Recombinant betatrophin (Angptl­8/lipasin) ameliorates streptozotocin­induced hyperglycemia and ß­cell destruction in neonatal rats.

Betatrophin [also known as lipasin, angiopoietin­like 8 (ANGPTL8), refeeding induced in fat and liver (RIFL), or hepatocellular carcinoma­associated gene TD26], a 22­kDa protein in the angiopoietin­like family, is a liver­derived hormone that promotes pancreatic ß­cell proliferation and lipid metabolism. The aim of the present study was to investigate the effect of recombinant betatrophin on ß­cell regeneration in a neonatal streptozotocin (STZ)­induced diabetic rat model. One­day­old Wistar rats were injected with STZ (100 mg/kg), followed by intraperitoneal administration of betatrophin to the STZ­injected rats for 6 days. Plasma glucose and body weight were monitored. On days 4 and 7, expression levels of pancreatic duodenal homeobox gene­1 (PDX­1), the Bax/B­cell lymphoma­2 (Bcl­2) ratio and plasma insulin were assessed, and the ß­cell proliferation rate was determined. Pancreatic islet area and number were determined at 10 weeks. It was found that betatrophin treatment alleviated STZ­induced hyperglycemia, elevated pancreatic expression levels of Bcl­2, PDX­1, plasma insulin levels and the ß­cell proliferation rate on days 4 and 7. Long­term betatrophin treatment improved glucose tolerance, associated with improved plasma insulin levels and ß­cell mass. These results suggest that early administration of betatrophin promotes ß­cell proliferation in STZ­induced diabetic neonates and prevents the development of diabetes in adults.

[Effects of lead exposure to rat placenta and pups during different gestation periods].

OBJECTIVE: To investigate the effects of lead exposure to rat placenta and pups during different gestation periods. METHODS: All 108 Wistar rats (72 females, 36 males) were randomly divided into four groups. All rats were orally fed with 0.025% lead acetate during different gestation periods. Blood was obtained from the abdominal vena cava and the lead level in maternal blood was measured by means of atomic absorption spectrometry at the end of the pregnancy. The number of pups, their body weight, body length and tail length were measured. The effects of lead to rat placenta were observed by level of microscopy, optical microscopy and electronic microscopy. RESULTS: Experimental groups the blood lead level at the end of gestation were above 0.483 micromol/L. There were significant differences among, of pups, during different groups (P < 0.01). Among them the drinking lead group of whole distant was the lowest in placenta weight [(0.31 +/- 0.13) g] body weight of pups [(2.08 +/- 0.88) g] length and tail length of pups [(2.37 +/- 0.32) cm, (0.98 +/- 0.09) cm]. There were significantly differences between the experimental groups and controls. Maternal blood lead level was negatively related to placenta weight (r = 0.652, P < 0.01), and had no relation with the body weight of pups (r = -0.107, P = 0.46). In the experimental groups of lead poisoned rats, the placenta showed focus necrosis in the deciduas, and increased the trophoblastic giant cells and light staining cells in the trophospongium. Trophoblast in the labyrinth and trophospongium showed degeneration; fibrin deposition around the villi was increased. Microvilli around the trophoblast were shorter and less, mitochondrion was swollen and decreased in number, rough endoplasmic reticulum was distended and ribosomal number on membrane decreased. CONCLUSION: Lead exposure during different gestation periods should have a traumatic effect on the trophoblast, leading to interference of nutrition and oxygen exchange. Furthermore, the blood supply to the placenta and nutrition and oxygen exchange between mother and pups were also interfered, leading to reduction of placenta weight and retardation of development of pups.

[Expression and significance of metallothionein in the placenta of women with low level lead exposure during pregnancy].

OBJECTIVE: To investigate the significance of metallothionein (MT) expression in the placenta of women exposed to low level lead during pregnancy. METHODS: Sixty-seven pregnant women with blood lead level ranging from 1.5 micromol/L to 4.8 micromol/L were randomly selected from the Department of Obstetrics of Qingdao Municipal Hospital between Mar 2005 and Mar 2006. Among them, 35 were with blood lead level less than 2.9 micromol/L (group A) and 32 more than 2.9 micromol/L (group B). Immunohistochemical streptavidin-peroxidase-biotin methods were used to observe the expression of MT in the placental tissue. RESULTS: (1) Among the 67 pregnant women, the highest level of blood lead was 4.7 micromol/L, and the lowest level was 1.6 micromol/L. The blood lead level of groups A and B was (1.7 +/- 0.3) micromol/L, and (3.1 +/- 0.4) micromol/L, with a significant difference between them (P < 0.05). (2) The positive expression of MT was mainly cytoplastic in the cytotrophoblast, decidual cell and small vascular endothelial cells. The positive cell staining was diffuse or scattered. (3) The positive staining of MT was 91% (29/32) and 74% (26/35) in the placental tissue of groups A and B, respectively, with a significant difference between them (P < 0.05). (4) The blood lead level of pregnant women was correlated with the expression of MT of placenta. CONCLUSIONS: Lead can induce the expression of MT in the placental tissue in a dose-dependent manner. MT is mainly located in the cytotrophoblast, decidual cell and small vascular endothelial cells of the placenta. MT expression in the placenta is important to the structural integrity and function of the placenta.

[Effects of intervening measures on postpartum depression].

OBJECTIVE: To study the related factors of postpartum depression (PPD) and the effects of intervening measures to PPD incidence. METHODS: 1 597 pregnant women selected from our antenatal care clinic were investigated by using the hospital anxiety and depression questionnaire (HAD) during pregnancy and the Edinburgh postpartum depression scale (EPDS) after childbirth. All the enrolled women were randomly divided into control group and intervening group by the proportion of 1 to 2. Six intervening measures were used in the latter group. RESULTS: (1) There were 49 women whose HAD >or= 11 score (anxiety-depression mood) with 28 cases (57.1%) had got postpartum depression in the control group. In the intervening group, however, there were 94 women whose HAD >or= 11 score with 24 cases (25.5%) had got postpartum depression. There is a significant difference between the two groups (P < 0.01). (2) There were 71 (13.0%) women whose EPDS >or= 13 score (postpartum depression) in the control group. In the intervening group, however, there were 63 (6.0%) women whose EPDS >or= 13 score. There had a significant difference between the two groups (P < 0.01). (3) PPD women had higher N and P scores than those of non-PPD women (P < 0.01). CONCLUSION: (1) Prenatal anxiety, depression, negative personality and postpartum psychological and physiological changes were high risk factors to PPD. (2) Psychological personality play an important role in PPD. (3) Incidence of PPD was significantly reduced by social support.