1. The results showed that VES downregulates the protein expressions of advanced glycation end products receptor, CCAAT/enhancer binding protein-, and upregulates the protein expressions of pancreatic-duodenal homeobox-1, nuclear factor-erythroid 2-related factor 2 and glyoxalases I from the pancreatic cells. The results also revealed that VES elevates glutathione, and antioxidant enzymes contents, and then downregulates c-Jun N-terminal kinase and p38 mitogen-activated protein kinases pathways to protect pancreatic -cells in MG-administrated rats.
  2. ALA improved hyperinsulinemia and the higher levels of free fatty acids of the T2DM rats. Behavioral experiments showed that the administration of ALA improved cognitive impairment in HFD/STZ-induced T2DM rats. ALA ameliorated insulin-related pathway proteins (phosphoinositide 3-kinase, phospho-protein kinase B (pAkt)/Akt, and insulin-degrading enzyme) and the long-term potentiation pathway, as well as synaptic plasticity proteins (calmodulin-dependent protein kinase II, cyclic AMP response element-binding protein, and postsynaptic density protein-95) of the cerebral cortex or hippocampus in HFD/STZ-induced T2DM rats.
  3. Our results demonstrate that tomatidine significantly decreases body weight and fat weight compared to HFD-fed mice. In addition, tomatidine decreased hepatic lipid accumulation and improved hepatocyte steatosis in HFD-induced obese mice. We also found that tomatidine significantly regulated serum total cholesterol, fasting blood glucose, low-density lipoprotein, and triglyceride levels, but the serum high-density lipoprotein and adiponectin concentrations were higher than in the HFD-fed obese mice. In vivo and in vitro, tomatidine significantly suppressed the expression of fatty acid synthase and transcription factors involved in lipogenesis, and increased the expression of adipose triglyceride lipase. Tomatidine promoted the sirtuin 1 (sirt1)/AMPK signaling pathway to increase lipolysis and β-oxidation in fatty liver cells. These findings suggest that tomatidine potentially ameliorates obesity and acts against hepatic steatosis by regulating lipogenesis and the sirt1/AMPK pathway.
  4. Our results showed that the ethyl acetate fraction (EAf2) from RTL significantly increased glucose uptake and suppressed lipid accumulation in TNF-α plus OA-treated FL83B cells. Western blot analysis showed that EAf2 from RTL ameliorated IR by upregulating the expression of insulin signaling-related proteins, including protein kinase B, glucose transporter-2, and peroxisome proliferator-activated receptor alpha in TNF-α plus OA-treated FL83B cells. The results of this study suggest that EAf2 from RTL may improve hepatic glucose uptake and alleviate lipid accumulation by ameliorating and suppressing the hepatic insulin signaling and lipogenesis pathways, respectively, in hepatocytes.
  5. Results showed that the liver triglyceride contents of T2DM rats was 11.35±1.84%, whereas the administration of 50, 100, and 200 mg/kg BW ALA significantly reduced the liver triglyceride contents of T2DM rats to 4.14±0.59%, 4.02±0.41%, and 3.01±1.07%, respectively. Moreover, 200 mg/kg BW ALA significantly decreased the hepatic levels of NLRP3 inflammasome activation-related proteins NLRP3, caspase-1, and interleukin-1 expression by 40.0%, 60.1%, and 24.5%, respectively, in T2DM rats. Furthermore, the expression levels of hepatic fat synthesis-related proteins decreased, namely a 45.4% decrease in sterol regulatory element-binding protein-1c, whereas the expression of hepatic lipid oxidation-related proteins increased, including a 27.5% increase in carnitine palmitoyltransferase, in T2DM rats after 200 mg/kg BW ALA treatment.
