Abstract:
:Studying ciliopathies, like the Bardet-Biedl syndrome (BBS), allow the identification of signaling pathways potentially involved in common diseases, sharing phenotypic features like obesity or type 2 diabetes. Given the close association between obesity and insulin resistance, obese BBS patients would be expected to be insulin resistant. Surprisingly, we found that a majority of obese BBS patients retained normal glucose tolerance and insulin sensitivity. Patient's adipose tissue biopsies revealed upregulation of adipogenic genes and decrease of inflammatory mediators. In vitro studies on human primary mesenchymal stem cells (MSCs) showed that BBS12 inactivation facilitated adipogenesis, increased insulin sensitivity, and glucose utilization. We generated a Bbs12(-/-) mouse model to assess the impact of Bbs12 inactivation on adipocyte biology. Despite increased obesity, glucose tolerance was increased with specific enhanced insulin sensitivity in the fat. This correlated with an active recruitment of MSCs resulting in adipose tissue hyperplasia and decreased in inflammation.
journal_name
Cell Metabjournal_title
Cell metabolismauthors
Marion V,Mockel A,De Melo C,Obringer C,Claussmann A,Simon A,Messaddeq N,Durand M,Dupuis L,Loeffler JP,King P,Mutter-Schmidt C,Petrovsky N,Stoetzel C,Dollfus Hdoi
10.1016/j.cmet.2012.08.005subject
Has Abstractpub_date
2012-09-05 00:00:00pages
363-77issue
3eissn
1550-4131issn
1932-7420pii
S1550-4131(12)00327-0journal_volume
16pub_type
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