Effect of Short-term Intensive Insulin Therapy on Post-challenge Hyperglucagonemia in Early Type 2 XXXX .

@entity1 @entity1720 @entity413 @entity6
CONTEXT: Hyperglucagonemia is a characteristic feature of type 2 @entity6 (T2DM) that has been postulated to be due to beta-cell dysfunction and the resultant loss of insulin-mediated alpha-cell suppression. When administered in early T2DM, short-term @entity1720 ( @entity1720 ) can improve beta-cell function, resulting in reduced glycemic variability. OBJECTIVE: To evaluate the impact of @entity1720 on hyperglucagonemia, and its associations with beta-cell function and glycemic variability. Design/Setting/ @entity1 /Intervention: Sixty-two @entity1 with T2DM of mean 3.0  2.1 years duration and A1c 6.8  0.7% underwent 4 weeks of @entity1720 , consisting of basal detemir and pre-meal insulin aspart. MAIN OUTCOME MEASURES: Glucagon response was measured by area-under-the-glucagon-curve (AUCglucagon) on oral @entity413 tolerance test at baseline and one day post- @entity1720 . Beta-cell function before and after @entity1720 was assessed by Insulin Secretion-Sensitivity Index-2 (ISSI-2) and   ISR0-120/  @entity413 0-120*Matsuda index (where ISR is the prehepatic insulin secretion rate determined by C-peptide deconvolution). @entity413 variability was assessed in both the first and last week by the coefficient of variation of capillary @entity413 on daily 6-point self-monitoring profiles. RESULTS: Both ISSI-2 and   ISR0-120/  @entity413 0-120*Matsuda index demonstrated improvement in beta-cell function following @entity1720 (both p <=0.02), accompanied by reduced glycemic variability (p=0.05). There was a marked reduction in AUCglucagon following @entity1720 , as compared to baseline (p<0.001). However, the decrease in AUCglucagon was not associated with the change in either beta-cell measure (both p>= 0.34) or in @entity413 variability (p=0.37). CONCLUSIONS: Short-term @entity1720 can reduce post-challenge hyperglucagonemia in early T2DM but this effect does not appear to be due to improved beta-cell function.
