01 across both diabetic and non-diabetic subjects). Fasting glucose concentrations were not affected by prior diet but postprandial glucose concentrations were (P = 0.018), with significantly
higher values after the high-fat Cytoskeletal Signaling inhibitor than the high-sugar diet (P = 0.03).
Conclusions: The short-term TG-raising effect of a very low-fat diet is dependent upon the nature of the carbohydrate, with a greater effect of a sugar-rich than a complex-carbohydrate-rich diet. (C) 2007 Elsevier B.V. All rights reserved.”
“The radial growth of Ge nanowire via chemical vapor deposition is discussed in detail. Vapor-solid-solid (VSS) growth mechanism is believed to dominate the nanowire growth in radial direction, which contributes to the increase of the diameter of nanowire. After the Au catalysts
on the tip are consumed for a long growth time, the nanowire with a rough surface will be grown due to the selective VSS radial growth. (C) 2009 American Institute of Physics. [DOI: 10.1063/1.3204471]“
“Background BIBW2992 order and aims: Healthy individuals counteract insulin-induced hypoglycaemia by increasing glutamine utilization but not proteolysis. Glucagon is important to this response because it increases glutamine uptake. In type 1 diabetes (T1DM) glucagon and epinephrine responses to hypoglycaemia are defective. We investigated whether glutamine and amino acid utilization during hypoglycaemia is altered in T1DM with defective counter-regulatory responses.
Methods and results: Eight T1DM patients (duration of diabetes 14 4 years and therefore with presumed defective counter-regulatory response) and eight controls (CON) received a 3 h hypoglycaemic hyperinsulinaemic (0.65 mU/kg per min) clamp coupled to [6,6-(2)H(2)]glucose, [1-(13)C]
leucine and [2-(15)N]glutamine to trace the relative kinetics.
Post-absorptive plasma glucose and glucose uptake were increased in T1DM (9.09 +/- 0.99 vs 5.01 +/- 0.22 mmol/l and 19.5 +/- 0.9 vs 12.6 +/- 0.8 mu mol/kg per min, p < 0.01). During the clamp T1DM but not CON required exogenous glucose (4.4 +/- 1.7 mu mol/kg per min) to maintain the hypoglycaemic plateau because the endogenous glucose p38 MAPK pathway production was significantly suppressed (p < 0.01). In T1DM the leucine and phenylatanine concentrations were less suppressed from basal (p < 0.05) despite a similar insulin suppression of proteolysis (-16 +/- 2 vs -20 +/- 4%, p = ns) indicating a defective stimulation of leucine metabolic clearance from basal (+18 +/- 3% vs +55 +/- 9%, p < 0.01). Glutamine concentration remained unchanged from basal (-7 +/- 3% vs -35 +/- 3%, p < 0.01) and the clearance of glutamine was markedly defective in T1DM (+6 +/- 2%) in comparison with controls (+22 +/- 4%; p = 0.02).
Conclusions: In T1DM, the counter-regulatory failure to hypoglycaemia seems to be associated with a defective glutamine utilization. The failure to clear circulating amino acids, specifically glutamine, during hypoglycaemia may adversely affect gluconeogenesis.