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Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 6/2008, Volume 105, Issue 24, pp. 8452 - 8457
Obesity is a principal risk factor for type 2 diabetes, and elevated fatty acids reduce β-cell function and survival. An unbiased proteomic screen was used to... 
Obesity | Gels | Nonesterified fatty acids | Palmitates | Type 2 diabetes mellitus | Diabetes | Islets of Langerhans | Insulin | Fatty acids | Apoptosis | Type 2 diabetes | 2D difference gel electrophoresis proteomics | Hyperproinsulinemia | Mechanisms of β-cell lipotoxicity | Free fatty acids | LEVELS PREDICT | HUMAN PANCREATIC-ISLETS | ENZYME-ACTIVITY | MULTIDISCIPLINARY SCIENCES | mechanisms of beta-cell lipotoxicity | INSULIN-SECRETION | free fatty acids | ENDOPLASMIC-RETICULUM STRESS | type 2 diabetes | PYRUVATE-DEHYDROGENASE ACTIVITY | PROHORMONE CONVERTASES | FREE FATTY-ACIDS | LINE INS-1 | TRIGLYCERIDE ACCUMULATION | hyperproinsulinemia | Endoplasmic Reticulum - enzymology | Golgi Apparatus - enzymology | Cell Survival | Diabetes Mellitus, Type 2 - genetics | Humans | Cells, Cultured | Diabetes Mellitus, Type 2 - enzymology | Apoptosis - genetics | Proteome | Hyperglycemia - genetics | Insulin-Secreting Cells - ultrastructure | Animals | Insulin-Secreting Cells - drug effects | Mice, Mutant Strains | Palmitates - pharmacology | Carboxypeptidase H - metabolism | Hyperglycemia - enzymology | Hyperinsulinism - enzymology | Hyperinsulinism - genetics | Mice | Palmitates - metabolism | Carboxypeptidase H - genetics | Insulin-Secreting Cells - enzymology | Biological Sciences | mechanisms of β-cell lipotoxicity
Journal Article
Journal Article
Science, ISSN 0036-8075, 1/2005, Volume 307, Issue 5708, pp. 384 - 387
Maintenance of normal blood glucose levels depends on a complex interplay between the insulin responsiveness of skeletal muscle and liver and... 
Obesity | Delta cells | B lymphocytes | Insulin resistance | Type 2 diabetes mellitus | Diabetes | Fatty acids | Insulin | Viewpoints | Insulin secretion | Type 1 diabetes mellitus | PATHOGENESIS | OBESITY | STIMULATED INSULIN-SECRETION | FREE FATTY-ACIDS | MULTIDISCIPLINARY SCIENCES | RESISTANCE | MUSCLE | MECHANISMS | UNCOUPLING PROTEIN-2 | FAILURE | BETA-CELL LIPOTOXICITY | Ion Channels | Humans | Muscle, Skeletal - metabolism | Mitochondrial Proteins - genetics | Adenosine Triphosphate | Islets of Langerhans - metabolism | Membrane Transport Proteins - genetics | Mitochondrial Proteins - metabolism | Islets of Langerhans - cytology | Superoxides - metabolism | Membrane Transport Proteins - metabolism | Hyperglycemia - physiopathology | Fatty Acids - metabolism | Insulin Secretion | Islets of Langerhans - physiology | Oxidation-Reduction | Liver - metabolism | Gene Expression Regulation | Insulin Resistance | Oxidative Phosphorylation | Obesity - physiopathology | Transcription Factors - metabolism | Insulin - metabolism | Animals | Diabetes Mellitus, Type 2 - physiopathology | Models, Biological | Glucose - metabolism | Uncoupling Protein 2 | Mitochondria - physiology | Type 2 diabetes | Care and treatment | Hyperglycemia | Causes of | Development and progression | Mitochondrial diseases | Research | Health aspects | Medical research | Glucose | Cellular biology
Journal Article
Journal Article
BIOLOGICAL RESEARCH, ISSN 0716-9760, 08/2019, Volume 52, Issue 1, pp. 44 - 12
Background: Free fatty acid receptor 1 (FFAR1) is G-protein coupled receptor predominantly expressed in pancreatic beta-cells that is activated by a variety of... 
