Supported Pt-Co catalysts for selective CO oxidation in a hydrogen-rich stream.
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Journal Article↗
Biomedical subjects
Hyun Chul Lee
Publications and source records attributed to Hyun Chul Lee.
Association of the Gly82Ser polymorphism in the receptor for advanced glycation end products (RAGE) gene with circulating levels of soluble RAGE and inflammatory markers in nondiabetic and nonobese Koreans.
We investigated the association between the Gly82Ser (G82S) polymorphism in the receptor for advanced glycation end products (RAGE) gene and circulating levels of soluble RAGE (sRAGE), advanced glycation end products (AGEs), and inflammatory markers in nondiabetic/nonobese Koreans. A total of 1096 men and 580 women aged 30 to 69 years and with body mass index of 18.5 to 29.9 kg/m(2) were recruited. Anthropometrics, lipid profiles, glucose, insulin, insulin resistance (IR), RAGE G82S polymorphism, sRAGE, AGEs, and inflammatory markers were measured. There was a significant association between G82S genotypes and plasma sRAGE concentrations (P < .001). sRAGE concentrations were significantly higher in subjects with the G/G genotype (1038 +/- 33 pg/mL) than in those with the G/S (809 +/- 19 pg/mL) or the S/S (428 +/- 43 pg/mL) genotype. Furthermore, the G82S genotypes in the RAGE gene were associated with serum AGE (P = .033), homeostasis model assessment for insulin resistance (HOMA-IR) (P < .001), plasma tumor necrosis factor alpha (TNF-alpha) (P = .033), serum C-reactive protein (CRP) (P= .002), and urinary excretion of 8-epi-prostaglandin F(2alpha) (P = .028) after adjusting for sex, age, body mass index, cigarette smoking, and alcohol drinking. Subjects with the S/S genotype showed higher levels of serum AGE, HOMA-IR, plasma TNF-alpha, serum CRP, and 8-epi-prostaglandin F(2alpha) than those with the G/G or G/S combination. The sRAGE levels showed a negative relation with high-sensitivity CRP (r = -0.250; P < .001). The AGE concentrations showed a positive relation with TNF-alpha levels (r = 0.398; P < .001). Subjects with homozygosity for the minor S allele (S/S) of the G82S polymorphism had higher risk factors for cardiovascular disease, such as low sRAGE levels, inflammation, oxidative stress, and IR, compared with those bearing at least one G allele.
5' Untranslated Regions↗
Effects of rosiglitazone and metformin on inflammatory markers and adipokines: decrease in interleukin-18 is an independent factor for the improvement of homeostasis model assessment-beta in type 2 diabetes mellitus.
OBJECTIVE: We examined the individual pharmacological effects of the addition of rosiglitazone and metformin to glimepiride on inflammatory markers and adipokines in patients with type 2 diabetes mellitus. We analysed the relationships between these variables, the measurements of insulin sensitivity and beta-cell function in patients treated with rosiglitazone plus glimepiride. DESIGN AND PATIENTS: One hundred twenty (120) patients with type 2 diabetes mellitus were randomized and treated with glimepiride plus rosiglitazone or glimepiride plus metformin for 12 weeks. The plasma concentrations of the inflammatory markers and adipokines were measured at baseline and after 12 weeks. MEASUREMENTS: Markers of insulin sensitivity and beta-cell function were determined by the quantitative insulin sensitivity check index (QUICKI) and the homeostasis model assessment of beta-cell function (HOMA-beta), respectively. Plasma concentrations of adiponectin were measured by radioimmunoassay. Plasma concentrations of resistin, tumour necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and interleukin-18 (IL-18) were measured using ELISA. RESULTS: Improvements in fasting insulin level, QUICKI and HOMA-beta were noted in the rosiglitazone-treated group. Only the QUICKI value improved in the metformin-treated group. Adiponectin concentrations significantly increased in the rosiglitazone-treated group after 12 weeks. Significant decreases in resistin, C-reactive protein, TNF-alpha, IL-6 and IL-18 were seen in the rosiglitazone-treated patients but not in the metformin-treated patients. The independent risk factor for the HOMA-beta change according to stepwise multivariate regression analysis was a change in IL-18. CONCLUSIONS: Rosiglitazone, but not metformin, improved the plasma concentrations of inflammatory markers and adipokines in patients with type 2 diabetes mellitus. A decrease in IL-18 is an independent factor for the improvement of HOMA-beta in type 2 diabetes mellitus.
