title: Dead adipocytes and metabolic dysfunction: recent progress.
abstract: OBJECTIVE
  Dead adipocytes are at the heart of crown-like structures (CLSs), which represent a still relatively novel interface of adipocytes and adipose tissue macrophages (ATMs) and may be significant to human health conditions such as obesity, insulin resistance, diabetes mellitus, atherosclerosis, and cardiovascular disease. In order to provide a concise and pertinent discussion, this review highlights recent reports examining CLSs and projects the likely directions of future research in this budding and fascinating field.
  
  
  RESULTS
  In mice, there is recent progress in understanding the differences in distribution of two distinct phenotypes of ATM classes with respect to dead adipocytes. Furthermore, a detailed atlas of fat depot-specific differences in adipocyte size and CLS prevalence has begun in two genetic models of mouse obesity. In humans, fat cell aging and turnover have been quantified. The correlation between human CLSs and early cardiovascular disease has also been established. The predominant ATM phenotype in obese humans may be M2, which would contrast with the M1 ATMs of obese mouse models. Finally, osteopontin has been established in both humans and mice as an important macrophage chemoattractant to dead adipocytes, in addition to monocyte chemoattractant protein 1 and C-C motif chemokine receptor 2.
  
  
  CONCLUSIONS
  Recent updates in research on dead adipocytes and the biology of CLSs with clinical implications for metabolic dysfunction are discussed.
authors.affiliation: Department of Medicine, Division of Endocrinology and Metabolism, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21224, USA. mwest12@jhmi.edu
authors.forename: Michael
authors.initials: M
authors.lastname: West
mesh_terms: D017667:Adipocytes / Q000378:metabolism* / Q000473:pathology / Q000502:physiology*; D000818:Animals; D017209:Apoptosis / Q000502:physiology; D006801:Humans; D008264:Macrophages / Q000502:physiology / Q000648:ultrastructure; D008659:Metabolic Diseases / Q000378:metabolism* / Q000473:pathology*; D051379:Mice; D009765:Obesity / Q000378:metabolism / Q000473:pathology