Type 2 diabetes | MAMMALIAN TARGET | ACTIVATION | IRS-1 | INSR | MECHANISMS | Akt | Palmitic acid | RECEPTOR SUBSTRATE-1 | STIMULATED INSULIN-SECRETION | FREE FATTY-ACIDS | GLUCOSE | BIOLOGY | mTOR | GENE-EXPRESSION | RESISTANCE | Insulin resistance | beta-cells | FFAR1 | Lipotoxicity | EXPOSURE
Journal Article
BBA - Gene Regulatory Mechanisms, ISSN 1874-9399, 09/2018, Volume 1861, Issue 9, pp. 803 - 814
Selective β-cell loss is a characteristic of type 2 diabetes mellitus (T2DM). Inhibition of glucose-stimulated β-cell proliferation is one of the results of... 
Egr-1 | Glucolipotoxicity | Wnt5a | β-cell | Lipotoxicity | Saturated fatty acids | INDUCED APOPTOSIS | BIOCHEMISTRY & MOLECULAR BIOLOGY | INSULIN-SECRETION | ENDOPLASMIC-RETICULUM STRESS | TESTICULAR NEOPLASMS | BIOPHYSICS | GLUCAGON-LIKE PEPTIDE-1 | beta-cell | SIGNALING PATHWAY | PRIMARY MECHANISM | FREE FATTY-ACIDS | GROWTH-FACTOR | TRANSCRIPTION FACTOR
Journal Article
by Li, J and Liu, X and Ran, X and Chen, J and Li, X and Wu, W and Huang, H and Huang, H and Long, Y and Liang, J and Cheng, J and Tian, H
Diabetes, Obesity and Metabolism, ISSN 1462-8902, 01/2010, Volume 12, Issue 1, pp. 35 - 46
Journal Article
PLoS ONE, ISSN 1932-6203, 02/2016, Volume 11, Issue 2, p. e0148686
Type 2 diabetes is characterized by peripheral insulin resistance and pancreatic beta cell dysfunction. Elevated free fatty acids (FFAs) may impair beta cell... 
SATURATED FATTY-ACID | UNFOLDED PROTEIN RESPONSE | INSULIN-RESISTANCE | ER STRESS | MULTIDISCIPLINARY SCIENCES | BETA-CELL DYSFUNCTION | MECHANISMS | ENDOPLASMIC-RETICULUM STRESS | KAPPA-B | PALMITATE | CALCIUM LEAK | RNA, Small Interfering - genetics | Palmitates - toxicity | Apoptosis - drug effects | Calcium - metabolism | Humans | Homeostasis | Protein Transport - drug effects | Recombinant Fusion Proteins - metabolism | Heat-Shock Proteins - genetics | RNA, Messenger - biosynthesis | Insulin-Secreting Cells - metabolism | Caspases - metabolism | Transfection | RNA Interference | Protein Translocation Systems - physiology | Puromycin - pharmacology | Ion Transport - drug effects | Insulin Secretion | Genes, Reporter | Endoplasmic Reticulum Stress - drug effects | RNA, Messenger - genetics | Cells, Cultured | Enzyme Activation - drug effects | Insulin - metabolism | Animals | Insulin-Secreting Cells - drug effects | Calcium Signaling - drug effects | Anisomycin - pharmacology | Mice | Heat-Shock Proteins - physiology | Type 2 diabetes | Pancreatic beta cells | Physiological aspects | Development and progression | Genetic aspects | Research | Fatty acids | Risk factors | Calcium | Laboratories | Leak channels | Recovery of function | Palmitic acid | Channels | Puromycin | Proteins | Rodents | Inhibition | Pretreatment | Pancreas | Calcium homeostasis | Stresses | Calcium channels | Calcium (intracellular) | Secretion | Diabetes mellitus | Pharmacology | Permeability | Insulin | Stress | Beta cells | Depletion | Anisomycin | Antibiotics | Insulin resistance | Diabetes | Endoplasmic reticulum | Endocrinology | Apoptosis | Life Sciences
Journal Article
BBA - Molecular Basis of Disease, ISSN 0925-4439, 11/2019, Volume 1865, Issue 11, p. 165525
Lipotoxicity has been considered a major cause for beta-cell dysfunction in type 2 diabetes mellitus. However, the underlying mechanisms are still unclear. To... 
Type 2 diabetes | ER stress | Lipotoxicity | Human pancreatic beta cell | Fatty acid | Apoptosis | OXIDATION | PEROXISOMES | BIOCHEMISTRY & MOLECULAR BIOLOGY | MITOCHONDRIA | MECHANISMS | INDUCTION | PROTECTS | OBESITY | BIOPHYSICS | LINE
Journal Article
Journal Article