  6. BALB/c mice were sensitized with ovalbumin, and received oral sesamol on days 14 to 27. Furthermore, BEAS-2B human bronchial epithelial cells were treated with sesamol to investigate inflammatory cytokine levels and oxidative responses in vitro. Our results demonstrated that oral sesamol administration significantly suppressed eosinophil infiltration in the lung, airway hyperresponsiveness, and T helper 2 cell-associated (Th2) cytokine expressions in bronchoalveolar lavage fluid and the lungs. Sesamol also significantly increased glutathione expression and reduced malondialdehyde levels in the lungs of asthmatic mice. We also found that sesamol significantly reduced proinflammatory cytokine levels and eotaxin in inflammatory BEAS-2B cells. Moreover, sesamol alleviated reactive oxygen species formation, and suppressed intercellular cell adhesion molecule-1 (ICAM-1) expression, which reduced monocyte cell adherence
  7. Our results showed that the EAF5 fraction was isolated from RTL by Sephadex LH20 gel packing chromatography and significantly increased glucose uptake in TNF-α-treated FL83B cells. Moreover, EAF5 was separated into five sub-fractions by MCI gel packing chromatography and no significant cytotoxic effect was found for these fractions at the concentration of 25 μg/ml treating in FL83B cells. Among them, EAF5-5 fraction markedly enhanced glucose uptake in TNF-α-treated FL83B cells. The possible bioactive compounds of EAF5-5 fraction were identified by HPLC assay including syringic acid, p-coumaric acid, and cirsimaritin. The p-coumaric acid was the bioactive compound with the best effect of increasing glucose intake among the three, but its effect was still not as good as the mix group of the above three compounds and the EAF5-5 fraction. Thus, we speculated that the anti-diabetes effect of RTL may be the result of multiple active ingredients.
  8. Phloretin significantly reduced excessive lipid accumulation and decreased sterol regulatory element-binding protein 1c, blocking the expression of fatty acid synthase in oleic acid-induced HepG2 cells. Phloretin increased Sirt1, and phosphorylation of AMP activated protein kinase to suppress acetyl-CoA carboxylase expression, reducing fatty acid synthesis in hepatocytes. Phloretin also reduced body weight and fat weight compared to untreated HFDfed mice. Phloretin also reduced liver weight and liver lipid accumulation and improved hepatocyte steatosis in obese mice. In liver tissue from obese mice, phloretin suppressed transcription factors of lipogenesis and fatty acid synthase, and increased lipolysis and fatty acid β-oxidation. Furthermore, phloretin regulated serum leptin, adiponectin, triglyceride, low-density lipoprotein, and free fatty acid levels in obese mice.
  9. Administration RTL aqueous extract (RTLW) or ethanolic extract (RTLE) at dosage of 100 or 400 mg/kg body weight for 4 weeks were carried out in HFD/STZ induced T2DM rats. Liver weight, adipose (epididymal and perirenal adipose tissues) weight, hepatic triglyceride level and de novo lipogenesis (DNL) associated proteins expression were monitored after scarification. The results revealed that RTLW and RTLE reduced relative liver weight and relative fat weights in HFD/STZ induced T2DM rats. RTLW and RTLE also ameliorated NAFLD and hepatic triglyceride (TG) accumulation in diabetic rats. Moreover, hepatic DNL regulated enzymes, such as sterol regulatory element-binding protein-1 (SREBP1) and fatty acid synthase (FAS) expression were significantly suppressed by RTLE (100 and 400 mg/kg body weight) in diabetic rats.
  10. Our results demonstrated that HFD-induced obese mice treated with licochalcone A had decreased body weight as well as inguinal and epididymal adipose tissue weights compared with HFD-treated mice. Licochalcone A also ameliorated hepatocyte steatosis and decreased liver tissue weight and lipid droplet accumulation in liver tissue. We also found that licochalcone A significantly regulated serum triglycerides, low-density lipoprotein, and free fatty acids, and decreased the fasting blood glucose value. Furthermore, in vivo and in vitro, licochalcone A significantly decreased expression of the transcription factor of lipogenesis and fatty acid synthase. Licochalcone A activated the sirt-1/AMPK pathway to reduce fatty acid chain synthesis and increased lipolysis and -oxidation in hepatocytes.
  11. Inflammatory human tracheal epithelial (BEAS-2B) cells were treated with licochalcone A to evaluate oxidative responses and inflammatory cytokine levels. In addition, BALB/c mice were sensitized with ovalbumin (OVA) and injected intraperitoneally with licochalcone A (5 or 10 mg/kg). Licochalcone A significantly inhibited reactive oxygen species, eotaxin, and proinflammatory cytokines in BEAS-2B cells. LicochalconeAalso decreased intercellular adhesion molecule 1 levels in inflammatory BEAS-2B cells, blocking monocyte cell adherence. We also found that licochalcone A significantly decreased oxidative responses,reduced malondialdehyde levels, and increased glutathione levels in the lungs of OVA-sensitized mice. Furthermore, licochalcone A decreased airway hyper-responsiveness, eosinophil infiltration,and Th2 cytokine production in the BALF.
