Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26248647
&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215
Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26248647
.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Diabetologia
2015 ; 58
(11
): 2459-68
Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
The new biology of diabetes
#MMPMID26248647
Pajvani UB
; Accili D
Diabetologia
2015[Nov]; 58
(11
): 2459-68
PMID26248647
show ga
Until recently, type 2 diabetes was seen as a disease caused by an impaired
ability of insulin to promote the uptake and utilisation of glucose. Work on
forkhead box protein O (FOXO) transcription factors revealed new aspects of
insulin action that have led us to articulate a liver- and beta cell-centric
narrative of diabetes pathophysiology and treatment. FOXO integrate a
surprisingly diverse subset of biological functions to promote metabolic
flexibility. In the liver, they controls the glucokinase/glucose-6-phosphatase
switch and bile acid pool composition, directing carbons to glucose or lipid
utilisation, thus providing a unifying mechanism for the two abnormalities of the
diabetic liver: excessive glucose production and increased lipid synthesis and
secretion. Moreover, FOXO are necessary to maintain beta cell differentiation,
and diabetes development is associated with a gradual loss of FOXO function that
brings about beta cell dedifferentiation. We proposed that dedifferentiation is
the main cause of beta cell failure and conversion into non-beta endocrine cells,
and that treatment should restore beta cell differentiation. Our studies
investigating these proposals have revealed new dimensions to the pathophysiology
of diabetes that can be leveraged to design new therapies.
free
free
free
