipose tissue of obese animals and humans are arranged around dead adipocytes, forming characteristic crown-like structures (CLS). In this study we quantified CLS in visceral and subcutaneous depots from two strains of genetically obese mice, db/db and ob/ob. In both strains, CLS were prevalent in visceral compared with subcutaneous fat. Adipocyte size and CLS density exhibited a positive correlation both in visceral and in subcutaneous depots; however, the finding that adipocyte size was smallest and CLS density highest in visceral fat suggests a different susceptibility of visceral and subcutaneous adipocytes to death. Visceral fat CLS density was 3.4-fold greater in db/db than in ob/ob animals, which at the age at which our experimental strain was used are more prone to glucose metabolic disorders. The incidence of obesity is rapidly increasing all over the world (1Bray G.A. Bellanger T. Epidemiology, trends, and morbidities of obesity and the metabolic syndrome.Endocrine. 2006; 29: 109-117Crossref PubMed Scopus (345) Google Scholar, 2Hill J.O. Understanding and addressing the epidemic of obesity: an energy balance perspective.Endocr. Rev. 2006; 27: 750-761Crossref PubMed Scopus (426) Google Scholar). The phenomenon is a major public health concern, mainly because it carries an increased risk of death from obesity-associated disorders (3Shetty P. Schmidhuber J. Introductory lecture the epidemiology and determinants of obesity in developed and developing countries.Int. J. Vitam. Nutr. Res. 2006; 76: 157-162Crossref PubMed Scopus (25) Google Scholar, 4Kuk J.L. Associations between abdominal adiposity, exercise, morbidity, and mortality.Appl. Physiol. Nutr. Metab. 2007; 32: 1210-1211Crossref Google Scholar). Obesity is frequently associated with metabolic syndrome; insulin resistance is widely suspected as the central starting event of the condition (1Bray G.A. Bellanger T. Epidemiology, trends, and morbidities of obesity and the metabolic syndrome.Endocrine. 2006; 29: 109-117Crossref PubMed Scopus (345) Google Scholar). Although the adipose organ of obese animals and humans is increased at both subcutaneous and visceral sites, visceral fat alone is responsible for the metabolic consequences of obesity (5Bjorntorp P. Rosmond R. Visceral obesity and diabetes.Drugs. 1999; 58 (Suppl.): 13-18Crossref PubMed Scopus (71) Google Scholar, 6Rodriguez A. Catalan V. Gomez-Ambrosi J. Fruhbeck G. Visceral and subcutaneous adiposity: are both potential therapeutic targets for tackling the metabolic syndrome?.Curr. Pharm. Des. 2007; 13: 2169-2175Crossref PubMed Scopus (120) Google Scholar, 7Thorne A. Lonnqvist F. Apelman J. Hellers G. Arner P. A pilot study of long-term effects of a novel obesity treatment: omentectomy in connection with adjustable gastric banding.Int. J. Obes. Relat. Metab. Disord. 2002; 26: 193-199Crossref PubMed Scopus (266) Google Scholar, 8Frayn K.N. Visceral fat and insulin resistance—causative or correlative?.Br. J. Nutr. 2000; 83 (Suppl.): 71-77Crossref PubMed Scopus (368) Google Scholar, 9Wajchenberg B.L. Subcutaneous and visceral adipose tissue: their relation to the metabolic syndrome.Endocr. Rev. 2000; 21: 697-738Crossref PubMed Scopus (2224) Google Scholar). The reasons for this effect are unclear. It has recently been shown that the adipose tissue of obese animals and humans is infiltrated by a pure macrophage population of bone marrow origin (10Weisberg S.P. McCann D. Desai M. Rosenbaum M. Leibel R.L. Ferrante Jr., A.W. Obesity is associated with macrophage accumulation in adipose tissue.J. Clin. Invest. 2003; 112: 1796-1808Crossref PubMed Scopus (7562) Google Scholar, 11Cinti S. Mitchell G. Barbatelli G. Murano I. Ceresi E. Faloia E. Wang S. Fortier M. Greenberg A.S. Obin M.S. Adipocyte death defines macrophage localization and function in adipose tissue of obese mice and humans.J. Lipid Res. 2005; 46: 2347-2355Abstract Full Text Full Text PDF PubMed Scopus (1792) Google Scholar, 12Yu R. Kim C.S. Kwon B.S. Kawada T. Mesenteric adipose tissue-derived monocyte chemoattractant protein-1 plays a crucial role in adipose tissue macrophage migration and activation in obese mice.Obesity (Silver Spring). 