Serotonin regulates maternal calcium homeostasis during the perinatal period of sheep.

The goal of this experiment was to demonstrate the ability of an infusion of serotonin (5-HT; 5-hydroxytryptamine) precursors to increase 5-HT production during the transition from pregnancy to lactation and its effects on gene expression related to calcium (Ca) transporters in the mammary gland and bone resorption markers in the femur. Thirty pregnant Bamei mutton sheep were randomly assigned to 3 experimental groups. All groups received a daily intravenous infusion of saline (control group; n = 10), saline containing 0.178 mg of L-tryptophan/kg body weight (BW) (TRP group, n = 10) or 0.178 mg of 5-hydroxytryptophan/kg BW (5-HTP group, n = 10), beginning on day 7 of prepartum and continuing until delivery. Serum (pre- and postpartum), milk (postpartum), and femur and mammary gland tissue (day 9) were collected. Sheep infused with 5-HTP had a larger total serum Ca concentration on days 3, 6, 15, and 30 of lactation and total milk Ca concentration on days 3, 6, 12, and 15 of lactation compared with that of the control group. Sheep infused with 5-HTP and TRP increased blood and milk concentrations of 5-HT on days 3, 6, 9, and 30 of lactation and parathyroid hormone-related protein (PTHrP) on day 3 of prepartum and on days 3, 6, and 15 of lactation (P < 0.05). In addition, compared to that of the control group, the TRP or 5-HTP infusion upregulated PTHrP, a sodium/calcium exchanger, plasma membrane Ca2+ ATPase 2, secretory pathway Ca2+ ATPase 1, and calcium sensing receptor mRNA expression in mammary gland and receptor-activated nuclear factor kappa-B ligand mRNA expression in the femur, but had no effect on receptor-activated nuclear factor kappa-B and osteoprotegerin mRNA expression in the femur (P < 0.05). This suggests that 5-HT and PTHrP may be involved in regulating maternal Ca homeostasis during the transition from pregnancy to lactation in the sheep.

The efficiency comparision of continuous glucose monitoring system and blood glucose self-monitoring in evaluating blood glucose excursion in type 1 diabetes mellitus complicated with pregnancy / 中国医师进修杂志

Objective To explore the efficiency of continuous glucose monitoring system(CGMS) and blood glucose self-monitoring (SMBG)in evaluating blood glucose excursion in type 1 diabetes mellitus (T1DM) complicated with pregnancy. Methods Twenty-five patients having suffered from T1DM complicated with pregnancy were selected randomly during June 2012 to July 2015. All subjects underwent blood glucose monitoring by CGMS and SMBG for 72 h, including the data of blood glucose before meal, 2 h post-meal blood glucose (2hBG) and blood glucose at 2:00 AM. Results The level of the highest blood glucose in CGMS was significantly higher than that in SMBG:(10.60 ± 2.11) mmol/L vs. (7.50 ± 1.18) mmol/L, P0.05. The rate of hypoglycemia(blood glucose<3.3 mmol/L) in CGMS was 4.6%, and in SMBG was 1.9%. Through adjusting the treatment by CGMS, the blood glucose before meal, 2hBG and blood glucose at 2:00 AM at 49-72 h were significantly lower than that at 0-24 h (P<0.05). Conclusions Compared with SMBG, CGMS has a relatively larger blood glucose monitoring range and can sensitively evaluate blood glucose excursion, CGMS provides a scientific basis to develop a more rational and effective strategies for controlling diabetes.

Small interfering RNA-mediated islet neogenesis associated protein gene silencing inhibits the proliferation of INS-1 islet cells / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the effect of small interfering RNA (siRNA)-mediated islet neogenesis associated protein (INGAP) gene silencing on the proliferation of islet cells.</p><p><b>METHODS</b>Different siRNAs targeting INGAP gene were designed and transfected into INS-1 islet cells, and the expression levels of INGAP mRNA and protein following the transfection were detected using RT-PCR, flow cytometry and Western blotting. The proliferation of the transfected INS-1 cells was evaluated using MTT assay.</p><p><b>RESULTS</b>Compared with those in the irrelevant siRNA, empty vector control, and un-transfected groups, the expression levels of INGAP mRNA and protein in the cells transfected with siRNA6 were reduced significantly. The cell proliferation rate significantly increased after transfection with siRNA6 (P<0.05).</p><p><b>CONCLUSION</b>siRNA targeting INGAP can effectively down-regulate INGAP expression and inhibit the proliferation of INS-1 cells.</p>

High glucose impairs mitochondrial respiratory chain function in pancreatic beta cells / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the effect of high glucose on mitochondrial respiratory chain function in INS-1 cells.</p><p><b>METHODS</b>The pancreatic beta cell line INS-1 was divided into the normal control (NC), high glucose (HG), and N-acetyl-L-cysteine (NAC) pretreatment groups, which were cultured for 72 h in the presence of 5.5 mmol/L glucose, 16.7 mmol/L glucose, and 16.7 mmol/L glucose with 1.0 mmol/L NAC, respectively. The activities of the enzyme complexes I and III of the respiratory chain in the cells were assessed with spectrophotometry, the ATP levels were examined using a luciferinluciferase kit, and insulin levels detected by radioimmunoassay.</p><p><b>RESULTS</b>The activities of the respiratory chain enzyme complexes I and III were 1.53-/+0.24 and 1.08-/+0.22 micromol.mg(-1).min(-1) in high glucose group, respectively, significantly lower than those in the normal control group (2.31-/+0.33 and 1.92-/+0.39 micromol.mg(-1).min(-1), P<0.01). ATP and insulin levels also decreased significantly in high glucose group as compared with those in the normal control group (P<0.01). The addition of NAC partially inhibited high glucose-induced decreases in the enzyme complex activities, ATP levels and insulin secretion (P<0.05).</p><p><b>CONCLUSION</b>The respiratory chain function is positively correlated to insulin secretion in INS-1 cells, and exposure to high glucose causes impairment of the two enzyme complexes activities through oxidative stress, resulting in the mitochondrial respiratory chain dysfunction. High glucose-induced damages of the mitochondrial respiratory chain function can be partially inhibited by NAC.</p>