Adiponectin↗
Frequent, aggressive behaviors of thyroid microcarcinomas in korean patients.
The incidence of thyroid microcarcinoma is rising due to the frequent use and improvement of fine-needle aspiration biopsy and ultrasonography. Since the recent update of the TNM (Tumor, Node, Metastasis) staging system for thyroid cancer, the importance of lymph node metastasis became more prominent. In the present study, we evaluated the prognostic factors and extension of thyroid microcarcinomas in Korean patients. The clinical and pathological findings in patients with thyroid microcarcinomas in a Korean hospital from January through December 2004 were evaluated. A total of 302 (50.2%) out of 601 cases of thyroid cancers were microcarcinomas. Evaluation of the histology revealed that nearly all of the cases (300 of 302) were of the papillary type. Analyzing patients of papillary thyroid microcarcinomas, 273 (91.0%) out of 300 patients of papillary microcarcinomas were women. Seventy-eight (26.0%) cases contained multiple tumor masses (> or =2), including 49 (16.3%) cases that were bilateral. There were 84 (28.0%) cases of extrathyroidal extensions and 89 cases (29.7%) of lymph node metastasis, but no cases of distant metastases. Application of the new staging system revealed 7 (2.3%) cases that changed from stage III to stage IVA. Thyroid microcarcinomas were also associated with poor prognostic factors and appear to exist at relatively higher cancer stages. Therefore, it is important to treat them as early and as vigorously as possible with extensive surgery, radioactive iodine therapy, and thyroxine suppression.
Adolescent↗
Adiponectin protects human neuroblastoma SH-SY5Y cells against acetaldehyde-induced cytotoxicity.
Acetaldehyde, an inhibitor of mitochondrial function, has been widely used as a neurotoxin because it elicits a severe Parkinson's disease-like syndrome with elevation of the intracellular reactive oxygen species (ROS) level and apoptosis. Adiponectin, secreted from adipose tissue, mediates systemic insulin sensitivity with liver and muscle as target organs. In this study, we investigated the protective effects of adiponectin on acetaldehyde-induced apoptosis in human neuroblastoma SH-SY5Y cells and attempted to examine its mechanism. Acetaldehyde-induced apoptosis was moderately reversed by adiponectin treatment. Our results suggest that the protective effects of adiponectin on acetaldehyde-induced apoptosis may be ascribed to ability to induce the expression of anti-oxidant enzymes and to regulate Bcl-2 and Bax expression. These data indicate that adiponectin may provide a useful therapeutic strategy for the prevention of progressive neurodegenerative disease such as Parkinson's disease.
Acetaldehyde↗
A novel 111/121 diplotype in the Calpain-10 gene is associated with type 2 diabetes.
Genetic variations in the Calpain-10 gene, CAPN10, have been reported to be associated with the risk of type 2 diabetes mellitus (T2DM) in Mexican-Americans and Northern Europeans whereas these variations are not associated with T2DM in other populations. The aim of this study was to determine whether there is an association between specific CAPN10 diplotype (SNP-43, -19, and -63) and T2DM in the Korean population. Overall, 454 Korean patients with T2DM (male 230, female 224) and 236 non-diabetic controls (male 124, female 112) with no family history of diabetes were enrolled in this study. All the subjects were genotyped according to CAPN10 SNP-43, -19, and -63. The restriction fragment length polymorphism method was used for the three SNPs. There were eight estimated haplotype allelic variations. After adjusting for gender and age, the 111 haplotype was associated with a high risk of T2DM (P <0.0001). The 111/121 diplotype was associated with a high risk of T2DM (odds ratio =2.580, 95% confidence interval =1.602-4.155, P =0.001). The high-risk haplotype (112/121) in Mexican-Americans was not significant in our study population. In conclusion, we found that a novel 111/121 diplotype in Calpain-10 gene is associated with T2DM in the Korean population.
