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Lipodystrophy and Fat Redistribution: From Molecular Basis to Therapies 2.0
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Lipodystrophy and Fat Redistribution: From Molecular Basis to Therapies 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (31 August 2022) | Viewed by 4064

Special Issue Editor

Dr. Elena Bresciani

E-Mail Website
Guest Editor
Department of Medicine and Surgery, University of Milano-Bicocca, 20900 Monza, Italy
Interests: pharmacology; molecular biology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Lipodystrophy encompasses a variety of disorders characterized by different degrees of body fat loss and predisposing to insulin resistance and its metabolic complications as well as diabetes, hypertriglyceridemia, and hepatic steatosis. The lipodystrophies could be of genetic or acquired origin. Among those acquired, highly active antiretroviral therapy (HART)-induced lipodystrophy in HIV-infected patients is a common subtype. Recent advances have led to the discovery of new genes associated with lipodystrophy and have improved the knowledge of underlying processes regulating adipose cells biology, differentiation, lipid droplet assembly, and metabolism. The effects of recent drugs used in HIV infection management on adipose tissue metabolism must still be investigated, however.

Original manuscripts and reviews dealing with specific and/or systematic aspects of adipose tissue phenotype alteration/redistribution, metabolism, hormonal or drug-related pathophysiology ranging from basic to translational or clinical research are very welcome from outstanding experts of the topic.

Dr. Elena Bresciani
Guest Editor

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Keywords

  • lipodystrophy
  • adipose tissue redistribution
  • metabolic alterations
  • mechanism of disease
  • highly active antiretroviral therapy (HART)

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Related Special Issue

Published Papers (6 papers)

