ReviewJournal of human genetics2014
Exploring the pathophysiology behind the more common genetic and acquired lipodystrophies.
Review in Journal of human genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 85 citations in OpenAlex.
- Potential Impact of Parental Origin of Inheritance on the Clinical Presentation of Familial Partial Lipodystrophy Type 2 Syndrome.Clinical endocrinology · 2025Article
- Lipodystrophy Syndromes: One Name but Many Diseases Highlighting the Importance of Adipose Tissue in Metabolism.Current diabetes reports · 2025Review
- Brazilian expert consensus on the diagnosis, classification, screening for complications and treatment of familial partial lipodystrophy.Diabetology & metabolic syndrome · 2025Article
- Article
- Role of Na/K-ATPase α1 caveolin-binding motif in adipogenesis.American journal of physiology. Cell physiology · 2024Article
- Loss-of-function variants affecting the STAGA complex component SUPT7L cause a developmental disorder with generalized lipodystrophy.Human genetics · 2024Article
- Familial Screening for the Prevention of Rare Diseases: A Focus on Lipodystrophy in Southern Saudi Arabia.Journal of epidemiology and global health · 2024Article
- Exploring lipodystrophy gene expression in adipocytes: unveiling insights into the pathogenesis of insulin resistance, type 2 diabetes, and clustering diseases (metabolic syndrome) in Asian Indians.Frontiers in endocrinology · 2024Article
- Identifying congenital generalized lipodystrophy using deep learning-DEEPLIPO.Scientific reports · 2023Article
- A new mutation in theFrontiers in endocrinology · 2023Review
- Lipodystrophy for the Diabetologist-What to Look For.Current diabetes reports · 2022Review
- Approach to the Patient With Lipodystrophy.The Journal of clinical endocrinology and metabolism · 2022Article
- Familial Partial Lipodystrophy-Literature Review and Report of a Novel Variant inDiagnostics (Basel, Switzerland) · 2022Article
- Type 2 Diabetes Partitioned Polygenic Scores Associate With Disease Outcomes in 454,193 Individuals Across 13 Cohorts.Diabetes care · 2022Article
- Acquired localised lipoatrophy secondary to transgluteal drainage.BMJ case reports · 2021Article
- Distinct Shades of Adipocytes Control the Metabolic Roles of Adipose Tissues: From Their Origins to Their Relevance for Medical Applications.Biomedicines · 2021Review
- Lipotransfer provides effective soft tissue replacement for acquired partial lipodystrophy.BMJ case reports · 2020Article
- Genotype-phenotype correlations of Berardinelli-Seip congenital lipodystrophy and novel candidate genes prediction.Orphanet journal of rare diseases · 2020Article
- Cardiac Alterations in Patients with Familial Lipodystrophy.Arquivos brasileiros de cardiologia · 2020Review
- Adipose tissue loss and lipodystrophy in xylosyltransferase II deficient mice.International journal of obesity (2005) · 2019Article
Corrections and comments
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lipodystrophies are an immense group of genetic or acquired metabolic disorders that are characterized by varying degrees of body fat loss and in some instances localized accumulation of subcutaneous fat. Lipodystrophies are often tightly linked with profound metabolic complications; this strong bond emphasizes and reinforces the significance of adipose tissue as a dynamic endocrine organ. The extent of fat loss determines the severity of associated metabolic complications such as diabetes mellitus, hypertriglyceridemia and hepatic steatosis. The lipodystrophies can be divided into generalized, partial or local, depending on the degree and locality of the observable fat loss; moreover, the generalized and partial divisions can be partitioned further into inherited or acquired forms. The major genetic factors in the generalized forms of the lipodystrophies, particularly Congenital generalized lipodystrophy (CGL)-Berardinelli-Seip syndrome, are the AGPAT2, BSCL2, caveolin 1 (CAV1) and polymerase-I-and-transcriptrelease factor (PTRF) genes. In the acquired forms, genes such as LMNA, PPARG, CIDEC (cell-death-inducing DNA fragmentation factor a-like effector c) and PLIN1 are heavily involved in familial partial lipodystrophy (FPLD) type 2 (also known as the Dunnigan-Variety) and WRN along with RECQL5 in Werner Syndrome (WS). Autoimmune causes are particularly noted in acquired partial lipodystrophy (APL)-Barraquer-Simons syndrome and in AGL-Lawrence syndrome; panniculitis has been shown to have a substantial role in the former as well as in other forms of localized lipodystrophies. Patients with human immunodeficiency virus (HIV) exposed to protease inhibitors, nucleoside reverse transcriptase inhibitors (NRTIs) (for example, zidovudine and stavudine) or non-nucleoside reverse transcriptase inhibitors (NNRTIs) (for example, efavirenz) while undergoing Highly Active Antiretroviral Therapy (HAART) have led to the current most-prevalent form of the lipodystrophies: lipodystrophy in HIV-infected patients (LD-HIV) and HAART-associated lipodystrophy syndrome (HALS).
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