中国蔬菜产业可持续发展研讨会将于4月在华中农大举行

由中国园艺学会主办．湖北省园艺学会、国家蔬菜改良中心华中分中心、华中农业大学园艺林学学院共同承办的2006中国蔬菜产业可持续发展研讨会定于2006年4月在华中农业大学（湖北武汉）举行，现将有关事宜通知如下。     

“2006中国蔬菜产业可持续发展研讨会”在华中农大成功召开

2006年4月13～15日．由中国园艺学会举办，华中农业大学园艺林学学院承办的“2006中国蔬菜产业可持续发展研讨会”在武汉华中农业大学国际学术交流中心成功召开。     

“全国茄子大会暨学术研讨会”在武汉召开

由中国园艺学会、武汉市人民政府、湖北省农业厅主办，湖北省园艺学会、武汉市农业局、武汉市农业科学院协办，武汉市蔬菜科学研究所、湖北省园艺学会蔬菜专业委员会承办的“全国茄子大会暨学术研讨会”于2008年6月5～7日在湖北省武汉市隆重召开，来自全国25个省市的逾50家科研、教学、推广部门以及种子种苗企业的200多位代表参加了本次会议。中国园艺学会理事长方智远院士、武汉市人民政府张学忙副市长、湖北省农业厅徐能海副厅长、湖北省园艺学会副理事长叶志彪教授等到会祝贺。     

“全国蔬菜和薯类种质资源研究与利用研讨会”会议纪要

由中国园艺学会蔬菜专业委员会和中国农业科学院蔬菜花卉研究所共同组织的“全国蔬菜和薯类种质资源研究与利用研讨会”于2006年4月26～28日在北京召开。来自全国15个省（市）和自治区32个单位的92名代表出席了会议。科技部农村司协调处许增泰处长、农业处魏勤芳副处长、农业部种植业司种子处李恩普处长、科教司交流与推广处刘艳处长、中国农业科学院刘旭副院长、科技管理局综合处张燕卿处长、中国园艺学会名誉理事长朱德蔚等有关部门领导出席了开幕式并讲话。     

林处发研究员

林处发,男,推广研究员,国务院津贴专家,武汉市农科院副院长,国家大宗蔬菜产业技术体系武汉功能实验站站长。中国园艺学会理事、中国园艺学会水生蔬菜分会理事长、中国园艺学会茄子分会副理事长、湖北省园艺学会副理事长兼蔬菜专业委员会主任、湖北省植物生理学会副理事长：《长江蔬菜》、《上海蔬菜》编委,     

第六届全国水生蔬菜学术及产业化研讨会圆满召开

2012年8月8～9日,"第六届全国水生蔬菜学术及产业化研讨会"在湖北仙桃召开。会议由中国园艺学会水生蔬菜分会、湖北省农业厅、湖北省仙桃市人民政府及武汉市农业科学技术研究院主办,湖北农鑫农产品科技发展专业合作社、华中农业大学食品科技学院、湖北省蔬菜办公室、仙桃市彭场镇人民政府、仙桃市     

“全国茄子育种工作交流会暨茄子新品种展示会”预备通知

全国茄子育种工作交流会暨茄子新品种展示会由中国园艺学会主办，中国农业科学院蔬菜花卉研究所、武汉市人民政府、湖北省农业厅、湖北省园艺学会、武汉市农业局和武汉市农业科学院协办，武汉市蔬菜科学研究所承办。会议预计于2008年5月下旬～6月上旬在湖北省武汉市召开，会期3天。欢迎从事茄子科研、教学、推广及生产等单位代表参加。     

全国首次“水生蔬菜学术及产业化研讨会”在汉召开

由中国园艺学会主办，湖北省园艺学会与武汉市蔬菜办公室协办，国家种质武汉水生蔬菜资源圃与武汉市蔬菜科学研究所承办的全国首次“水生蔬菜学术及产业化研讨会”于２００１年８月２０日至２２日在湖北武汉举行。中国园艺学会副理事长、中国农科院蔬菜花卉研究所李树德研究员出席并主持会议。武汉市蔬菜科学研究所名誉所长孔庆东教授主持会议开幕式。来自北京、湖北、江苏、河南、湖南、浙江、江西、福建、广东、云南、广西、上海、重庆等１２个省市的１０８位代表参加了会议。会议广泛深入地交流了水生蔬菜的资源征集、保存、分布与利用研…     

第一届国际园艺学会蔬菜嫁接研讨会论文征集通知

<正>第一届国际园艺学会蔬菜嫁接研讨会定于2014年3月17—21日在湖北武汉举行。本次大会由国际园艺学会主办,中国园艺学会和华中农业大学承办,武汉维尔福生物科技股份有限公司和武汉如意种苗高科技开发有限公司等单位协办。     