Adult↗
The association of total and differential white blood cell count with metabolic syndrome in type 2 diabetic patients.
AIMS: We investigated the relation between total and differential white blood cell (WBC) count and metabolic syndrome (MS) in type 2 diabetic patients. METHODS: Eight-hundred and twenty-two patients (males 430, females 392, BMI 25.4+/-3.2 kg/m2, duration of diabetes 5.7+/-6.8 years) were enrolled in this study. We measured total WBC count and differential count, anthropometry, blood pressure, fasting glucose, insulin and lipid profiles. RESULTS: The number of components of MS and prevalence of MS were increased from 1st quartile to 4th quartile of WBC count. Total WBC, neutrophil, lymphocyte, monocyte and eosinophil counts were increased with the increase of number of components of MS except basophil count. Total WBC, neutrophil, lymphocyte, monocyte and eosinophil counts were higher in the patients with MS features than those without MS features. WBC count was positively correlated with waist circumference (gamma=0.134), systolic blood pressure (gamma=0.082), diastolic blood pressure (gamma=0.083), triglyceride (gamma=0.241), insulin (gamma=0.222), and HOMA-IR (gamma=0.225), and negatively with HDL cholesterol (gamma=-0.146) (p<0.05, respectively). CONCLUSIONS: Chronic inflammation, as indicated by a higher WBC count, may be related with the increased number of components of MS in type 2 diabetic patients.
Aged↗
Rosiglitazone relieves acute ethanol-induced hangover in Sprague-Dawley rats.
AIMS: To assess the efficacy of rosiglitazone in blocking ethanol-induced hangover in rats. METHODS: Rats injected with ethanol (4 g/kg body weight) were subjected to social interaction tests. Levels of aldehyde dehydrogenase 2 (ALD2), involved in an anti-hangover mechanism, were measured by semi-quantitative RT-PCR and western blot analysis. RESULTS: Rosiglitazone caused an upregulation of mitochondrial ALD2, thus significantly detoxifying acetaldehyde. CONCLUSIONS: Rosiglitazone alleviated the symptoms of ethanol-induced hangover by inducing ALD2 expression; this result was reconfirmed by eliminating the effect of rosiglitazone by injecting cyanamide, an ALD2 inhibitor.
Animals↗
Haplotype combination of Calpain-10 gene polymorphism is associated with metabolic syndrome in type 2 diabetes.
Patients with metabolic syndrome are at increased risk of developing cardiovascular disease. The combinations of the haplotype created by the alleles of three single nucleotide polymorphisms (SNPs): SNP-43, -19, and -63 of the Calpain-10 gene (CAPN10), have been reported to be associated with the risk of type 2 diabetes in many populations. The aim of this study was to examine the association of the CAPN10 polymorphism with metabolic syndrome in patients with type 2 diabetes in Korea. Overall, 382 patients with type 2 diabetes were enrolled in this study. All the subjects were genotyped according to CAPN10 SNP-43, -19, and -63. The restriction fragment length polymorphism method was used for the three SNPs. The baseline presence of components of metabolic syndrome was determined. Two hundred and sixty-five (69.4%) patients had metabolic syndrome. Patients with the 111/121 haplotype combination showed a higher risk of hypertension than the other haplotype combinations (odd ratio (OR)=2.334, P=0.010). Patients with the 111/121 haplotype combination had a significantly high risk of metabolic syndrome (OR=1.927, P=0.042). The results of this study suggest that a novel 111/121 haplotype combination created by the CAPN10 SNP-43, -19, and -63 increases the susceptibility to the metabolic syndrome in patients with type 2 diabetes.