2006; 14: 1353-1362Crossref PubMed Scopus (145) Google Scholar, 13Chen A. Mumick S. Zhang C. Lamb J. Dai H. Weingarth D. Mudgett J. Chen H. MacNeil D.J. Reitman M.L. et al.Diet induction of monocyte chemoattractant protein-1 and its impact on obesity.Obes. Res. 2005; 13: 1311-1320Crossref PubMed Scopus (183) Google Scholar, 14R Cancello Taleb S. Poitou C. Tordjman J. Lacasa D. Guerre-Millo M. Clement K. [Is obesity an inflammatory disease?].Journ. Annu. Diabetol. Hotel Dieu. 2006; : 115-128PubMed Google Scholar) expressing C-C chemokine receptor 2 (CCR2) (15Lumeng C.N. Bodzin J.L. Saltiel A.R. Obesity induces a phenotypic switch in adipose tissue macrophage polarization.J. Clin. Invest. 2007; 117: 175-184Crossref PubMed Scopus (3401) Google Scholar). This phenomenon correlates with adipocyte size and body mass index (10Weisberg S.P. McCann D. Desai M. Rosenbaum M. Leibel R.L. Ferrante Jr., A.W. Obesity is associated with macrophage accumulation in adipose tissue.J. Clin. Invest. 2003; 112: 1796-1808Crossref PubMed Scopus (7562) Google Scholar). It is especially important because it is temporally associated with the appearance of insulin resistance (10Weisberg S.P. McCann D. Desai M. Rosenbaum M. Leibel R.L. Ferrante Jr., A.W. Obesity is associated with macrophage accumulation in adipose tissue.J. Clin. Invest. 2003; 112: 1796-1808Crossref PubMed Scopus (7562) Google Scholar, 16Xu H. Barnes G.T. Yang Q. Tan G. Yang D. Chou C.J. Sole J. Nichols A. Ross J.S. Tartaglia L.A. et al.Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance.J. Clin. Invest. 2003; 112: 1821-1830Crossref PubMed Scopus (5240) Google Scholar, 17Goossens G.H. The role of adipose tissue dysfunction in the pathogenesis of obesity-related insulin resistance.Physiol. Behav. 2007; (Epub ahead of print. October 22. doi: 10.1016/j.physbeh.2007.10.010.)PubMed Google Scholar). Furthermore, some cytokines held to have an important role in the pathogenesis of insulin resistance (TNF-α, IL-6, iNOS) seem to be more abundantly expressed in the macrophage-containing stromal-vascular part of adipose tissue than in the mature adipocyte fraction, suggesting that macrophages, not adipocytes, are the main producers of the cytokines responsible for the onset of insulin resistance (10Weisberg S.P. McCann D. Desai M. Rosenbaum M. Leibel R.L. Ferrante Jr., A.W. Obesity is associated with macrophage accumulation in adipose tissue.J. Clin. Invest. 2003; 112: 1796-1808Crossref PubMed Scopus (7562) Google Scholar, 16Xu H. Barnes G.T. Yang Q. Tan G. Yang D. Chou C.J. Sole J. Nichols A. Ross J.S. Tartaglia L.A. et al.Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance.J. Clin. Invest. 2003; 112: 1821-1830Crossref PubMed Scopus (5240) Google Scholar). Recent immunohistochemical experiments have confirmed that TNF-α and IL-6 are confined to macrophage-containing areas in the adipose tissue of obese mice (18Strissel K.J. Stancheva Z. Miyoshi H. Perfield 2nd, J.W. DeFuria J. Jick Z. Greenberg A.S. Obin M.S. Adipocyte death, adipose tissue remodeling, and obesity complications.Diabetes. 2007; 56: 2910-2918Crossref PubMed Scopus (700) Google Scholar). The reason for macrophage infiltration of obese adipose tissue was largely unknown until our group observed that the vast majority (>90%) of macrophages in obese mice and humans are found around dead adipocytes, where they may be resorbing the lipid remnants of these cells (11Cinti S. Mitchell G. Barbatelli G. Murano I. Ceresi E. Faloia E. Wang S. Fortier M. Greenberg A.S. Obin M.S. Adipocyte death defines macrophage localization and function in adipose tissue of obese mice and humans.J. Lipid Res. 2005; 46: 2347-2355Abstract Full Text Full Text PDF PubMed Scopus (1792) Google Scholar). This biological reaction results in characteristic morphological elements that we termed crown-like