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Journal Article
Kidney International, ISSN 0085-2538, 08/2011, Volume 80, Issue 4, pp. 358 - 368
Enhanced transforming growth factor-β1 (TGF-β1) expression in renal cells promotes fibrosis and hypertrophy during the progression of diabetic nephropathy. The... 
TGF-β | fibrosis | diabetic nephropathy | gene expression | cell signaling | Up-Regulation | Diabetes Mellitus, Type 2 - genetics | Homeodomain Proteins - metabolism | Transforming Growth Factor beta1 - metabolism | Diabetes Mellitus, Experimental - genetics | Diabetes Mellitus, Type 1 - metabolism | Homeostasis | MicroRNAs - metabolism | Diabetes Mellitus, Type 2 - metabolism | Transfection | Time Factors | Kruppel-Like Transcription Factors - metabolism | Upstream Stimulatory Factors - metabolism | Diabetes Mellitus, Type 1 - chemically induced | Diabetes Mellitus, Experimental - chemically induced | 3' Untranslated Regions | Diabetes Mellitus, Experimental - metabolism | Binding Sites | Collagen Type IV - metabolism | Promoter Regions, Genetic | Diabetic Nephropathies - pathology | Collagen Type I - metabolism | Diabetic Nephropathies - metabolism | Cells, Cultured | Diabetes Mellitus, Type 1 - pathology | Diabetes Mellitus, Type 1 - genetics | Diabetic Nephropathies - genetics | Transforming Growth Factor beta1 - genetics | Mesangial Cells - metabolism | Oligonucleotides - metabolism | Animals | Fibrosis | Diabetes Mellitus, Experimental - pathology | Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - metabolism | Mice | Diabetes Mellitus, Type 2 - pathology | Mutation | Zinc Finger E-box-Binding Homeobox 1 | Index Medicus
Journal Article
Journal of Cellular and Molecular Medicine, ISSN 1582-1838, 11/2017, Volume 21, Issue 11, pp. 2732 - 2747
Metastasis associated lung adenocarcinoma transcript 1( MALAT 1) is a long non‐coding RNA , broadly expressed in mammalian tissues including kidney and... 
MALAT | β‐catenin | SRSF | high glucose | diabetic nephropathy | podocyte | β-catenin | MALAT1 | SRSF1 | beta-catenin | MEDICINE, RESEARCH & EXPERIMENTAL | APOPTOSIS | RETAINED NONCODING RNA | PROLIFERATION | MESENCHYMAL TRANSITION | CELL BIOLOGY | GLOMERULAR SLIT DIAPHRAGM | ROLES | DYSFUNCTION | WNT | SPLICING FACTOR | RNA, Small Interfering - genetics | Diabetes Mellitus, Experimental - genetics | Male | Serine-Arginine Splicing Factors - metabolism | Serine-Arginine Splicing Factors - genetics | Glucose - toxicity | Diabetes Mellitus, Experimental - chemically induced | Diabetes Mellitus, Experimental - metabolism | Wnt Signaling Pathway | Promoter Regions, Genetic | Diabetic Nephropathies - pathology | Podocytes - metabolism | Diabetic Nephropathies - metabolism | Mice, Inbred C57BL | Diabetic Nephropathies - chemically induced | Gene Expression Regulation | Diabetic Nephropathies - genetics | RNA, Long Noncoding - genetics | Podocytes - pathology | beta Catenin - metabolism | beta Catenin - genetics | Protein Transport | Serine-Arginine Splicing Factors - antagonists & inhibitors | Feedback, Physiological | Animals | Podocytes - drug effects | beta Catenin - antagonists & inhibitors | Diabetes Mellitus, Experimental - pathology | Protein Binding | Mice | Streptozocin - toxicity | RNA, Long Noncoding - antagonists & inhibitors | RNA, Long Noncoding - metabolism | Cell Line, Transformed | RNA, Small Interfering - metabolism | Index Medicus | Original
Journal Article
Journal Article
Journal of Ethnopharmacology, ISSN 0378-8741, 11/2016, Volume 192, pp. 382 - 389
Liuwei Dihaung decoction (LWDHT) is a well-known classic traditional Chinese medicine formula, consists of six herbs including Rehmannia glutinosa... 