Adult↗
Adiponectin protects human neuroblastoma SH-SY5Y cells against MPP+-induced cytotoxicity.
1-Methyl-4-phenylpyridinium ion (MPP+), an inhibitor of mitochondrial complex I, has been widely used as a neurotoxin because it elicits a severe Parkinson's disease-like syndrome characterized by elevation of intracellular reactive oxygen species level and apoptotic death. Adiponectin, secreted from adipose tissue, mediates systemic insulin sensitivity with liver and muscle as target organs. Adiponectin can also suppress superoxide generation in endothelial cells. In the present study, we investigated the protective effects of adiponectin on MPP+-induced cytotoxicity in human neuroblastoma SH-SY5Y cells, as well as the underlying mechanism. Our results suggest that the protective effects of adiponectin on MPP+-induced apoptosis may be ascribed to its anti-oxidative properties, anti-apoptotic activity via inducing expression of SOD and catalase, and regulation of Bcl-2 and Bax expression. These data indicated that adiponectin might provide a useful therapeutic strategy for the treatment of progressive neurodegenerative diseases such as Parkinson's disease.
1-Methyl-4-phenylpyridinium↗
Effects of lifestyle modification on metabolic parameters and carotid intima-media thickness in patients with type 2 diabetes mellitus.
The aim of this study was to examine the effects of a 6-month intensive lifestyle modification intervention on metabolic parameters and carotid intima-media thickness (IMT) in patients with type 2 diabetes mellitus. Fifty-eight subjects with type 2 diabetes mellitus were randomly assigned to the intervention group or the control group. The subjects in the intervention group participated in a 16-week intensive lifestyle modification program and subsequent monthly meetings during the 6-month study period. Control subjects received basic dietary education and usual care. Anthropometric data, metabolic parameters, and carotid IMT were examined before the intervention and after 6 months. Lifestyle modification intervention group patients showed a significant reduction in HbA1c (-1.0% +/- 1.3% vs +0.1% +/- 1.2%, P = .002), fasting blood glucose (-1.6 +/- 1.5 vs +0.3 +/- 2.5 mmol/L, P = .001), and 2-hour postprandial plasma glucose (-2.1 +/- 2.5 vs +0.8 +/- 4.4 mmol/L, P = .003) compared with control patients after 6 months. Body weight (-2.0 +/- 2.6 vs +0.2 +/- 1.7 kg, P = .001), body mass index (-0.8 +/- 1.0 vs 0.0 +/- 0.8 kg/m2, P = .003), and systolic blood pressure (-8.2 +/- 15.9 vs +0.4 +/- 14.1 mm Hg, P = .041) were significantly decreased in the intervention group. A significantly reduced carotid mean IMT progression was seen in the intervention group after 6 months (-0.040 +/- 0.136 vs +0.083 +/- 0.167 mm, P = .007). Changes in HbA1c (r = 0.34, P = .028), fasting plasma glucose (r = 0.31, P = .045), and 2-hour postprandial plasma glucose (r = 0.37, P = .015) correlated with the mean carotid IMT change after adjustment for age and sex. In conclusion, a 6-month intensive lifestyle modification intervention in patients with type 2 diabetes mellitus resulted in improved glycemic control and decreased progression of carotid IMT.
Aged↗
Clinical and biochemical characteristics of nonobese type 2 diabetic patients with glutamic acid decarboxylase antibody in Korea.