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Research

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17 pages, 1318 KiB  
Article
The Longitudinal Changes in Subcutaneous Abdominal Tissue and Visceral Adipose Tissue Volumetries Are Associated with Iron Status
by Alejandro Hinojosa-Moscoso, Anna Motger-Albertí, Elena De la Calle-Vargas, Marian Martí-Navas, Carles Biarnés, María Arnoriaga-Rodríguez, Gerard Blasco, Josep Puig, Diego Luque-Córdoba, Feliciano Priego-Capote, José María Moreno-Navarrete and José Manuel Fernández-Real
Int. J. Mol. Sci. 2023, 24(5), 4750; https://doi.org/10.3390/ijms24054750 - 1 Mar 2023
Cited by 3 | Viewed by 3393
Abstract
Excess iron is known to trigger adipose tissue dysfunction and insulin resistance. Circulating markers of iron status have been associated with obesity and adipose tissue in cross-sectional studies. We aimed to evaluate whether iron status is linked to changes in abdominal adipose tissue [...] Read more.
Excess iron is known to trigger adipose tissue dysfunction and insulin resistance. Circulating markers of iron status have been associated with obesity and adipose tissue in cross-sectional studies. We aimed to evaluate whether iron status is linked to changes in abdominal adipose tissue longitudinally. Subcutaneous abdominal tissue (SAT) and visceral adipose tissue (VAT) and its quotient (pSAT) were assessed using magnetic resonance imaging (MRI), at baseline and after one year of follow-up, in 131 (79 in follow-up) apparently healthy subjects, with and without obesity. Insulin sensitivity (euglycemic– hyperinsulinemic clamp) and markers of iron status were also evaluated. Baseline serum hepcidin (p = 0.005 and p = 0.002) and ferritin (p = 0.02 and p = 0.01)) were associated with an increase in VAT and SAT over one year in all subjects, while serum transferrin (p = 0.01 and p = 0.03) and total iron-binding capacity (p = 0.02 and p = 0.04) were negatively associated. These associations were mainly observed in women and in subjects without obesity, and were independent of insulin sensitivity. After controlling for age and sex, serum hepcidin was significantly associated with changes in subcutaneous abdominal tissue index (iSAT) (β = 0.406, p = 0.007) and visceral adipose tissue index (iVAT) (β = 0.306, p = 0.04), while changes in insulin sensitivity (β = 0.287, p = 0.03) and fasting triglycerides (β = −0.285, p = 0.03) were associated with changes in pSAT. These data indicated that serum hepcidin are associated with longitudinal changes in SAT and VAT, independently of insulin sensitivity. This would be the first prospective study evaluating the redistribution of fat according to iron status and chronic inflammation. Full article
(This article belongs to the Special Issue Lipodystrophy and Fat Redistribution: From Molecular Basis to Therapies 2.0)
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13 pages, 1549 KiB  
Article
eNAMPT Is Localised to Areas of Cartilage Damage in Patients with Hip Osteoarthritis and Promotes Cartilage Catabolism and Inflammation
by Ashleigh M. Philp, Sam Butterworth, Edward T. Davis and Simon W. Jones
Int. J. Mol. Sci. 2021, 22(13), 6719; https://doi.org/10.3390/ijms22136719 - 23 Jun 2021
Cited by 10 | Viewed by 3017
Abstract
Obesity increases the risk of hip osteoarthritis (OA). Recent studies have shown that adipokine extracellular nicotinamide phosphoribosyltransferase (eNAMPT or visfatin) induces the production of IL-6 and matrix metalloproteases (MMPs) in chondrocytes, suggesting it may promote articular cartilage degradation. However, neither the functional effects [...] Read more.
Obesity increases the risk of hip osteoarthritis (OA). Recent studies have shown that adipokine extracellular nicotinamide phosphoribosyltransferase (eNAMPT or visfatin) induces the production of IL-6 and matrix metalloproteases (MMPs) in chondrocytes, suggesting it may promote articular cartilage degradation. However, neither the functional effects of extracellular visfatin on human articular cartilage tissue, nor its expression in the joint of hip OA patients of varying BMI, have been reported. Hip OA joint tissues were collected from patients undergoing joint replacement surgery. Cartilage explants were stimulated with recombinant human visfatin. Pro-inflammatory cytokines and MMPs were measured by ELISA and Luminex. Localisation of visfatin expression in cartilage tissue was determined by immunohistochemistry. Cartilage matrix degradation was determined by quantifying proteoglycan release. Expression of visfatin was elevated in the synovial tissue of hip OA patients who were obese, and was co-localised with MMP-13 in areas of cartilage damage. Visfatin promoted the degradation of hip OA cartilage proteoglycan and induced the production of pro-inflammatory cytokines (IL-6, MCP-1, CCL20, and CCL4) and MMPs. The elevated expression of visfatin in the obese hip OA joint, and its functional effects on hip cartilage tissue, suggests it plays a central role in the loss of cartilage integrity in obese patients with hip OA. Full article
(This article belongs to the Special Issue Lipodystrophy and Fat Redistribution: From Molecular Basis to Therapies)
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14 pages, 23159 KiB  
Article
Complement Factor D (adipsin) Levels Are Elevated in Acquired Partial Lipodystrophy (Barraquer–Simons syndrome)
by Fernando Corvillo, Laura González-Sánchez, Alberto López-Lera, Emilia Arjona, Giovanni Ceccarini, Ferruccio Santini, David Araújo-Vilar, Rebecca J Brown, Joan Villarroya, Francesc Villarroya, Santiago Rodríguez de Córdoba, Teresa Caballero, Pilar Nozal and Margarita López-Trascasa
Int. J. Mol. Sci. 2021, 22(12), 6608; https://doi.org/10.3390/ijms22126608 - 21 Jun 2021
Cited by 8 | Viewed by 3141
Abstract
Complement overactivation has been reported in most patients with Barraquer–Simons syndrome (BSS), a rare form of acquired partial lipodystrophy. Complement Factor D (FD) is a serine protease with a crucial role in the activation of the alternative pathway of the complement system, which [...] Read more.