structures (CLS). CLS are easy to recognize at the light microscopic level, especially when macrophages are immunolabeled with specific antibodies. CLS thus identify dead adipocytes, and their number is a fair indication of the number of dead adipocytes and macrophages infiltrating the obese adipose tissue. If the cytokines responsible for insulin resistance are indeed produced by macrophages, CLS should be preponderant in visceral depots compared with subcutaneous fat in obese animals. Two recent papers seem to support this hypothesis, although one examined a visceral depot that is not found in humans (18Strissel K.J. Stancheva Z. Miyoshi H. Perfield 2nd, J.W. DeFuria J. Jick Z. Greenberg A.S. Obin M.S. Adipocyte death, adipose tissue remodeling, and obesity complications.Diabetes. 2007; 56: 2910-2918Crossref PubMed Scopus (700) Google Scholar) and the other analyzed only a small amount of adipose tissue in a heterogeneous population (19Harman-Boehm I. Bluher M. Redel H. Sion-Vardy N. Ovadia S. Avinoach E. Shai I. Kloting N. Stumvoll M. Bashan N. et al.Macrophage infiltration into omental versus subcutaneous fat across different populations: effect of regional adiposity and the comorbidities of obesity.J. Clin. Endocrinol. Metab. 2007; 92: 2240-2247Crossref PubMed Scopus (450) Google Scholar). In this study, we thoroughly examined the visceral and subcutaneous fat depots of two different types of obese mice, db/db (strain Ks) and ob/ob (strain 6J), to establish whether dead adipocytes surrounded by macrophages (i.e., CLS) are more numerous in visceral than in subcutaneous fat. Such a finding would further support the adverse effect of visceral depots. We analyzed a large amount of adipose tissue from the depots that are most frequently responsible for human visceral obesity, whose portal drainage may have an important role in the pathogenesis of obesity-associated metabolic disorders. Twenty 14 week-old female mice were purchased from Harlan (Udine, Italy): five obese B6.V-Lepob/OlaHsd (hereafter ob/ob) and five lean control mice; five diabetic BKS.Cg−+Leprdb/+Leprdb/OlaHsd (db/db) and five lean control mice. Their weight is reported in Fig. 1. All animal procedures were in accordance with National Institute of Medical Research guidelines. Mice were euthanized with an overdose of anesthetic (Avertin; Fluka Chemie, Buchs, Switzerland) and immediately perfused with 4% paraformaldehyde in 0.1 M phosphate buffer (PB), pH 7.4, for 5 min. Subcutaneous (inguinal) and visceral (mesenteric, omental, and perirenal) white adipose tissue depots were dissected using a Zeiss OPI1 surgical microscope (Carl Zeiss, Oberkochen, Germany) and assessed by light microscopy, immunohistochemistry, and morphometry. The omental depot is seldom investigated in mouse studies (20Crossno Jr., J.T. Majka S.M. Grazia T. Gill R.G. Klemm D.J. Rosiglitazone promotes development of a novel adipocyte population from bone marrow-derived circulating progenitor cells.J. Clin. Invest. 2006; 116: 3220-3228Crossref PubMed Scopus (211) Google Scholar), owing to its small size in these animals. Its anatomical site corresponds to that of other mammals, man included; its gross anatomy is shown in Fig. 2. After dissection, depots were further fixed by immersion in 4% paraformaldehyde in 0.1 M sodium PB, pH 7.4, overnight at 4°C, then dehydrated, cleared, and paraffin embedded. Two visceral depots with portal drainage (mesenteric and omental) (Fig. 2), a visceral depot with systemic drainage (perirenal) as well as the principal mouse subcutaneous depot (inguinal) were studied. Three sections from different levels (every 0.5 mm) of each depot were analyzed for adipocyte size and CLS density. For each level, 3 μm-thick serial sections were obtained, one for hematoxylin and eosin staining to assess morphology, and the others for immunohistochemical processing. Adipocyte size was calculated as the mean adipocyte area of 300 random adipocytes (100 per section) in each mouse using a drawing tablet and