We evaluated the prevalence of glutamic acid decarboxylase autoantibody (GADA) in nonobese patients with type 2 diabetes mellitus in Korea and investigated the characteristics of GADA-positive and GADA-negative patients. Two years later, we assessed the progression of beta-cell function in these patients. Of the 647 nonobese patients with type 2 diabetes mellitus enrolled in the study, 10.1% was positive for GADA. Glutamic acid decarboxylase antibody-positive patients had lower fasting and stimulated C-peptide levels compared with GADA-negative patients (1.70 +/- 0.72 vs 1.24 +/- 0.59 microg/L, P < .001; 2.59 +/- 1.51 vs 1.99 +/- 0.82 microg/L, P < .001). Patients treated with insulin had lower fasting and stimulated C-peptide levels than those not treated (1.13 +/- 0.52 vs 1.66 +/- 0.73 microg/L, P = .002; 1.85 +/- 0.69 vs 2.49 +/- 0.91 microg/L, P = .004) and had higher titers of GADA (30.5 +/- 7.3 vs 6.0 +/- 4.8 U/mL, P < .001). In terms of progression of beta-cell function, fasting and stimulated C-peptide levels were significantly lower in GADA-positive patients after 2 years (from 1.24 +/- 0.59 to 0.95 +/- 0.54 microg/L, P = .004; from 1.99 +/- 0.82 to 1.61 +/- 0.77 microg/L, P = .007), whereas no such difference was observed in the GADA-negative patients. We demonstrate that a significant proportion of Korean patients may be positive for GADA; this is consistent with studies of white subjects, although disagrees with previous reports on Korean subjects. By assessing the presence of GADA in Korean type 2 diabetic patients, we are able to predict their course of beta-cell function and identify in advance those who are likely to require insulin treatment.
Adult↗
Relationship of low-density lipoprotein particle size to insulin resistance and intima-media thickness in nondiabetic Koreans.
The aim of this study was to investigate whether low-density lipoprotein (LDL) particle size is associated with insulin resistance and to explore the association between LDL particle size and preclinical atherosclerosis in nondiabetic Korean population. We measured the carotid intima-media thickness (IMT), LDL particle size, and insulin resistance in 136 nondiabetic subjects. Low-density lipoprotein particle size was significantly correlated with insulin resistance, but the independent risk factors of LDL particle size determined by the multiple regression analysis were age, triglyceride, and high-density lipoprotein cholesterol (HDL-C). Carotid IMT was associated with traditional risk factors of atherosclerosis, which are age, HDL-C, LDL cholesterol, systolic and diastolic blood pressure, but LDL particle size was not correlated with carotid IMT. We conclude that LDL particle size was associated with insulin resistance, but age, triglyceride, and HDL-C contributed independently to the variability in LDL particle size, and LDL particle size was not a predictor of preclinical atherosclerosis in nondiabetic Koreans.
Adult↗
Does birthweight predict adolescent adiponectin levels?
OBJECTIVE: Low birthweight is associated with insulin resistance later in life, and adiponectin is known to play an important role in insulin resistance. We have investigated whether birthweight has a relationship with adiponectin levels in adolescence. PATIENTS: An at-home questionnaire survey was completed by 660 middle-school students (aged 12-15 years) in Seoul, Korea, and 152 participants were selected randomly based on their birthweight. MEASUREMENTS Subjects were separated into three groups according to birthweight. We recorded the birthweight and measured anthropometric factors including blood pressure, lipid profile, homeostasis model assessment of insulin resistance (HOMA-IR) and beta-cell function (HOMA-beta), and adiponectin levels of the subjects. These parameters were compared among the groups. The relationship between birthweight and physiological characteristics in adolescence was examined. RESULTS: Systolic blood pressure, lipid profiles and fasting plasma glucose were not significantly different among the groups, but diastolic blood pressure was lower in the third tertile. Insulin, C-peptide and HOMA-IR were higher in the low birthweight tertile. After adjustment for confounding factors, birthweight was inversely related to diastolic blood pressure, insulin, C-peptide and HOMA-IR. Adiponectin level had a significant relationship with current body mass index (BMI) (r=-0.291; P< 0.001) but not with birthweight (r = 0.117; P = 0.166). CONCLUSIONSP: Although birthweight is closely related to insulin resistance during adolescence, adiponectin levels during adolescence had no significant relationship with birthweight. This result implies that low birthweight may not permanently affect adiponectin levels, but current body size is more closely associated with a decreased adiponectin level. However, the limited importance of birthweight as a determining factor on the adiponectin level later in life needs to be further evaluated.