Complement overactivation has been reported in most patients with Barraquer–Simons syndrome (BSS), a rare form of acquired partial lipodystrophy. Complement Factor D (FD) is a serine protease with a crucial role in the activation of the alternative pathway of the complement system, which is mainly synthesized by adipose tissue. However, its role in the pathogenesis of BSS has not been addressed. In this study, plasma FD concentration was measured in 13 patients with BSS, 20 patients with acquired generalized lipodystrophy, 22 patients with C3 glomerulopathy (C3G), and 50 healthy controls. Gene expression and immunohistochemistry studies were assayed using atrophied adipose tissue from a patient with BSS. We found significantly elevated FD levels in BSS cases compared with the remaining cohorts (p < 0.001). There were no significant differences in FD levels between sexes but FD was strongly and directly associated with age in BSS (r = 0.7593, p = 0.0036). A positive correlation between FD and C3 was seen in patients with C3G, characterized by decreased FD levels due to chronic C3 consumption, but no correlation was detected for BSS. Following mRNA quantification in the patient’s adipose tissue, we observed decreased CFD and C3 but elevated C5 transcript levels. In contrast, the increased FD staining detected in the atrophied areas reflects the effects of persistent tissue damage on the adipose tissue, thus providing information on the ongoing pathogenic process. Our results suggest that FD could be a reliable diagnostic biomarker involved in the pathophysiology of BSS by promoting unrestrained local complement system activation in the adipose tissue environment. Full article
(This article belongs to the Special Issue Lipodystrophy and Fat Redistribution: From Molecular Basis to Therapies)
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15 pages, 6397 KiB  
Article
Cellular Mechanism Underlying Highly-Active or Antiretroviral Therapy-Induced Lipodystrophy: Atazanavir, a Protease Inhibitor, Compromises Adipogenic Conversion of Adipose-Derived Stem/Progenitor Cells through Accelerating ER Stress-Mediated Cell Death in Differentiating Adipocytes
by Sadanori Akita, Keiji Suzuki, Hiroshi Yoshimoto, Akira Ohtsuru, Akiyoshi Hirano and Shunichi Yamashita
Int. J. Mol. Sci. 2021, 22(4), 2114; https://doi.org/10.3390/ijms22042114 - 20 Feb 2021
Cited by 7 | Viewed by 2644
Abstract
Lipodystrophy is a common complication in human immunodeficiency virus (HIV)-infected patients receiving highly active antiretroviral therapy (HAART) or antiretroviral therapy (ART). Previous studies demonstrated that endoplasmic reticulum (ER) stress-mediated unfolded protein response (UPR) is involved in lipodystrophy; however, the detailed mechanism has not [...] Read more.
Lipodystrophy is a common complication in human immunodeficiency virus (HIV)-infected patients receiving highly active antiretroviral therapy (HAART) or antiretroviral therapy (ART). Previous studies demonstrated that endoplasmic reticulum (ER) stress-mediated unfolded protein response (UPR) is involved in lipodystrophy; however, the detailed mechanism has not been fully described in human adipogenic cell lineage. We utilized adipose tissue-derived stem cells (ADSCs) obtained from human subcutaneous adipose tissue, and atazanavir (ATV), a protease inhibitor (PI), was administered to ADSCs and ADSCs undergoing adipogenic conversion. Marked repression of adipogenic differentiation was observed when ATV was administered during 10 days of ADSC culture in adipogenic differentiation medium. Although ATV had no effect on ADSCs, it significantly induced apoptosis in differentiating adipocytes. ATV treatment also caused the punctate appearance of CCAAT-enhancer-binding (C/EBP) protein homologous protein (CHOP), and altered expression of CHOP and GRP78/Bip, which are the representation of ER stress, only in differentiating adipocytes. Administration of UPR inhibitors restored adipogenic differentiation, indicating that ER stress-mediated UPR was induced in differentiating adipocytes in the presence of ATV. We also observed autophagy, which was potentiated in differentiating adipocytes by ATV treatment. Thus, adipogenic cell atrophy leads to ATV-induced lipodystrophy, which is mediated by ER stress-mediated UPR and accelerated autophagy, both of which would cause adipogenic apoptosis. As our study demonstrated for the first time that ADSCs are unsusceptible to ATV and its deleterious effects are limited to the differentiating adipocytes, responsible target(s) for ATV-induced lipodystrophy may be protease(s) processing adipogenesis-specific protein(s). Full article
(This article belongs to the Special Issue Lipodystrophy and Fat Redistribution: From Molecular Basis to Therapies)
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19 pages, 4032 KiB  
Article
White Adipose Tissue Expansion in Multiple Symmetric Lipomatosis Is Associated with Upregulation of CK2, AKT and ERK1/2
by Marta Sanna, Christian Borgo, Chiara Compagnin, Francesca Favaretto, Vincenzo Vindigni, Mariangela Trento, Silvia Bettini, Alessandra Comin, Anna Belligoli, Massimo Rugge, Franco Bassetto, Arianna Donella-Deana, Roberto Vettor, Luca Busetto and Gabriella Milan
Int. J. Mol. Sci. 2020, 21(21), 7933; https://doi.org/10.3390/ijms21217933 - 26 Oct 2020
Cited by 10 | Viewed by 3106
Abstract
Multiple symmetric lipomatosis (MSL) is a rare disorder characterized by overgrowing lipomatous tissue (LT) in the subcutaneous adipose tissue (SAT). What LT is and how it expands are not completely understood; previous data suggested that it could derive from brown AT precursors. In [...] Read more.
Multiple symmetric lipomatosis (MSL) is a rare disorder characterized by overgrowing lipomatous tissue (LT) in the subcutaneous adipose tissue (SAT). What LT is and how it expands are not completely understood; previous data suggested that it could derive from brown AT precursors. In six MSL type I patients, we compared LT morphology by histological and immunohistochemistry (IHC) analysis, gene expression, by qPCR, kinase activity, by Western Blot and in vitro assay to paired-control SAT using AT from patients with pheochromocytoma as a human browning reference. In the stromal vascular fraction (SVF), we quantified adipose stem cells (ASCs) by flow cytometry, the proliferation rate, white and beige adipogenic potential and clonogenicity and adipogenicity by a limiting dilution assay. LT displayed white AT morphology and expression pattern and did not show increased levels of the brown-specific marker UCP1. In LT, we evidenced AKT, CK2 and ERK1/2 hyperactivation. LT-SVF contained increased ASCs, proliferated faster, sprouted clones and differentiated into adipocytes better than the control, displaying enhanced white adipogenic potential but not increased browning compared to SAT. In conclusion, LT is a white AT depot expanding by hyperplasia through increased stemness and enhanced white adipogenesis upregulating AKT, CK2 and ERK1/2, which could represent new targets to counteract MSL. Full article
(This article belongs to the Special Issue Lipodystrophy and Fat Redistribution: From Molecular Basis to Therapies)
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Review