the Nikon LUCIA IMAGE (version 4.61; Laboratory Imaging, Praha, Czech Republic) of the morphometric program. Tissue sections were observed with a Nikon Eclipse E800 light microscope using a ×20 objective, and digital images were captured with a Nikon DXM 1200 camera. CLS density was obtained by counting the total number of CLS in each section compared with the total number of adipocytes and was expressed as CLS number/10,000 adipocytes. For immunohistochemistry, 3 μm dewaxed serial sections were incubated with anti-MAC-2 (1:2,800; Cedarlane Laboratories, Paletta Court, Burlington,Ontario, Canada) and anti-perilipin (PREK 1:300, AS Greenberg, Boston,MA) primary antibodies according to the Avidin Biotin Complex method (16Xu H. Barnes G.T. Yang Q. Tan G. Yang D. Chou C.J. Sole J. Nichols A. Ross J.S. Tartaglia L.A. et al.Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance.J. Clin. Invest. 2003; 112: 1821-1830Crossref PubMed Scopus (5240) Google Scholar), as previously described (11Cinti S. Mitchell G. Barbatelli G. Murano I. Ceresi E. Faloia E. Wang S. Fortier M. Greenberg A.S. Obin M.S. Adipocyte death defines macrophage localization and function in adipose tissue of obese mice and humans.J. Lipid Res. 2005; 46: 2347-2355Abstract Full Text Full Text PDF PubMed Scopus (1792) Google Scholar). We used 3% hydrogen to by or to serial sections were incubated overnight with and anti-perilipin primary antibodies. antibodies were and were using and as were with tissue were fixed in paraformaldehyde in 0.1 M PB, pH 7.4, for in and in an sections were with sections were obtained with an with and examined with a microscope The are as mean between group were analyzed by between were considered when were calculated by correlation using for The body weight of the two strains of obese animals and was not although both strains were than the (Fig. In lean mice, white adipocyte size was in all fat depots mouse adipocytes were (Fig. than of their In both genetically obese mouse strains, white adipocytes were than in lean mice in all fat depots (Fig. In db/db mice, adipocytes were in omental in and in the was in subcutaneous fat were in obese than in lean mice in omental in and in the size was in the subcutaneous depots that adipocyte size was greater in the subcutaneous depots of both strains than in the visceral both in and in obese mice (Fig. macrophages were found in all depots of lean and obese mice. than were CLS (Fig. surrounded dead adipocytes of lipid remnants and all the and microscopic described in our (11Cinti S. Mitchell G. Barbatelli G. Murano I. Ceresi E. Faloia E. Wang S. Fortier M. Greenberg A.S. Obin M.S. Adipocyte death defines macrophage localization and function in adipose tissue of obese mice and humans.J. Lipid Res. 2005; 46: 2347-2355Abstract Full Text Full Text PDF PubMed Scopus (1792) Google Scholar). adipocytes and macrophage infiltration in fat depots were quantified by CLS density as CLS number/10,000 adipocytes (Fig. Fig. CLS were more numerous in visceral than in subcutaneous fat in both mouse strains The in CLS density was found between the subcutaneous depots and the and depots in db/db mice, and between the subcutaneous depots and the and omental depots in ob/ob light microscopic of CLS found in the depot of a obese mouse macrophages around remnants of lipid of dead adipocytes. anti-MAC-2 antibodies Avidin Biotin Complex method in tissue. images from omental and and and fat depots of lean and obese mice by CLS are by only when than were found in the images from omental and and and fat depots of lean and obese mice by CLS are by only when than were found in the Such of dead adipocytes and macrophage infiltration was because visceral depots exhibited the smallest adipocytes (Fig. the positive correlation found between adipocyte size and CLS density in both visceral and subcutaneous depots (Fig. CLS density in the visceral depots of db/db mice was 3.4-fold greater than in the visceral depots of ob/ob mice CLS number/10,000 The was found in the where CLS density was greater in the animals. CLS density in the omental and depots of db/db mice was that of ob/ob mice It is well that metabolic disorders in obese are most associated with visceral fat accumulation (5Bjorntorp P. Rosmond R. Visceral obesity and diabetes.Drugs. 