  12. The results of Morris water maze indicated that, by administrating CA (30 mg/kg b.w./day) for 30 weeks, the memory and learning impairments in HF-induced hyperinsulinemic rats were significantly ameliorated. CA also enhanced superoxide dismutase and glutathione free radical scavenger activity in hyperinsulinemic rats. The western blot data further confirmed that protein expressions of phosphorylated-glycogen synthase kinase 3β (GSK3β) were significantly increased, whereas the expression of phosphorylated-tau protein decreased in hippocampus of rats administered with CA in comparison with the HF group. Moreover, the expression of amyloid precursor protein (APP) and β-site APP cleaving enzyme were attenuated, subsequently lowering the level of β-amyloid 1-42 (Aβ 1-42) in the hippocampus of CA treated hyperinsulinemic rats. CA also significantly increased the expression of synaptic proteins in HF rats.
  13. Results showed that RTL ethanol extract (100 and 400 mg/kg BW/d) ameliorated serum lipid profiles, including triglyceride (TG), free fatty acid (FFA), low-density lipoprotein cholesterol (LDL-C), very low-density lipoprotein cholesterol (VLDL-C) and high-density lipoprotein cholesterol (HDL-C) levels. It also significantly reduced the level of serum cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in T2DM rats. Additionally, RTL extract decreased endothelin-1 (ET-1) and endothelial nitric oxide (eNOS) contents, reduced the level of cell adhesion factors, including monocyte chemoattractant protein-1 (MPC-1) and cell adhesion factor vascular cell adhesion molecule-1 (VCAM-1), while decreasing content of damage factors, namely tissue factor (TF) and von Willebrand factor (vWF) in aortic tissues of diabetic rats.
  14. This study investigated the ameliorative effect of gallic acid (GA) on hypertriglyceridemia and fat accumulation in perirenal adipose tissues of high-fructose diet (HFD)-induced diabetic rats. The previous results showed that orally administered GA (30 mg/kg body weight) for four weeks significantly reduced the levels of plasma glucose and triglyceride (TG) in HFD rats. GA also markedly decreased the perirenal adipose tissues weight of HFD rats in present study. Western blot assay indicated that GA restored expression of insulin signaling-related proteins, such as insulin receptor, protein kinase C-zeta, and glucose transporter-4 in the perirenal adipose tissues of HFD rats. Moreover, GA enhanced expression of glycolysis-related proteins, such as phosphofructokinase (PFK) and pyruvate kinase (PK), and increased the expression of lipolysis-related proteins, such as adipose triglyceride lipase (ATGL), which is involved in lipolysis in the perirenal adipose tissues of HFD rats.
  15. Ruellia tuberosa L. (RTL) exhibits a wide range of phytochemical activities, for example on treatment of diabetes mellitus (DM), in Orient. There is, however, few study regarding the effect of RTL on glycemic-related homeostasis in type 2 DM (T2DM). We investigated the effect of RTL aqueous and ethanolic extracts on hypoglycemia in high-fat diet (HFD)-fed plus streptozotocin (STZ)-induced T2DM rats, and examined the effect of RTL on glucose uptake in TNF-α-induced insulin resistant mouse C2C12 myoblasts, a mouse skeletal muscle cell line. The administration of 100 or 400 mg/kg BW/day of RTL aqueous or ethanolic extracts once a day for 4 weeks significantly ameliorated hyperglycemia, hyperinsulinemia, and the insulin resistance index in diabetic rats. RTL either aqueous or ethanolic extract at a concentration of 25–800 μg/mL significantly improved glucose uptake in insulin-resistant mouse C2C12 myoblasts, indicating inhibiting the insulin resistance in skeletal muscles.
  16. This study we uses a model marination solution comprising 0.2 M glucose–0.2 M glycine buffered to pH 4.3 containing either 0% or 50% ethanol and mimicked the cooking process by heating for 12 h. Antioxidative and antimutagenic characteristics of Maillard reaction products (MRPs) were investigated. Reducing power, antioxidant activity (Fe2+ chelating ability) and free radical neutralization ability generated from DPPH and ABTS were determined. Ames testing was performed.Results indicate that MRPs from aqueous and alcoholic solution exhibit four antioxidative assays in a dose-dependent manner from 0.16 to 10.00 mg mL−1. However, MRPs from the alcoholic model were superior. In Ames testing, MRPs from both models are neither toxic nor mutagenic at the test concentrations of 0.63–10.00 mg plate−1. However, MRPs from the alcoholic model exhibited a higher inhibitory effect on the direct-acting mutagen 4-NQNO compared to the aqueous model.