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15 pages, 257 KiB  
Review
Lipodystrophies—Disorders of the Fatty Tissue
by Birgit Knebel, Dirk Müller-Wieland and Jorg Kotzka
Int. J. Mol. Sci. 2020, 21(22), 8778; https://doi.org/10.3390/ijms21228778 - 20 Nov 2020
Cited by 23 | Viewed by 4467
Abstract
Lipodystrophies are a heterogeneous group of physiological changes characterized by a selective loss of fatty tissue. Here, no fat cells are present, either through lack of differentiation, loss of function or premature apoptosis. As a consequence, lipids can only be stored ectopically in [...] Read more.
Lipodystrophies are a heterogeneous group of physiological changes characterized by a selective loss of fatty tissue. Here, no fat cells are present, either through lack of differentiation, loss of function or premature apoptosis. As a consequence, lipids can only be stored ectopically in non-adipocytes with the major health consequences as fatty liver and insulin resistance. This is a crucial difference to being slim where the fat cells are present and store lipids if needed. A simple clinical classification of lipodystrophies is based on congenital vs. acquired and generalized vs. partial disturbance of fat distribution. Complications in patients with lipodystrophy depend on the clinical manifestations. For example, in diabetes mellitus microangiopathic complications such as nephropathy, retinopathy and neuropathy may develop. In addition, due to ectopic lipid accumulation in the liver, fatty liver hepatitis may also develop, possibly with cirrhosis. The consequences of extreme hypertriglyceridemia are typically acute pancreatitis or eruptive xanthomas. The combination of severe hyperglycemia with dyslipidemia and signs of insulin resistance can lead to premature atherosclerosis with its associated complications of coronary heart disease, peripheral vascular disease and cerebrovascular changes. Overall, lipodystrophy is rare with an estimated incidence for congenital (<1/1.000.000) and acquired (1–9/100.000) forms. Due to the rarity of the syndrome and the phenotypic range of metabolic complications, only studies with limited patient numbers can be considered. Experimental animal models are therefore useful to understand the molecular mechanisms in lipodystrophy and to identify possible therapeutic approaches. Full article
(This article belongs to the Special Issue Lipodystrophy and Fat Redistribution: From Molecular Basis to Therapies)
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