Adiponectin↗
Effects of growth hormone on insulin resistance and atherosclerotic risk factors in obese type 2 diabetic patients with poor glycaemic control.
OBJECTIVE: We aimed to evaluate the combined effects of GH treatment and diet restriction on lipolysis and anabolism, insulin resistance and atherosclerotic risk factors in obese patients with type 2 diabetes mellitus (T2DM). SUBJECTS: This randomized, double-blind, placebo-controlled study included 24 obese T2DM patients (male : female = 12 : 12, mean age 53.7 +/- 7.2 years) with poor glycaemic control (fasting plasma glucose 10.673 +/- 1.121 mmol/l, HbA(1C) 9.9 +/- 2.3%). Sixteen of these patients were treated with recombinant human GH (1-1.5 units/day, 5 days/week) while undergoing diet restriction and exercise for 12 weeks. METHODS: Anthropometric and bioelectrical impedance measurements were undertaken to determine the lean body mass and total body fat. Computed tomography (CT) was performed to estimate visceral and subcutaneous fat distribution at the umbilicus level and the muscle area of the midthigh. Insulin resistance was measured by the insulin tolerance test (ITT) and by the homeostasis model assessment of insulin resistance (HOMA-IR). RESULTS: The ratios VSR (visceral fat area/subcutaneous fat area) and VMR (visceral fat area/thigh muscle area) were significantly decreased in the GH-treated group compared to the control group. An increase in lean body mass was observed in the GH-treated group. Levels of total cholesterol, triglyceride, free fatty acid (FFA), fibrinogen, and plasminogen activator inhibitor-1 (PAI-1) were significantly decreased after GH treatment. Fasting glucose levels decreased similarly (P < 0.05 anova) in both groups during the treatment period. Fasting C-peptide levels significantly increased, whereas insulin levels significantly decreased, in the GH-treated group, but no changes were observed in the control group. The insulin sensitivity index (ISI) was significantly increased in the GH-treated group (1.3 +/- 1.4 vs. 1.9 +/- 1.0%/min, P < 0.05). CONCLUSIONS: GH treatment in obese T2DM patients with poor glycaemic control is beneficial in decreasing the amount of visceral fats, and may therefore result in improvements in insulin resistance, atherosclerotic risk factors and dyslipidaemia.
Analysis of Variance↗
The long-term effects of rosiglitazone on serum lipid concentrations and body weight.
OBJECTIVE: Although rosiglitazone, an insulin sensitizer, is known to have beneficial effects on high density lipoprotein cholesterol (HDL-C) concentrations and low density lipoprotein (LDL) particle size, it has unwanted effects on total cholesterol (TC) and LDL cholesterol (LDL-C) concentrations and body weight in some short-term studies. The aim of this study was to evaluate the long-term effects of rosiglitazone on serum lipid levels and body weight. DESIGN: Open labelled clinical study. PATIENTS AND MEASUREMENTS: We prospectively evaluated fasting serum glucose, haemoglobin A(1c) (HbA(1c)), lipid profiles and body weight at baseline and every 3 months after the use of rosiglitazone (4 mg/day) for 18 months in 202 type 2 diabetic patients. RESULTS: TC levels increased maximally at 3 months and decreased thereafter. However, overall, TC levels remained significantly higher at 18 months than those at baseline. LDL-C levels from the 3-month to the 12-month timepoint were significantly higher than those at baseline. However, after 15 months, LDL-C concentrations were not significantly different from basal LDL-C concentrations. HDL-C levels increased after the first 3 months and these levels were maintained. The increment of change in HDL-C was more prominent in patients with low basal HDL-C concentrations than in patients with high basal HDL-C concentrations. Body weight increased after the first 3 months and these levels were maintained. CONCLUSIONS: HDL-C and body weight increased and remained elevated for the duration of the study. There was an initial increase in LDL-C but this attenuated and by the end of the study was not significantly elevated above baseline levels.