  17. Subsequently, rats received oral administrations of 100 or 400 mg/kg body weight RTL extrThe real-time PCR analyses showed that the abnormality of hepatic phase I and II detoxification enzymes expression were observed in diabetic rats. However, both RTLW and RTLE significantly normalized the expression of hepatic phase I detoxification enzymes such as CYP 2E1, and expression of phase II detoxification enzymes such as UGT 1A7 and GST M1 in diabetic rats. Furthermore, we found that fasting serum glucose, hemoglobin A1C (HbA1C) and the areas under the curve of oral glucose tolerance test (AUCOGTT) levels were significantly reduced in both RTLW and RTLE treatment diabetic rats. Moreover, both RTLW and RTLE significantly increased the activity of hepatic anti-oxidative enzymes such as superoxide dismutase (SOD) in diabetic rats.
  18. This study investigates the ameliorative effect of vescalagin (VES) isolated from Pink wax apple fruit on hepatic insulin resistance and abnormal carbohydrate metabolism in high-fructose diet (HFD)-induced hyperglycemic rats. The results show that in HFD rats, VES significantly reduced the values of the area under the curve for glucose in an oral glucose tolerance test and the homeostasis model assessment of insulin resistance index. VES significantly enhanced the activity of hepatic antioxidant enzymes while reducing thiobarbituric acid–reactive substances in HFD rats. Western blot assay revealed that VES reduced hepatic protein expression involved in inflammation pathways while upregulating expression of hepatic insulin signaling–related proteins. Moreover, VES upregulated the expression of hepatic glycogen synthase and hepatic glycolysis-related proteins while downregulating hepatic gluconeogenesis-related proteins in HFD rats.
  19. We investigated the hypoglycemic effect of plant phenol gallic acid (GA). We first tested its ability to enhance glucose uptake in an insulin-resistant cell-culture model and then determined its effects on hepatic carbohydrate metabolism in rats with high-fructose diet (HFD)-induced diabetes. GA increased glucose uptake activity by 19.2% at a concentration of 6.25 μg/mL in insulin-resistant FL83B mouse hepatocytes. In HFD-induced diabetic rats, GA significantly alleviated hyperglycemia, reduced the values of the area under the curve for glucose (AUCglucose) in an oral glucose tolerance test, and reduced the scores of the homeostasis model assessment insulin resistance (HOMA-IR) index. The levels of serum C-peptide and fructosamine and cardiovascular risk index scores were also significantly decreased in HFD rats treated with GA.
  20. Excess free fatty acid accumulation from abnormal lipid metabolism results in the insulin resistance in peripheral cells, subsequently causes hyperinsulinemia, hyperglycemia and/or hyperlipidemia in diabetes mellitus (DM) patients. Herein, we investigated the effect of phenolic acids on glucose uptake in an insulin-resistant cell-culture model and on hepatic insulin resistance and inflammation in rats fed a high-fructose diet (HFD). The results show that vanillic acid (VA) demonstrated the highest glucose uptake ability among all tested phenolic acids in insulin-resistant FL83B mouse hepatocytes. Furthermore, rats fed HFD for 16 weeks were orally administered with VA daily (30 mg/kg body weight) at Week 13-16. The results show that levels of serum insulin, glucose, triglyceride, and free fatty acid were significantly decreased in VA-treated HFD rats (P < 0.05), indicating the protective effects of VA against hyperinsulinemia, hyperglycemia and hyperlipidemia in HFD rats.
  21. This study investigated the effect of phenolic acid on memory decline and cerebral carbohydrate metabolism in rats fed a high-fat diet (HFD), which induced hyperinsulinemia. First, among eleven tested phenolic acids, caffeic acid (CA) was demonstrated to induce the highest glucose uptake capacity in insulin-resistant Neuro 2a mouse neuroblastoma cells. Next, male rats fed a HFD were treated with daily oral CA (30 mg/kg body weight) for 30 weeks. Cognitive performance trials were conducted to investigate the effect of CA on ameliorating memory impairment. Cerebral tissues were analyzed to determine whether CA affected brain carbohydrate metabolism and/or alleviated insulin and leptin resistances.