PI3K/Akt signaling pathway | Liuwei Dihuang decoction | Type 2 diabetes mellitus | CHEMISTRY, MEDICINAL | INTEGRATIVE & COMPLEMENTARY MEDICINE | GENES | PHARMACOLOGY & PHARMACY | PLANT SCIENCES | Diabetes Mellitus, Experimental - drug therapy | Liver - pathology | Phosphorylation | Liver - enzymology | Diabetes Mellitus, Experimental - enzymology | Streptozocin | Drugs, Chinese Herbal - pharmacology | Male | Insulin Receptor Substrate Proteins - metabolism | Insulin - blood | RNA, Messenger - metabolism | Proto-Oncogene Proteins c-akt - genetics | Diabetes Mellitus, Experimental - blood | Liver - drug effects | Time Factors | Diabetes Mellitus, Experimental - chemically induced | Insulin Receptor Substrate Proteins - genetics | Proto-Oncogene Proteins c-akt - metabolism | Phosphatidylinositol 3-Kinase - metabolism | Pancreas - enzymology | RNA, Messenger - genetics | Diabetes Mellitus, Type 2 - enzymology | Insulin Resistance | Pancreas - drug effects | Pancreas - pathology | Biomarkers - blood | Rats, Sprague-Dawley | Hypoglycemic Agents - pharmacology | Blood Glucose - drug effects | Gene Expression Regulation, Enzymologic | Diabetes Mellitus, Type 2 - blood | Animals | Phosphatidylinositol 3-Kinase - genetics | Signal Transduction - drug effects | Diabetes Mellitus, Type 2 - chemically induced | Blood Glucose - metabolism | Diabetes Mellitus, Type 2 - drug therapy | Type 2 diabetes | Insulin resistance | Medicine, Chinese | Liver | Physiological aspects | Blood sugar | Index Medicus
Journal Article
PLoS ONE, ISSN 1932-6203, 2011, Volume 6, Issue 2, pp. e16556 - e16556
Berberine (BBR) is a compound originally identified in a Chinese herbal medicine Huanglian (Coptis chinensis French). It improves glucose metabolism in type 2... 
ACTIVATED PROTEIN-KINASE | MECHANISM DISTINCT | INSULIN-RESISTANCE | MUSCLE ATROPHY | LIVER | BIOLOGY | CARBOHYDRATE | ELEMENT-BINDING PROTEIN | FOXO TRANSCRIPTION FACTORS | LIPID HOMEOSTASIS | EXPRESSION | Diabetes Mellitus, Experimental - drug therapy | Streptozocin | Gluconeogenesis - drug effects | Male | Diabetes Mellitus, Type 2 - metabolism | Insulin - blood | Diabetes Mellitus, Experimental - blood | Liver - drug effects | Diabetes Mellitus, Experimental - chemically induced | Diabetes Mellitus, Experimental - metabolism | Drug Evaluation, Preclinical | Hypoglycemic Agents - therapeutic use | Blood Glucose - analysis | Liver - metabolism | Rats | Down-Regulation - drug effects | Rats, Sprague-Dawley | Hypoglycemic Agents - pharmacology | Blood Glucose - drug effects | Berberine - pharmacology | Diabetes Mellitus, Type 2 - blood | Insulin - metabolism | Animals | Glucose - metabolism | Berberine - therapeutic use | Diabetes Mellitus, Type 2 - chemically induced | Blood Glucose - metabolism | Diabetes Mellitus, Type 2 - drug therapy | Type 2 diabetes | Phosphatases | Blood sugar | Genes | DNA binding proteins | Muscle proteins | Fatty acids | Insulin | Glucose metabolism | Synthesis | Adenylic acid | Protein kinases | Adenosine triphosphate | Protein binding | Transcription factors | Peptides | Liver | Glucose | Blood | Proteins | Signal transduction | Mitochondria | Hyperglycemia | Forkhead protein | Inhibition | Drug dosages | Gluconeogenesis | Binding | Carbohydrates | Berberine | AMP | Metabolism | Fatty-acid synthase | Hepatocytes | Protein synthesis | Glucose-6-phosphatase | Endocrinology | Biomedical research | Kinases | High fat diet | Fatty liver | FOXO1 protein | Rodents | Statins | Fasting | Adenosine monophosphate | Diabetes mellitus | Oxygen consumption | Steatosis | Herbal medicine | Musculoskeletal system | Signaling | Protein kinase | Adenosine kinase | Coronary vessels | Insulin resistance | Diabetes | Respiration | Laboratory animals | ATP | Index Medicus
Journal Article
Diabetes, ISSN 0012-1797, 11/2011, Volume 60, Issue 11, pp. 2872 - 2882
OBJECTIVE-To evaluate whether healthy or diabetic adult mice can tolerate an extreme loss of pancreatic a-cells and how this sudden massive depletion affects... 
