RESUMO
<p><b>OBJECTIVE</b>To investigate the relationship of serum omentin-1 and chemerin with gestational diabetes mellitus (GDM).</p><p><b>METHODS</b>Serum levels of omentin-1 chemerin, glycolipids biochemical index, inflammation index, fasting insulin (FINS), and insulin resistance indexes (HOMA-IR) were determined in 85 women with GDM and 85 pregnant women with normal glucose tolerance (NGT).</p><p><b>RESULTS</b>BMI, FPG, hs-CRP, blood lipids, blood glucose, FINS, HOMA-IR and serum chemerin level were all significantly higher while serum omentin-1 significantly lower in GDM group than in NGT group (P<0.05). In both groups, serum omentin-1 level was significantly lower and serum chemerin was significantly higher in obese subjects than in the non-obese subjects (P<0.05). Obesity before delivery and/or HOMA-IR ≥2 was associated with a significantly decreased serum omentin-1 level; serum chemerin increased significantly in obese women before delivery but was not associated with HOMA-IR. Serum omentin-1 level was positively correlated with HDL but inversely with BMI (at pregnancy and before delivery), FPG, FINS and HOMA-IR; Chemerin was positively correlated with TC, TG, hs-CRP and FPG; serum omentin-1 and chemerin levels were not significant correlated (P=0.301). In women with GDM, BMI at pregnancy, TG, FPG, and FINS were all independent factors affecting serum omentin-1; TG, LDL, and hs-CRP were independent factors affecting serum chemerin.</p><p><b>CONCLUSION</b>An decreased serum omentin-1 can be indicative of glucose and lipid metabolism disorder and insulin resistance, and an increased serum chemerin level indicates hyperlipidemia and chronic inflammation in pregnant women. Both of the adipokines are closed associated with GDM and probably participate in the occurrence and development of GDM.</p>
RESUMO
<p><b>OBJECTIVE</b>To investigate the effects of chronic aluminum exposure on the learning and memory abilities and brain-derived nerve growth factor (BDNF) in Sprague-Dawley (SD) rats.</p><p><b>METHODS</b>Thirty-two male SD rats were randomly and equally divided into 4 groups: control group and high-, middle-, and low-dose exposure groups. The rats in high-, middle-, and low-dose exposure groups were fed with the feed mixed with AlCl(3) (120.0, 12.0, and 1.2 mg/kg, respectively), while the rats in control group were fed conventionally. After 6 months of feeding, brain aluminum levels were determined by inductively coupled plasma mass spectrometry; Morris water maze was employed to test the learning and memory abilities; the expression and content of BDNF in brain tissue were measured by Western blot and enzyme-linked immuno sorbent assay (ELISA).</p><p><b>RESULTS</b>The high- and middle-dose exposure groups had significantly higher brain aluminum levels than the control group (P<0.05). The Morris water maze test showed that the high- and middle-dose exposure groups had significantly prolonged escape latency (P<0.05), significantly prolonged time taken to first reach the target quadrant (P<0.01), and significantly decreased number of platform crossings and time spent in the target quadrant (P<0.05), as compared with the control group. The Western blot and ELISA showed that the expression and content of BDNF in brain tissue decreased as the dose of AlCl(3) increased, and they were significantly lower in the high- and middle-dose exposure groups than in the control group (P<0.05).</p><p><b>CONCLUSION</b>Chronic aluminum exposure (12.0 and 120.0 mg/kg) can lead to cognitive dysfunction in rats, and the decreased expression of BDNF may be one of the mechanisms of learning and memory deficits induced by aluminum.</p>