  22. Vescalagin, an active component from Pink wax apple [Syzygium samarangense (Blume) Merrill and Perry
  23. This study investigated the glucose uptake activity of the water extracts from the leaves and fruit of edible Myrtaceae plants in FL83B mouse hepatocytes. The fluorescent dye 2-(N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino)-2-deoxyglucose (2-NBDG) was used to estimate the uptake ability of the cells. Glucose uptake test showed that pink wax apple fruit water extract (PWFE) exhibits the highest glucose uptake activity, at an increment of 21 % in the insulin-resistant FL83B mouse hepatocytes as compared with the tumour necrosis factor-α (TNF-α)-treated control group. Vescalagin was isolated using column chromatography of PWFE. This compound, at the concentration of 6.25 μg/mL, exhibits the same glucose uptake improvement in insulin-resistant cells as PWFE at 100 μg/mL does. We postulate that vescalagin is an active component in PWFE that may alleviate the insulin resistance in mouse hepatocytes.
  24. The unbalance of glucose metabolism in humans may cause the excessive formation of methylglyoxal (MG), which can react with various biomolecules to form the precursor of advanced glycation end products (AGEs). Vescalagin (VES) is an ellagitannin that alleviates insulin resistance in cell study. Results showed that VES reduced the value of oral glucose tolerance test, cardiovascular risk index, AGEs, and tumor necrosis factor-α contents while increasing C-peptide and d-lactate contents significantly in rats orally administered MG and VES together. The preventive effect of VES on MG-induced inflammation and carbohydrate metabolic disorder in rats was thus proved. On the basis of the experiment data, a mechanism, which involves the increase in d-lactate to retard AGE formation and the decrease in cytokine release to prevent β-cell damage, is proposed to explain the bioactivities of VES in antiglycation and in the alleviation of MG-induced carbohydrate metabolic disorder in rats
  25. FL83B mouse hepatocytes were treated with tumor necrosis factor-α (TNF-α) to induce insulin resistance to investigate the effect of a wax apple aqueous extract (WAE) in insulin-resistant mouse hepatocytes. The results show that WAE significantly improves the uptake of glucose and enhances glycogen content in insulin-resistant FL83B mouse hepatocytes. The results from Western blot analysis also reveal that WAE increases the expression of glycogen synthase (GS), hexokinase (HXK), glucose-6-phosphate dehydrogenase (G6PD), phosphofructokinase (PFK) and aldolase in TNF-α treated cells, indicating that WAE may ameliorate glucose metabolism by promoting glycogen synthesis and the glycolysis pathways in insulin-resistant FL83B mouse hepatocytes.
  26. Inflammation is associated with the development of insulin resistance in Type 2 diabetes mellitus. In the present study, mouse FL83B cells were treated with tumor necrosis factor-alpha (TNF-α) to induce insulin resistance, and then co-incubated with a fraction from wax apple fruit extract (FWFE). This fraction significantly increased the uptake of the nonradioactive fluorescent indicator 2-[N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl) amino]-2-deoxy-d-glucose (2-NBDG) in insulin resistant cells. Western blot analysis revealed that, compared with the TNF-α-treated control group, FWFE increased the expression of the insulin receptor (IR), insulin receptor substrate-1 (IRS-1), protein kinase B (Akt/PKB), phosphatidylinositol-3 kinase (PI3K), and glucose transporter 2 (GLUT-2), and increased IR tyrosyl phosporylation, in insulin resistant FL83B cells.
  27. Tumour necrosis factor-α (TNF-α) plays a pivotal role in cellular insulin resistance and can induce insulin resistance in mouse FL83B hepatocytes. Caffeic acid and cinnamic acid were found to improve glucose uptake in TNF-α-treated insulin-resistant mouse FL83B hepatocytes. The mechanism of glucose metabolism by caffeic acid and cinnamic acid was further investigated. The result from western blot analysis revealed that caffeic acid and cinnamic acid increased expression of glycogen synthase, whereas the expression of glycogen synthase kinase and phosphorylation of glycogen synthase at Ser641 in insulin-resistant mouse hepatocytes was decreased. Caffeic acid and cinnamic acid suppressed the expression of hepatic nuclear factor-4 in TNF-α-treated mouse FL83B hepatocytes. The activity of phosphoenolpyruvate carboxykinase was also inhibited.