中国园艺学会黄瓜分会2012年年会暨新品种展示会在山东沂南举行

<正>中国园艺学会黄瓜分会第3届年会暨新品种展示会于2012年4月19-20日在山东省沂南县举办。本次会议由中国园艺学会黄瓜分会、国家大宗蔬菜产业技术体系和山东省园艺学会主办,山东省沂南县政府、中国农业科学院蔬菜花卉研究所、山东省农业科学院蔬菜研究所、山东农业大学、青岛市农业科学院、烟台市农业科学院、潍坊市农业科学院联合承办。出席本次会议的主要领导有:中国园艺学会理事长杜永臣、中国园艺学会黄瓜分会理事长杜胜利、沂南县委副书记吴昌力。邀     

Effect of pioglitazone on glucose metabolism and PPAR-γ expression in lipid-infused rats

AIM: To investigate the effect of pioglitazone (Pio) on glucose metabolism and peroxisome proliferators-activated receptor (PPAR)-γ expression in free fatty acid (FFA) -induced insulin resistance in rats. METHODS: A hyperinsulinaemic-euglycaemic clamp and ［3-3H］-glucose tracing technique were used in awake rats. Glucose metabolism in vivo and PPAR-γ in adipose tissue expression were assessed with elevation FFA by lipid infusion over 4 h in rats pretreated with or without Pio.RESULTS: During steady-state of clamp, there was a significant increase in plasma FFA in two lipid-infused groups, compared to control rats (P<0.01). The glucose infusion rates (GIR) in Pio-treated rats (P/L group), compared with controls, were significantly reduced ［(20.6±0.4) mg·kg^-1·min^-1 vs (33.6±0.6)mg·kg^-1· min^-1, P<0.01］, whereas the GIR was lower in the lipid group (L group) than that in the P/L group［(12.6±0.8) mg·kg^-1·min^-1 vs (20.6±0.4) mg·kg^-1·min^-1, P<0.01］. The hepatic glucose production (HGP) was significantly suppressed (85%) ［(18.3±2.1)mg· kg^-1·min^-1 (basal) vs (2.7±2.4)mg· kg^-1·min^-1, and (17.5±2.6) mg· kg^-1·min^-1 vs (2.6±1.0)mg· kg^-1·min^-1］, all P<0.01 during clamp in control and P/L groups. The suppressive effect of insulin on HGP was significantly blunted in L group［(17.3±2.1)mg· kg^-1·min^-1 vs (15.8±1.5)mg· kg^-1·min^-1］. The rate of glucose disappearance (GRd) was significantly reduced in two lipid-infused rats compared with controls［(26.6±1.6)mg· kg^-1·min^-1 and (23.2±0.9)mg· kg^-1·min^-1 vs (37.7±2.6)mg·kg^-1·min^-1,P<0.01］. The PPAR-γ expression of adipose tissue in P/L group was significantly upregulated. CONCLUSION: Lipid-infusion induces an acute insulin-resistance in vivo. Pio treatment upregulates the PPAR-γ of adipose tissue and suppresses HGP. Pio can protect partly against lipid-induced insulin resistance.     

Effects of phosphodiesterase inhibitor-induced insulin resistance on glucose and lipid metabolism in rats

AIM:To investigate the effects of milrinone (a selective phosphdiesterase III inhibitor PDE₃) on insulin secretion, blood glucose, plasma free fatty acids (FFA) and dose-response relationship, and assess possible effects of milrinone on glucose metabolism and insulin sensitivity in conscious rats.METHODS:The catheterized nonstressed rats were administered by the varying doses of milrinone (1, 5, 25 μmol/kg) and were compared with controls. A hyperinsulinaemic- euglycaemic clamp was established in awake rats, and milrinone(25 μmol/kg) and 25% dimethyl sulfoxide (DMSO, as a control) were given at 120 min during hyperinsulinaemic- euglycaemic clamp. Glucose turnover was decided by gas chromatograph mass spectrometer (GC-MS).RESULTS:After dosing, plasma FFA levels in 3 milrinone groups significantly increased compared with the controls and before dosing. The percentages of elevation of FFA by the different milrinone doses were very similar, 50%, 52%, 55% for 1, 5, 25 μmol/kg respectively at 2 min after dosing. Plasma insulin levels were significantly elevated in the 5 and 25 μmol/kg groups, and the effect of milrinone on glucose concentration was detectable only 25 μmol/kg group. During hyperinsulinaemic clamp, there were significant increase in plasma FFA (from 173.1±15.2 to 633.8±87.3 μEq/L) and hepatic glucose production (HGP), and a significant decrease in glucose infusion rates (GIR) (to about 21%).CONCLUSION:These data suggest that milrinone impaires the abilities of insulin to suppress lipolysis and HGP, and insulin-mediated glucose utilization in peripheral tissue. Therefore, milrinone administration may induce an acute insulin resistancein vivo.     