Adult↗
Decrement of postprandial insulin secretion determines the progressive nature of type-2 diabetes.
OBJECTIVE: Type-2 diabetes is a progressive disease. However, little is known about whether decreased fasting or postprandial pancreatic beta-cell responsiveness is more prominent with increased duration of diabetes. The aim of this study was to evaluate the relationship between insulin secretion both during fasting and 2 h postprandial, and the duration of diabetes in type-2 diabetic patients. DESIGN: Cross-sectional clinical investigation. METHODS: We conducted a meal tolerance test in 1466 type-2 diabetic patients and calculated fasting (M0) and postprandial (M1) beta-cell responsiveness. RESULTS: The fasting C-peptide, postprandial C-peptide, M0, and M1 values were lower, but HbA1c values were higher, in patients with diabetes duration > 10 years than those in other groups. There was no difference in the HbA1c levels according to the tertiles of their fasting C-peptide level. However, in a group of patients with highest postprandial C-peptide tertile, the HbA1c values were significantly lower than those in other groups. After adjustment of age, sex, and body mass index (BMI), the duration of diabetes was found to be negatively correlated with fasting C-peptide (gamma = -0.102), postprandial C-peptide (gamma = -0.356), M0 (gamma = -0.263), and M1 (gamma = -0.315; P < 0.01 respectively). After adjustment of age, sex, and BMI, HbA1c was found to be negatively correlated with postprandial C-peptide (gamma = -0.264), M(0) (gamma = -0.379), and M1 (gamma = -0.522), however, positively correlated with fasting C-peptide (gamma = 0.105; P < 0.01 respectively). In stepwise multiple regression analysis, M0, M1, and homeostasis model assessment for insulin resistance (HOMA-IR) emerged as predictors of HbAlc after adjustment for age, sex, and BMI (R2 = 0.272, 0.080, and 0.056 respectively). CONCLUSIONS: With increasing duration of diabetes, the decrease of postprandial insulin secretion is becoming more prominent, and postprandial beta-cell responsiveness may be a more important determinant for glycemic control than fasting beta-cell responsiveness.
Adult↗
Antidiabetic agents from medicinal plants.
Currently available therapeutic options for non-insulin-dependent diabetes mellitus, such as dietary modification, oral hypoglycemics, and insulin, have limitations of their own. Many natural products and herbal medicines have been recommended for the treatment of diabetes. The present paper reviews medicinal plants that have shown experimental or clinical antidiabetic activity and that have been used in traditional systems of medicine; the review also covers natural products (active natural components and crude extracts) isolated from the medicinal plants and reported during 2001 to 2005. Many kinds of natural products, such as terpenoids, alkaloids, flavonoids, phenolics, and some others, have shown antidiabetic potential. Particularly, schulzeines A, B, and C, radicamines A and B, 2,5-imino-1,2,5-trideoxy-L-glucitol, beta-homofuconojirimycin, myrciacitrin IV, dehydrotrametenolic acid, corosolic acid (Glucosol), 4-(alpha-rhamnopyranosyl)ellagic acid, and 1,2,3,4,6-pentagalloylglucose have shown significant antidiabetic activities. Among active medicinal herbs, Momordica charantia L. (Cucurbitaceae), Pterocarpus marsupium Roxb. (Leguminoceae), and Trigonella foenum graecum L. (Leguminosae) have been reported as beneficial for treatment of type 2 diabetes.
Alkaloids↗