1999; 58 (Suppl.): 13-18Crossref PubMed Scopus (71) Google Scholar, 6Rodriguez A. Catalan V. Gomez-Ambrosi J. Fruhbeck G. Visceral and subcutaneous adiposity: are both potential therapeutic targets for tackling the metabolic syndrome?.Curr. Pharm. Des. 2007; 13: 2169-2175Crossref PubMed Scopus (120) Google Scholar, 7Thorne A. Lonnqvist F. Apelman J. Hellers G. Arner P. A pilot study of long-term effects of a novel obesity treatment: omentectomy in connection with adjustable gastric banding.Int. J. Obes. Relat. Metab. Disord. 2002; 26: 193-199Crossref PubMed Scopus (266) Google Scholar, 8Frayn K.N. Visceral fat and insulin resistance—causative or correlative?.Br. J. Nutr. 2000; 83 (Suppl.): 71-77Crossref PubMed Scopus (368) Google Scholar, 9Wajchenberg B.L. Subcutaneous and visceral adipose tissue: their relation to the metabolic syndrome.Endocr. Rev. 2000; 21: 697-738Crossref PubMed Scopus (2224) Google Scholar). is for the that the mild chronic inflammation of adipose tissue in obese and animals is associated with insulin which is the main of the other metabolic disorders (16Xu H. Barnes G.T. Yang Q. Tan G. Yang D. Chou C.J. Sole J. Nichols A. Ross J.S. Tartaglia L.A. et al.Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance.J. Clin. Invest. 2003; 112: 1821-1830Crossref PubMed Scopus (5240) Google Scholar, J. Chen of the of in adipose tissue of obesity and insulin J. Physiol. Endocrinol. Metab. 2007; PubMed Scopus Google Scholar, M. C. Kim M. H. J. Recent in the between obesity, and insulin 2006; Google Scholar). A has been shown between adipose tissue infiltration by macrophages weight and onset of insulin resistance (10Weisberg S.P. McCann D. Desai M. Rosenbaum M. Leibel R.L. Ferrante Jr., A.W. Obesity is associated with macrophage accumulation in adipose tissue.J. Clin. Invest. 2003; 112: 1796-1808Crossref PubMed Scopus (7562) Google Scholar, 16Xu H. Barnes G.T. Yang Q. Tan G. Yang D. Chou C.J. Sole J. Nichols A. Ross J.S. Tartaglia L.A. et al.Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance.J. Clin. Invest. 2003; 112: 1821-1830Crossref PubMed Scopus (5240) Google Scholar, 17Goossens G.H. The role of adipose tissue dysfunction in the pathogenesis of obesity-related insulin resistance.Physiol. Behav. 2007; (Epub ahead of print. October 22. doi: 10.1016/j.physbeh.2007.10.010.)PubMed Google Scholar). In a we showed that >90% of macrophages infiltrating the adipose tissue of obese humans and animals are found around dead adipocytes, forming characteristic elements that we termed crown-like structures (11Cinti S. Mitchell G. Barbatelli G. Murano I. Ceresi E. Faloia E. Wang S. Fortier M. Greenberg A.S. Obin M.S. Adipocyte death defines macrophage localization and function in adipose tissue of obese mice and humans.J. Lipid Res. 2005; 46: 2347-2355Abstract Full Text Full Text PDF PubMed Scopus (1792) Google Scholar). of CLS a number of the macrophages infiltrating the fat depots. In this of different visceral and subcutaneous fat depots of two strains of genetically obese mice that visceral depots are the prevalent of adipocyte death and macrophage The that the incidence of metabolic disorders associated with visceral fat accumulation be to a greater susceptibility to death of the adipocytes found at this anatomical site compared with found in the subcutaneous This is in with the that adipocytes found in different depots have different T. J.L. in potential impact of 2007; PubMed Scopus Google Scholar, B.L. D. E. and R. F. M. of subcutaneous and visceral adipose tissue and their relation to the metabolic Metab. Res. 2002; PubMed Scopus Google Scholar). Visceral adipocytes have been to be than their subcutaneous both in lean and in obese animals J. of adipose depots in strains of genetically obese Lipid Res. 13: Full Text PDF PubMed Google Scholar), and our are with this visceral adipocytes were to be The positive correlation found between adipocyte size and CLS density in all depots suggests that increased adipocyte size is the factor macrophage as in other studies (10Weisberg S.P. McCann D. Desai M. Rosenbaum M. Leibel R.L. Ferrante Jr., A.W. Obesity is associated with macrophage accumulation in adipose tissue.J. Clin. Invest. 