Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29053727
&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
Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\29053727
.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 PLoS+One
2017 ; 12
(10
): e0185371
Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Impaired glucose metabolism in subjects with the Williams-Beuren syndrome: A
five-year follow-up cohort study
#MMPMID29053727
Lunati ME
; Bedeschi MF
; Resi V
; Grancini V
; Palmieri E
; Salera S
; Lalatta F
; Pugliese G
; Orsi E
PLoS One
2017[]; 12
(10
): e0185371
PMID29053727
show ga
OBJECTIVE: The Williams-Beuren syndrome (WS) is associated with impaired glucose
metabolism (IGM) early in adulthood. However, the pathophysiology of IGM remains
poorly defined, due to the lack of longitudinal studies investigating the
contribution of ?-cell dysfunction and impaired insulin sensitivity. This study
aimed at assessing incidence of IGM and the underlying mechanisms in WS adults.
METHODS: This observational, longitudinal (5-year), cohort study enrolled
thirty-one consecutive WS subjects attending a tertiary referral center. An oral
glucose tolerance test (OGTT) was performed yearly and used to classify patients
as normal or IGM, including impaired fasting glucose (IFG) and/or impaired
glucose tolerance (IGT) and diabetes mellitus (DM), and to calculate surrogate
measures of insulin secretion and/or sensitivity. RESULTS: IGM patients were 18
(58.1%, three DM) at baseline and 19 (61.3%, five DM) at end-of-follow-up.
However, 13 individuals changed category of glucose homeostasis in both
directions during follow-up (8 progressors, 5 regressors) and 18 did not (8
non-progressors, 10 non-regressors). New cases of IGM and DM were 11.1 and 2.53
per 100 persons-year, respectively, and were treated non-pharmacologically. In
the whole cohort and, to a higher extent, in progressors, indices of early-phase
insulin secretion and insulin sensitivity decreased significantly from baseline
to end-of-follow-up, with concurrent reduction of the oral disposition index and
insulin secretion-sensitivity index-2 (ISSI-2), compensating insulin secretion
for the level of insulin resistance. No baseline measure independently predicted
progression, which correlated with change from baseline in ISSI-2. Compared with
patients with normal glucose homeostasis, IGT subjects had impaired insulin
sensitivity, whereas insulin secretion was reduced only in those with IFG+IGT or
DM. CONCLUSIONS: IGM incidence is high in young adults with WS, suggesting the
need of early screening and timed intervention. As in classical type 2 diabetes,
impaired insulin sensitivity and ?-cell dysfunction contribute, in this sequence,
to progression to IGM and DM.