Correlation among plasma leptin,resistin an type 2 diabetes mellitus

AIM：To assess the association of resistin,obesity,serum lipid levels and insulin resistance with plasma leptin.METHODS：The concentrations of fasting serum glucose,insulin,lipid profiles,plasma resistin and leptin were assayed in 80 cases (including 37 controls with normal glucose tolerance and 43 patients with type 2 diabetes mellitus).RESULTS：Fasting plasma leptin level was positively correlated with sex,body mass index (BMI),waist circumference (WC),waist-hip ratio and fasting serum insulin (F Ins) （P<0.01）.Fasting plasma leptin level was negatively correlated with insulin sensitivity index (r=-0.373,P<0.01).There was no correlation between the concentrations of plasma leptin and FPG,TG,TC and resistin （P>0.05）.CONCLUSION：Fasting plasma leptin level is positively correlated with obesity and insulin resistance,not resistin.Leptin may play a role in the pathogenesis of type 2 diabetes mellitus.     

Correlation of serum omentin-1 level and insulin resistance in rats

AIM：To establish the insulin resistance rat model for evaluating the correlation of omentin-1 level and insulin resistance. METHODS：SPF male Wistar rats (n=30) were randomly divided into normal control group (NC, n=15) and high-fat diet group (HF, n=15). The rats in NC group were fed with basic diet. The insulin resistant model was established by feeding the rats with high-fat diet in HF group. After 10 weeks, 5 rats in each group were assessed by the technique of hyperinsulinaemic-euglycaemic clamp. After the insulin resistant model was successfully established, the body weight and fasting blood glucose were detected. The concentration of fasting serum omentin-1 was analyzed by ELISA. Fasting serum insulin was measured by radioimmunoassay. RESULTS：No difference of fasting blood glucose between the 2 groups was observed. The level of fasting serum insulin in HF group was significantly higher than that in NC group (P<0.05). The level of serum omentin-1 in HF group were significantly decreased compared with NC group (P<0.01). Pearson’s correlation analysis showed that negative correlations between serum omentin-1 and fasting serum insulin (r=-0.654,P<0.01), serum omentin-1 and free fatty acid (r=-0.446, P<0.05) was found. CONCLUSION：In rats, serum omentin-1 level began to decrease at insulin resistance stage. As serum omentin-1 level decreased, the basal insulin level increased, indicating that decreased serum omentin-1 level may be an early factor of IR, diabetes and cardiovascular diseases.     

Effect of micronised fenofibrate on lipotoxicity and insulin sensitivity in spontaneously hypertensive rats treated with high-fat diet

AIM: To observe the effect of micronised fenofibrate (lipanthyl) on lipotoxicity and insulin sensitivity (IS) in spontaneously hypertensive rats (SHR) with high-fat diet.METHODS: Twenty-seven SHR were randomly divided into three groups: normal chow group (n=9), high-fat diet group (n=9) and micronised fenofibrate treatment group (n=9). Micronised fenofibrate 100 mg·kg-1·d-1 was given orally to SHR, which diet on high-fat diet for three months. Intramuscular lipids were observed and lipids accumulation index (LAI) was calculated. Nonesterified fatty acid, glucose and insulin were determined in all rats.RESULTS: (1) Compared to SHR in normal chow diet group, body weight and the level of serum TG and TC increased significantly and the level of HDL-C decreased significantly in SHR fed with high-fat diet (P<0.05). Micronised fenofibrate significantly decreased systolic blood pressure, body weight, the level of serum TG and TC, increased the level HDL-C (P<0.05). (2) Fasted blood glucose, free fatty acid (FFA), GLU-AUC obviously increased in high-fat diet group compared with normal chow diet group. Insulin sensitivity index (ISI) in high-fat diet group was much lower than that in normal chow diet group (0.0038±0.0007 vs 0.0053±0.0013, P<0.05). No difference was found between fenofibrate-treated group and normal chow diet group. (3) There were more lipid drops in intramuscular cells of SHR treated with high-fat diet than those in fenofibrate-treated group and normal chow diet group (LAI: 6.42±0.59 vs 3.32±0.77 and 1.98±0.97, P<0.05). After covariance analysis, the results above-mentioned also made sense (F=10.46, P<0.05). (4) Inverse association was found between LAI and ISI (r=-0.58, P<0.05). Positive correlations were found between LAI and TG, FFA, body weight.CONCLUSION: In addition to regulating lipid, micronised fenofibrate may reduce BP, body weight, FFA, lipid accumulation in intramuscular cells and improve insulin sensitivity of SHR treated with high-fat diet.     