  28. Nonenzymatic browning occurs readily in alcoholic beverages and degrades their color quality. Ascorbic acid degradation in the presence of phenolic compounds is a major browning pathway in alcoholic beverages with fruit or fruit juice as the raw material or an ingredient. In the present study ethanolic solutions of ascorbic acid and catechin were prepared to simulate the alcoholic beverages. Ascorbic acid degradation and browning in these model solutions were investigated. Glycerol solutions with the same water activity (Aw) values as those of the ethanolic model solutions were used as controls in the evaluation of browning rate.
  29. The Maillard reaction of foods is essential part of cooking because it enhances the flavor and color presentation of foods. Maillard reaction occurred via the chemical reaction between amino acids and a reducing sugar. The present study mimics cooking meats in alcohol or distilled spirit marinades by using a 0.1 M creatinine / 0.05 M sugars / 0.1 M threonine ethanolic model solution in an attempt to investigate the formation of carcinogenic compounds containing imidazole quinoline (IQ) and imidazole quinoxaline (IQx) compounds via Maillard reaction. The results showed that ethanol accelerated the formation of carcinogenic IQ and IQx compounds. The contents of IQ and IQx increase with the increasing of ethanol concentration in the model solutions with a dose-dependent manner. In the aqueous model solution of 0.1 M creatinine / 0.05 M glucose / 0.1 M threonine after 8 hours heating at 150oC, the contents of IQ and IQx are 16.5±2.2 and 26.2±4.2 ×103 ng/g, respectively.
  30. The present study investigated the stability of green color in 1% to 60% ethanolic solutions of chlorophyll a. Kinetics studies were performed. The results show that the color loss follows first order reaction kinetics, similar to that in aqueous systems, with a reaction rate constant between 0.013 and 13.575 day-1 at 20oC and an activation energy between 18.4 and 85.1 kJ mol-1. The rate of color loss increases with the temperature and varies with the ethanol concentration. It reaches the maximum at 40% ethanol concentrations. The difference among the absorption spectra of the ethanolic solutions suggests that the interaction between water and ethanol molecules may be the major factor affecting the color stability of chlorophyll in the solutions. The bathochromic shift is most obvious around 40% ethanol concentration. We postulate that the formation of clusters of water-ethanol molecules is responsible for the increase in the rate of color loss.

名稱 開始日期 結束日期 委託單位 編號 參與身份別
本土臺灣天仙果減緩第二型糖尿病周邊神經病變之評估及其機制探討 2024/08/01 2025/07/31 國科會 NSTC 111-2320-B-003 -005 -MY3 主持人