INSULIN | HYPERGLUCAGONEMIA | ENDOCRINE PANCREAS | GLUCOSE-HOMEOSTASIS | ENDOCRINOLOGY & METABOLISM | RECEPTOR GENE | SECRETION | DIFFERENTIATION | HYPERPLASIA | ISLET CELLS | EXPRESSION | Insulin-Secreting Cells - secretion | Apoptosis - drug effects | Cell Count | Glucagon - genetics | Male | Diphtheria Toxin - toxicity | Insulin - blood | Glucagon - blood | Diabetes Mellitus, Experimental - blood | Hypoglycemia - prevention & control | Intercellular Signaling Peptides and Proteins - metabolism | Glucagon-Secreting Cells - drug effects | Insulin-Secreting Cells - metabolism | Hyperglycemia - chemically induced | Glucagon-Secreting Cells - metabolism | Diabetes Mellitus, Experimental - chemically induced | Diabetes Mellitus, Experimental - metabolism | Glucagon-Secreting Cells - secretion | Hyperglycemia - prevention & control | Promoter Regions, Genetic | Signal Transduction | Glucagon-Secreting Cells - pathology | Intercellular Signaling Peptides and Proteins - genetics | Pancreas - drug effects | Pancreas - pathology | Receptors, Glucagon - metabolism | Mice, Transgenic | Pancreas - metabolism | Heparin-binding EGF-like Growth Factor | Insulin - metabolism | Animals | Insulin-Secreting Cells - drug effects | Tamoxifen - pharmacology | Diabetes Mellitus, Experimental - pathology | Glucagon - metabolism | Mice | Streptozocin - toxicity | Insulin-Secreting Cells - pathology | Selective Estrogen Receptor Modulators - pharmacology | Index Medicus | Abridged Index Medicus | Islet Studies
Journal Article
Journal of the American Society of Nephrology, ISSN 1046-6673, 03/2012, Volume 23, Issue 3, pp. 458 - 469
Journal Article
Cardiovascular Pathology, ISSN 1054-8807, 2015, Volume 24, Issue 6, pp. 375 - 381
Abstract Introduction Hyperglycemia-induced reactive oxygen species (ROS) generation contributes to the development of diabetic cardiomyopathy. However, little... 
Pathology | Diabetic cardiomyopathy | Oxidative stress | Nuclear factor-erythroid 2-related factor 2 | MicroRNA-144 | Streptozotocin | CARDIAC & CARDIOVASCULAR SYSTEMS | PROTECTION | KINASE | RATS | RECEPTOR | DEATH | CARDIOMYOCYTES | PATHOLOGY | TRANSLATION | NRF2 | ENDOTHELIAL-CELLS | EXPRESSION | Diabetic Cardiomyopathies - metabolism | Reactive Oxygen Species - metabolism | Oxidative Stress | Ventricular Function, Left | Streptozocin | Diabetes Mellitus, Experimental - genetics | Diabetes Mellitus, Type 1 - metabolism | Male | MicroRNAs - metabolism | Diabetes Mellitus, Type 1 - therapy | Diabetes Mellitus, Experimental - therapy | Transfection | Diabetes Mellitus, Type 1 - chemically induced | Diabetic Cardiomyopathies - prevention & control | NF-E2-Related Factor 2 - genetics | Diabetes Mellitus, Experimental - chemically induced | 3' Untranslated Regions | Diabetes Mellitus, Experimental - metabolism | Signal Transduction | Mice, Inbred C57BL | Cells, Cultured | Diabetes Mellitus, Type 1 - pathology | Diabetes Mellitus, Type 1 - genetics | Diabetic Cardiomyopathies - genetics | Myocytes, Cardiac - pathology | Animals | NF-E2-Related Factor 2 - metabolism | Diabetes Mellitus, Experimental - pathology | Glucose - metabolism | Myocytes, Cardiac - metabolism | Diabetic Cardiomyopathies - pathology | MicroRNAs - genetics | Oligonucleotides - administration & dosage | Diabetic Cardiomyopathies - chemically induced | Apoptosis | MicroRNA | Index Medicus
Journal Article