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题名:The metabolic responses induced by acute dexamethasone predict glucose tolerance and insulin secretion over 10y in relatives of Type 2 diabetic subjects.
作者:DURCK TT; HENRIKSEN JE; EGEDE MB; LEVIN K; RANTZAU C; WARD G; BECK-NIELSEN H; ALFORD FP;
来源:Diabetes Metab Res Rev. 2013 Apr 9. doi: 10.1002/dmrr.2418. [ IF= 0.00 ] ]
URL :10.1002/dmrr.2418
日期:20130430
摘要:BACKGROUND: This study aimed to compare the metabolic and insulin secretory
responses to dexamethasone (DEX) with the metabolic responses observed at 10y in
normoglycaemic relatives of Type 2 diabetic and healthy control subjects.
METHODS: Twenty Relatives (REL) and 20 matched Control (CON) subjects were
studied twice at 0y (pre-DEX and post-DEX) and at 10y, employing a 75 g OGTT,
with serial measurements of glucose and insulin, for determination of glucose
tolerance and calculations of acute insulin release (DeltaI30 /DeltaG30;
insulinogenic index) and insulin sensitivity (SIHOMA ). RESULTS: Following DEX,
the REL group developed varying degrees of glucose intolerance, associated with
reduced SIHOMA and insulinogenic index. By 10y, fasting glucose and 2 h OGTT
glucose were raised in the REL group, especially in the REL most metabolically
affected by DEX, including a reduced insulinogenic index. Multiple regression
analysis of the REL data demonstrated that the 2 h OGTT glucose and fasting
glucose values at 10y depended on the 0y post-DEX 2 h OGTT glucose, post-DEX
fasting glucose and post-DEX SIHOMA , r2 adj = 56% (p < 0.001) and r2 adj = 60%
(p < 0.0001), respectively. No pre-DEX metabolic or insulin secretory responses
entered these models. CONCLUSIONS: In REL, fasting and 2 h OGTT glucose
concentrations and beta-cell responses to acute DEX-induced insulin resistance
are similar to those observed at 10y, especially in REL who develop the most
disturbed DEX-induced glucose intolerance and impaired acute insulin secretion.
The combined 0y, post-DEX fasting and 2 h OGTT glucose concentrations and SIHOMA
are the best predictors in REL of future dysglycaemia. This article is protected
by copyright. All rights reserved.

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