Charles, MO, USA) . HbA1c was measured using high-performance liquid chromatography (Biorad, Hercules, FL, USA). After prevention of in vitro lipolysis by collection of blood into orlistat-containing vials, NEFAs were assayed microfluorimetrically (Wako Chem USA, http://www.wakousa.com/
). Triglycerides, total, HDL and LDL cholesterol, and alanine and aspartate aminotransferase were measured using routine laboratory methods (Abbot Aeroset LN09D05-01, A1522460). All analyses were performed using spss 14.0 software (SPSS, http://www.spss.com
). Data in the Selleck Pritelivir
text and tables are presented as means?��?standard deviation (SD). In the figures, data are presented as means?��?standard error (SE). Comparisons between two groups were performed using unpaired two-tailed Student��s t test. Within group differences were determined using two-tailed Student��s paired t-test. Linear correlations are Pearson product-moment correlations. Spearman correlations were used for parameters with skewed distribution. selleck chemical
P values of <0.05 were considered to indicate significant differences. Fasting plasma glucose concentrations were not different between type 1 diabetic patients and nondiabetic volunteers (6.4?��?2.7 and 4.8?��?0.4?mmol?L?1, respectively, P?=?0.126). The variable insulin supplementation required to maintain near-normoglycaemia prior to the clamp resulted in higher plasma insulin concentrations in type 1 diabetic patients compared with controls (29?��?14 and 8?��?2?��U?mL?1, respectively, P?=?0.001). Except for HbA1c, anthropometric and metabolic parameters did not differ between groups (Table?1). Basal myocellular g6p and fATP (Fig.?2b,c), IMCL, Pi and fCK were also comparable between the groups (Table?2). There were no differences during the clamp between <a href="http://www.selleck.cn/products/CAL-101.html
">CAL 101 type 1 diabetic and nondiabetic subjects with regard to mean concentrations of plasma glucose (5.5?��?0.2 vs. 5.5?��?0.4?mmol?L?1, respectively, P?=?0.92) and insulin (99?��?18 vs. 88?��?10?��U?mL?1, respectively, P?=?0.16). Plasma NEFAs were also similarly suppressed by insulin in both groups compared with basal levels (type 1 diabetics: 0.02?��?0.02?mmol?L?1, P?=?0.007; controls: 0.01?��?0.01?mmol?L?1, P = 0.004). Whole-body glucose disposal expressed as M value was ?50% lower in type 1 diabetic patients compared to controls (P?=?0.001) (Fig.?2a). Similarly, whole-body insulin sensitivity expressed as M/I was ?53% lower in type 1 diabetic patients compared with controls (0.06?��?0.02 and 0.13?��?0.05?mg?kg?1?min?1 per ��U?mL?1, respectively, P?=?0.001). During the clamp, g6p did not change from baseline in type 1 diabetic patients, but almost doubled in the controls (P?=?0.004 vs. baseline). Insulin-stimulated g6p was therefore greater in the controls than in type 1 diabetic patients (P?=?0.003) (Fig.?2b).