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Microglial Proliferation in Obesity: When, Where, Why, and What Does It Mean?

  1. Julie A. Chowen1⇑,
  2. Tamas L. Horvath2 and
  3. Jesús Argente1,3
  1. 1Department of Endocrinology, Hospital Infantil Universitario Niño Jesús, Instituto de Investigación del Hospital de la Princesa, Centro de Investigación Biomédica en Red de Obesidad y Nutrición, Instituto de Salud Carlos III, Madrid, Spain
  2. 2Program in Integrative Cell Signaling and Neurobiology of Metabolism, Section of Comparative Medicine, Yale School of Medicine, New Haven, CT
  3. 3Department of Pediatrics, Universidad Autónoma de Madrid, Madrid, Spain
  1. Corresponding author: Julie A. Chowen, julieann.chowen{at}salud.madrid.org.
Diabetes 2017 Apr; 66(4): 804-805. https://doi.org/10.2337/dbi16-0073
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    André et al. (6) report that microglia proliferate specifically in the medial basal hypothalamus in response to an HFD. This is associated with increased weight gain, fat mass, energy intake, POMC expression, and serum leptin and IL-1β levels. When treated intracerebroventricularly with AraC, microglia do not proliferate in response to HFD intake, and HFD-induced weight gain and fat mass are reduced, while plasma leptin and IL-1β levels remain at control levels. Hypothalamic neuropeptide expression is modified, such that the mRNA levels of POMC are unchanged and AgRP decreased. Thus, although microglial proliferation is blocked, weight and fat mass accrual are only partially inhibited but systemic inflammation is constrained. AgRP, agouti-related protein; POMC, proopiomelanocortin.

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Diabetes: 66 (4)

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April 2017, 66(4)
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Microglial Proliferation in Obesity: When, Where, Why, and What Does It Mean?
Julie A. Chowen, Tamas L. Horvath, Jesús Argente
Diabetes Apr 2017, 66 (4) 804-805; DOI: 10.2337/dbi16-0073

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Microglial Proliferation in Obesity: When, Where, Why, and What Does It Mean?
Julie A. Chowen, Tamas L. Horvath, Jesús Argente
Diabetes Apr 2017, 66 (4) 804-805; DOI: 10.2337/dbi16-0073
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