Role of asiatic acid in treatment of insulin resistance in mouse adipocytes

AIM：To investigate the effects of asiatic acid, one of triterpenoids from Psidium guajava leaves, on the proliferation and differentiation of 3T3-L1 preadipocytes, and glucose and lipid metabolism of insulin-resistant adipocytes. METHODS：The proliferation of 3T3-L1 preadipocytes was tested by MTT assay, and the accumulation of lipid droplets in differentiated preadipocytes was measured by oil red O staining. The insulin-resistant cell model was established by exposure of the cells to dexamethasone. The cellular glucose uptake was determined by glucose oxidase-peroxidase assay. The free fat acid (FFA) concentration was detected by colorimetric method. Secreted adiponectin were measured by ELISA. The protein levels of peroxisome proliferator-activated receptor γ (PPARγ) and protein tyrosine phosphatase 1B (PTP1B) in insulin-resistant adipocytes were analyzed by Western blotting. RESULTS：Compared with medium group, asiatic acid increased the proliferation of 3T3-L1 preadipocytes and inhibited their differentiation at a concentration range of 10~100 μmol/L (P<0.05 or P<0.01). At concentrations of 30 μmol/L and 100 μmol/L, asiatic acid enhanced cellular glucose uptake in the insulin-resistant adipocytes both in basic and insulin-stimulation states. Asiatic acid decreased FFA production (P<0.05), and down-regulated the protein expression of PTP1B (P<0.05, or P<0.01). However, no effect on the secretion of adiponectin and the protein expression of PPARγ was observed (P>0.05). CONCLUSION：Asiatic acid enhances glucose uptake and inhibits FFA production in insulin-resistant adipocytes via down-regulating the protein expression of PTP1B, all of which play the roles of increasing insulin signaling sensitivity to improve insulin resistance.     

Effects of intranasal Escherichia coli on glucolipid metabolism in high-fat diet-induced obese mice

AIM: To study whether the pulmonary infection of Escherichia coli (E. coli) interferes the glucolipid metabolism in high-fat diet-induced obese mice. METHODS: High-fat diet-induced obese mice (n=48) and normal chow-fed control mice (n=48) were intranasally infused with 40 μL fluid containing 4×10⁹ CFUs E. coli. The serum, periepididymal adipose tissue and liver were obtained at 0 d, 1 d, 2 d, 3 d and 4 d after infection. The body mass, periepididymal adipose tissue and liver were weighed, and the levels of fasting blood glucose (FBG), fasting blood insulin (FINS), free fatty acid (FFA) and very-low-density lipoprotein (VLDL) were measured by ELISA. The serum total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C), and hepatic TG contents were detected, and the hepatic steatosis was observed under microscope with oil red O staining. RESULTS: Compared with day 0, the body mass, fat mass and fat index were decreased significantly from day 1 to day 4 after infection (P<0.05). The levels of FBG, FINS and HOMA-IR were apparently raised from day 2 to day 4 after infection (P<0.05). The contents of serum FFA, TG and VLDL were increased markedly from day 1 to day 4 after infection (P<0.05). However, the concentrations of serum TC, LDL-C and HDL-C were decreased obviously from day 1 to day 3 (P<0.05). The liver mass, liver index and TG content were significantly increased from day 1 to day 4 (P<0.05). Consistently, the lipid droplet accumulation in the liver cells was increased obviously at day 2 and day 4 after infection. Compared with control group, except the levels of serum TC, LDL-C and HDL-C in obese group substantially decreased, the other indexes were increased by different degrees during the whole experiment period (P<0.05). CONCLUSION: Pulmonary infection of Escherichia coli exacerbates the disorder of glucose and lipid metabolism in high-fat diet-induced obese mice, which contributes the development of insulin resistance and hepatic steatosis.     