功能性便秘與睡眠問題在學齡前兒童：直腸菌叢機制及可能使用的益生質 2023/11/01 2024/10/31 國科會 NSTC 112-2320-B-003-005 協同/共同主持人
本土臺灣天仙果減緩第二型糖尿病周邊神經病變之評估及其機制探討 2023/08/01 2024/07/31 國科會 NSTC 111-2320-B-003 -005 -MY3 主持人
本土臺灣天仙果減緩第二型糖尿病周邊神經病變之評估及其機制探討 2022/08/01 2023/07/31 國科會 NSTC 111-2320-B-003 -005 -MY3 主持人
以生體外、內模式探討丙烯醛於庫氏細胞（Kupffer cells）發炎及肝臟胰島素阻抗生成扮演之角色及食品源胺基酸減緩烘焙油酥餅乾產品熱加工過程丙烯醛生成與第二型糖尿病進程之研究 2021/08/01 2022/07/31 科技部(原國科會) MOST 110-2320-B-003-002 主持人
甲型硫辛酸(alpha-lipoic acid)調控肝臟庫弗細胞(Kupffer cells) NLRP3發炎體活化以改善糖尿病型肝疾病大鼠高血糖及非酒精性脂肪肝之評估及機制探討(3/3) 2020/08/01 2021/07/31 科技部(原國科會) MOST 107-2320-B-003 -004 -MY3 主持人
甲型硫辛酸(alpha-lipoic acid)調控肝臟庫弗細胞(Kupffer cells) NLRP3發炎體活化以改善糖尿病型肝疾病大鼠高血糖及非酒精性脂肪肝之評估及機制探討(2/3) 2019/08/01 2020/07/31 科技部(原國科會) MOST 107-2320-B-003 -004 -MY3 主持人
甲型硫辛酸(alpha-lipoic acid)調控肝臟庫弗細胞(Kupffer cells) NLRP3發炎體活化以改善糖尿病型肝疾病大鼠高血糖及非酒精性脂肪肝之評估及機制探討(1/3) 2018/08/01 2019/07/31 科技部(原國科會) MOST 107-2320-B-003 -004 -MY3 主持人
消渴草改善糖尿病型肝疾病大鼠肝臟胰島素阻抗、能量代謝與解毒相關功能的評估及其機制探討(3/3) 2017/08/01 2018/07/31 科技部(原國科會) MOST 104-2320-B-003 -003 -MY3 主持人
消渴草改善糖尿病型肝疾病大鼠肝臟胰島素阻抗、能量代謝與解毒相關功能的評估及其機制探討(2/3) 2016/08/01 2017/07/31 科技部(原國科會) MOST 104-2320-B-003 -003 -MY3 主持人
消渴草改善糖尿病型肝疾病大鼠肝臟胰島素阻抗、能量代謝與解毒相關功能的評估及其機制探討(1/3) 2015/08/01 2016/07/31 科技部(原國科會) MOST 104-2320-B-003 -003 -MY3 主持人
天然酚酸改善高熱量飲食引起之混合型失智症大鼠學習與記憶損傷的評估及其機制探討 2014/08/01 2015/07/31 國科會 NSC 101-2320-B-003 -004 -MY3 主持人
天然酚酸改善高熱量飲食引起之混合型失智症大鼠學習與記憶損傷的評估及其機制探討 2013/08/01 2014/07/31 國科會 NSC 101-2320-B-003 -004 -MY3 主持人
天然酚酸改善高熱量飲食引起之混合型失智症大鼠學習與記憶損傷的評估 2012/08/01 2013/07/31 國科會 NSC 101-2320-B-003 -004 -MY3 主持人
由食療性素材及食品加工副產品開發抗老化食品 2011/08/01 2012/07/31 國科會 NSC 100-2622-B-002-005-CC2 協同/共同主持人
酚酸及其衍生物之降血糖生理活性、機制探討及改善因腦部組織胰島素抗性引起之失智症的評估 2011/08/01 2012/07/31 國科會 NSC 100-2313-B-003 -001 主持人
修飾性果膠生理活性之探討 2011/08/01 2012/07/31 國科會 NSC 98-2313-B-020 -013 -MY3-3 協同/共同主持人
藥用與食用桃金孃科植物對第二型糖尿病胰島素阻抗研究、蛋白質體學探討與降血糖功能性評估 2010/08/01 2011/07/31 國科會 NSC 97-2313-B-214-002-MY3-3 主持人
由食療性素材及食品加工副產品開發抗老化食品 2010/08/01 2011/07/31 國科會 NSC 99-2622-B-002-003-CC2 協同/共同主持人
修飾性果膠生理活性之探討 2010/08/01 2011/07/31 國科會 NSC 98-2313-B-020 -013 -MY3-2 協同/共同主持人
由食療性素材及食品加工副產品開發抗老化食品 2009/08/01 2010/07/31 國科會 NSC 98-2622-B-002-005-CC2 協同/共同主持人
藥用與食用桃金孃科植物對第二型糖尿病胰島素阻抗研究、蛋白質體學探討與降血糖功能性評估 2009/08/01 2010/07/31 國科會 NSC 97-2313-B-214-002-MY3-2 主持人
修飾性果膠生理活性之探討 2009/08/01 2010/07/31 國科會 NSC 98-2313-B-020-013-MY3-1 協同/共同主持人
藥用與食用桃金孃科植物對第二型糖尿病胰島素阻抗研究、蛋白質體學探討與降血糖功能性評估 2008/08/01 2009/07/31 國科會 NSC 97-2313-B-214-002-MY3-1 主持人
以蛋白質體學探討胰島素阻抗形成與降血糖藥物、番石榴成分改善第二型糖尿病胰島素阻抗之機制 2007/08/01 2008/07/31 國科會 NSC 96-2313-B-214-005 主持人
純化番石榴葉降血糖成分對第二型糖尿病胰島素敏感性及葡萄糖代謝之影響 2006/08/01 2007/07/31 國科會 NSC 95-2313-B-214-001 主持人
番石榴對第二型糖尿病降血糖之評估及其對碳水化合物代謝之研究 2005/08/01 2006/07/31 國科會 NSC 94-2313-B-214-001 主持人