Insulin-like growth factor binding protein (IGFBP)-3 binds to IGF and modulates their actions and also possesses intrinsic activities. We investigated its effects on insulin action and found that when IGFBP-3 was added to fully differentiated 3T3-L1 adipocytes in culture, insulin-stimulated glucose transport was significantly inhibited to 60% of control in a time-and dose-dependent manner. Tumor necrosis factor (TNF)-␣ treatment also inhibited glucose transport to the same degree as IGFBP-3 and, in addition, increased IGFBP-3 levels 3-fold. Co-treatment with TNF-␣ and IGFBP-3 antisense partially prevented the inhibitory effect of TNF-␣ on glucose transport, indicating a role for IGFBP-3 in cytokine-induced insulin resistance. Insulin-stimulated phosphorylation of the insulin receptor was markedly decreased by IGFBP-3 treatment. IGFBP-3 treatment suppressed adiponectin expression in 3T3-L1 adipocytes. Infusion of IGFBP-3 to Sprague-Dawley rats for 3 h decreased peripheral glucose uptake by 15% compared with controls as well as inhibiting glycogen synthesis. Systemic administration of IGFBP-3 to rats for 7 d resulted in a dramatic 40% decrease in peripheral glucose utilization and glycogen synthesis. These in vitro and in vivo findings demonstrate that IGFBP-3 has potent insulin-antagonizing capability and suggest a role for IGFBP-3 in cytokine-induced insulin resistance and other mechanisms involved in the development of type-2 diabetes. (Pediatr Res 61: 159-164, 2007)
We report a case of a girl with clinical features of Peters' Plus Syndrome (PPS) (association of anterior eye chamber defects; peculiar facies; cleft lip/palate; brachymelia; developmental delay; growth retardation) and documented growth hormone deficiency (height -3.5 SDS at chronological age 5 years 8 months; low growth factors; bone age delay; growth velocity 4.4 cm/year (<3rd centile); and peak growth hormone levels of 1.7 and 4.7 ng/ml by clonidine and insulin provocative testing, respectively). Treatment with recombinant human growth hormone (0.3 mg/kg/week) resulted in a dramatic increase in growth velocity, increasing the height from -3.5 to -1.5 SDS over 2.3 years of therapy, indicative of an excellent response. Growth retardation is a known association in PPS: a condition that includes other midline facial defects. This case supports a role for GHD in the pathogenesis of the short stature observed in these children; demonstrates the efficacy of GH treatment; and further reinforces the relationship of pituitary anomalies with common congenital defects.
Carbosilane dendrimers adorned with either triarylamine or carbazole units in their periphery exhibit novel electrochemical behavior in which the electrochemical deposition is controlled by dendrite generation. In addition, the deposited layers remained intact in the depositing solvent, methylene chloride, allowing a second layer to be deposited on top of the first layer. We have sought to establish the suitability of this electrochemical deposition technique for use in the construction of multi-layer OLEDs, which cannot be fabricated via conventional spin-coating with a polymeric precursor. Thus, the electrochemical deposition-based process could potentially offer an ideal combination of deposition control on the one hand and multi-layer fabrication on the other. We report herein the novel electrochemical deposition behavior of arylamine or carbazole end-capped carbosilane dendrimers of the type GnNPB or GnCBP (n = 1-4) and their use for the formation of multi-layer devices for OLEDs.
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