Role of resistin in hepatic insulin resistance and the underlying mechanism

AIM: To investigate the role of resistin in hepatic insulin resistance and its mechanism. METHODS: A mouse model of hyperresistinemia in C57BL/6 mice was established by intravenous administration of the recombinant adenovirus encoding mouse resistin. Using periodic acid-Schiff staining we observed the effects of resistin on hepatic glycogen storage. Western blotting was used to measure AMPK-α protein and phosphrylated AMPK-α (Thr172) protein. mRNA levels of phosphoenolpyruvate carboxykinase gene and glucose-6-phosphatase gene were measured by real-time PCR. RESULTS: On day 5 after Adv injection, the concentration of plasma resistin was much higher in Adv-resistin-EGFP-treated mice than that in saline- or Adv-EGFP-treated mice. Semiquantitation of hepatic glucogen storage by PAS showed that the mice with hyperresistinemia had decreased glycogen particles compared to normal control and Adv-EGFP groups. The ratio of phosphorylated AMPK (Thr172)-α to total AMPK-α was used to evaluate hepatic AMPK activation. Compared with normal control and Adv-EGFP groups, the Adv-resistin-EGFP-treated mice had significantly lower ratio of p-AMPK/AMPK, and higher expression levels of G6Pase and PEPCK mRNA in liver. CONCLUSION: Resistin may decrease AMPK activation with downregulating expression of gluconeogenic enzymes, resulting in increased glucose production and decreased hepatic glycogen storage. Resistin may play an important role in hepatic insulin resistance.     

The correlation of serum ghrelin level with the total BMC,LM and body weight in premenopausal women with different thyroid functional status

AIM: To investigate the relationship between serum ghrelin level and body composition including bone mineral content (BMC), fat mass(FM) & lean mass(LM) in premenopausal women with different thyroid functional status. METHODS: We measured the serum ghrelin levels by radioimmunoassay (RIA), the serum levels of free triiodothyronine (FT3), free thyroxine (FT4) and sensitive thyroid-stimulating hormone (sTSH) by chemiluminescene immune assay. The total body composition including total BMC, FM and LM was measured by dual-energy X-ray absorptiometry (DXA) in 71 premenopausal women with different thyroid functional status (33 hyperthyroidism, 18 hypothyroidism and 20 normal subjects). RESULTS: (1) The level of serum ghrelin in patients with hyperthyroidism was significantly lower than that in patients with hypothyroidism (P<0.01) and normal subjects (P<0.01), but the serum ghrelin level in patients with hypothyroidism patients was similar to that in normal subjects (P>0.05). The serum ghrelin level was correlated negatively with FT3 (r=-0.318, P<0.01) and FT4 (r=-0.350, P<0.01), simultaneously correlated positively with serum sTSH (r=0.281, P<0.05). (2) The serum ghrelin level in 71 premenopausal women with different thyroid functional status correlated positively with the total BMC (r=0. 284, P<0.05), the total LM (r=0.259, P<0.05), body weight （r=0.279, P<0.05）but there was not correlation with total FM (P>0.05). CONCLUSION: The serum ghrelin level in the premenopausal women with different thyroid functional status may correlate with the total BMC, LM and body weight.     

Hypolipemic and hypoglycemic effects of total triterpenoids from Psidium guajava leaves on type 2 diabetic rats

AIM: To investigate the effects of total triterpenoids from Psidium guajava leaves (TTPGL) on blood glucose and lipids in type 2 diabetic rats. METHODS: The diabetic rats were induced by intraperitoneal injection of streptozotocin at dose of 35 mg/kg and feeding with high-fat diet. The animals were divided into 5 groups: diabetic model control group (model), TTPGL treatment groups (with the doses of 60, 120 and 240 mg/kg, respectively) and rosiglitazone treatment group (3 mg/kg). Another 12 normal SD rats were used as the normal controls. The rats received daily treatment for 6 weeks, and then the levels of fasting blood glucose (FBG), fasting insulin (FINS), triglyceride (TG), total cholesterol (TCH), free fatty acid (FFA), glycosylated hemoglobin (GHb) and glycosylated serum proteins (GSP) were measured. The protein expression of peroxisome proliferator-activated receptor γ (PPARγ) in adipose tissues was detected by Western blotting. RESULTS: Compared with normal control group, the levels of FBG, GHb and blood lipids were increased in type 2 diabetic rats. The FINS, insulin sensitivity index, and the protein expression of PPARγ in adipose tissues were decreased. Compared with model group, the levels of FBG and GSP were decreased,and the FINS, insulin sensitivity index, and the protein expression of PPARγ in adipose tissues significantly increased in TTPGL treatment groups (with the doses of 120 and 240 mg/kg). The levels of serum TG,TCH and FFA were significantly lower in TTPGL treatment groups (P<0.01 or P<0.05) as compared with the model controls. CONCLUSION: TTPGL decreases the levels of blood glucose and lipids in diabetic rats. TTPGL also increases serum insulin level and improves insulin sensitivity. The action mechanism of TTPGL may be related to the increase in the protein expression of PPARγ.