2003; 112: 1796-1808Crossref PubMed Scopus (7562) Google Scholar). This suggests that visceral adipocytes the size death subcutaneous adipocytes. The that adipocytes with greater insulin resistance J.S. N. J. size and insulin levels in obese and PubMed Scopus Google Scholar) thus to be in its with recent on CLS density in a visceral and a subcutaneous depot in mice an (18Strissel K.J. Stancheva Z. Miyoshi H. Perfield 2nd, J.W. DeFuria J. Jick Z. Greenberg A.S. Obin M.S. Adipocyte death, adipose tissue remodeling, and obesity complications.Diabetes. 2007; 56: 2910-2918Crossref PubMed Scopus (700) Google however, the depot is not found in humans and is not with portal with systemic A recent a visceral versus subcutaneous macrophage infiltration in obese human (19Harman-Boehm I. Bluher M. Redel H. Sion-Vardy N. Ovadia S. Avinoach E. Shai I. Kloting N. Stumvoll M. Bashan N. et al.Macrophage infiltration into omental versus subcutaneous fat across different populations: effect of regional adiposity and the comorbidities of obesity.J. Clin. Endocrinol. Metab. 2007; 92: 2240-2247Crossref PubMed Scopus (450) Google Scholar). have that the in and potential to shown by the different fat depots may be to regional in T. J.L. in potential impact of 2007; PubMed Scopus Google Scholar, M. The of white adipocyte Rev. PubMed Scopus Google Scholar). The greater of visceral compared with subcutaneous adipocytes to thus be by different fat depots. most other genetically obese mice, et (18Strissel K.J. Stancheva Z. Miyoshi H. Perfield 2nd, J.W. DeFuria J. Jick Z. Greenberg A.S. Obin M.S. Adipocyte death, adipose tissue remodeling, and obesity complications.Diabetes. 2007; 56: 2910-2918Crossref PubMed Scopus (700) Google Scholar), recently reported that fat macrophage infiltration in mice a different at different be It is to that CLS density in the visceral depots of db/db mice was than in ob/ob mice. Although we not db/db mice with the and at the age of used in the study seem to a more B.L. of (db/db) and obese of female Tissue Res. PubMed Scopus Google Scholar). In our that a positive correlation between size of adipocytes and macrophage infiltration both in visceral and in subcutaneous the visceral depots a more adipocytes in visceral depots are than found in subcutaneous depots. The susceptibility of visceral adipocytes to death be to different of the different and be to the appearance of metabolic as by other (18Strissel K.J. Stancheva Z. Miyoshi H. Perfield 2nd, J.W. DeFuria J. Jick Z. Greenberg A.S. Obin M.S. Adipocyte death, adipose tissue remodeling, and obesity complications.Diabetes. 2007; 56: 2910-2918Crossref PubMed Scopus (700) Google Scholar, I. Bluher M. Redel H. Sion-Vardy N. Ovadia S. Avinoach E. Shai I. Kloting N. Stumvoll M. Bashan N. et al.Macrophage infiltration into omental versus subcutaneous fat across different populations: effect of regional adiposity and the comorbidities of obesity.J. Clin. Endocrinol. Metab. 2007; 92: 2240-2247Crossref PubMed Scopus (450) Google Scholar). The are to F. and R. of for the

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The record

Venue

Journal of Lipid Research

Topic

Adipokines, Inflammation, and Metabolic Diseases

Field

Medicine

Canadian institutions

—

Funders

Università Politecnica delle Marche

Keywords

AdipocyteAdipose tissueInternal medicineEndocrinologyCLs upper limitsInflammationObesityInsulin resistanceDiabetes mellitusVisceral fatMedicineBiology

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