Endocrine Abstracts

Since 2003 there is a large consensus on the fact that obese adipose tissues of mice and humans are inflammed. This low-grade chronic inflammation is linked to insulin resistance inducing to type2 diabetes (T2D). In 2005 we showed that inflammation is due to death of obese adipocytes whose debris require macrophages infiltration of the tissue and consequent formation of crown like structures (CLS) as the basic histopathology aspect of inflammation. In 2008 we showed that visceral adipocytes have a critical death size smaller that that of subcutaneous adipocytes and, accordingly, inflammation of visceral fat is more severe. This offer an explanation to the well known clinical data claiming visceral obesity as the condition more frequently linked to the usual obesity related disorders and mainly to the T2D. In 2013 we showed that obese adipocytes die for pyroptosis. Here we show data suggesting that in adipose tissues of obese humans (66 fat biopsies from 33 bariatric patients) a large proportion (about 13%) of hypertrophic adipocytes die for self-choking due to fibrosis. Histochemistry, immunohistochemistry, electron microscopy and gene expression data showed that single or groups of obese adipocytes are surrounded by thick bands of fibrous collagen with evidence of hypoxia and correlation with signs of death (loss of perilipin1 immunoreactivity). Inflammation was mainly sustained by macrophages, but only a minority of them formed CLS. While the increased fibrous collagen is widely accepted the amount of collagen VI in obese fat is debated. Our data showed a reduction in gene expression and the analysis of tissue from a patient with the rare mutation inducing a reduction of active collagen VI production showed fibrosis comparable with that in obese fat suggesting a causative role for this gene.