DOCSLIB.ORG

09.Subjectindex ADA 13.Indd

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text

Load more

SUBJECT INDEX (-)-Epigallocatechin-3-gallate 2919-PO Add-on to basal insulin 1102-P Aggressiveness factor 2526-PO 1,5-Anhydroglucitol 928-P Add-on to metformin 1092-P Aging 1284-P, 1396-P, 1399-P, 1797-P, 1966-P, 11 β-HSD 1993-P Add-on to metformin + SU 1082-P 1972-P, 1981-P, 2007-P, 2209-P, 2308-PO, 11beta-HSD, glucocorticosteroids, type 2 diabetes Add-on to pioglitazone 1120-P 2481-PO, 2693-PO, 2697-PO 1128-P Adenine nucleotide translocase 28-OR, 29-OR Aging society 2657-PO 11β-HSD1 1875-P Adenosine A1 receptor 1854-P Agreement 2508-PO SUBJECT INDEX 12(S)-HETE 2057-P Adenovirus, shrna, over expression 340-OR Agrp neurons 1917-P 12/15-Lipoxygenase 2057-P Adherence 652-P, 789-P, 802-P, 814-P, 821-P, 857-P, AICAR 1815-P 12-Lipoxygenase 338-OR 889-P, 894-P, 1227-P, 1259-P, 1423-P, 2504-PO Akita 1643-P 14-3-3 142-OR Adhesive capsulitis 2887-PO Akt 25-OR 18FDG PET 2026-P Adipocyte 100-OR, 1644-P, 1748-P, 1748-P, 1749-P, Akt mediated signaling pathway 2321-PO 18F-TTCO-cys40-exendin-4 2163-P 1751-P, 1752-P, 1755-P, 1756-P, 1758-P, 1761-P, Akt, glucose uptake 1802-P 1-h plasma glucose 1457-P, 2808-PO 1763-P, 1765-P, 1769-P, 1769-P, 2056-P, 2943-PO Akt/GSK3 signaling pathway 488-P 25(OH)D 679-P Adipocyte differentiation 144-OR, 1745-P, 1745-P, Akt2 1818-P 25-hydroxivitamin D 2035-P 2013-P Alanine 1916-P 26S Proteasomes 498-P Adipocyte fatty acid-binding protein 2003-P Alanine aminotransferase 1460-P, 2860-PO 2-Aminobicyclo-(2,2,1)-heptane-2-carboxylic acid Adipocyte precursor cells 2081-P Alaska native people 183-OR 2079-P Adipocytes 94-OR, 95-OR, 1750-P Albiglutide 68-OR, 1010-P, 1044-P, 2590-PO 2-hour plasma glucose 1399-P Adipocytokines 1753-P, 2338-PO Albumin to creatinine ratio 2722-PO 3D microscopy 361-OR Adipogenesis 142-OR, 302-OR, 1752-P, 1763-P, Albuminuria 103-OR, 108-OR, 417-P, 419-P, 472-P, 3-hydroxybutyrate 2521-PO 2069-P, 2074-P, 2086-P, 2113-P 520-P, 555-P, 557-P, 559-P, 572-P, 719-P, 719-P, 3T3-L1 2921-PO Adipokine 1296-P, 1331-P, 1386-P, 2109-P, 2109-P, 1293-P, 1293-P, 1307-P, 1523-P, 2377-PO, 4-1BB 1719-P 2677-PO, 2686-PO 2387-PO, 2629-PO, 2725-PO 6q24 129-OR Adiponectin 202-OR, 250-OR, 446-P, 474-P, 624-P, Alcohol consumption 2267-P 7-point profile 906-P 650-P, 761-P, 1356-P, 1463-P, 1467-P, 1506-P, Aldose reductase inhibitor 577-P 9p21 locus 1505-P 1610-P, 1884-P, 2092-P, 2131-P, 2209-P, 2591-PO Aldosterone 566-P, 762-P, 2000-P A meta-analysis 1521-P Adiponectin multimer 741-P Aleglitazar 1142-P A1C 861-P, 877-P, 900-P, 1152-P, 1474-P, 1487-P, Adiponectin receptor 1807-P Aliskiren 566-P, 1191-P 1497-P, 1516-P, 1640-P, 2542-PO Adipor 64-OR, 202-OR All-cause mortality 278-OR A1c registry 2-OR Adipose 1637-P, 1743-P, 2102-P, 2102-P Alloreactive T cells 287-OR AATK 195-OR Adipose tissue 63-OR, 168-OR, 1744-P, 1803-P, All-trans retinoic acid 2907-PO Abdominal obesity 1909-P 1812-P, 1951-P, 2105-P, 2105-P, 2110-P, 2159-P Alogliptin 1143-P, 2621-PO, 2647-PO Abnormal glucose tolerance 1466-P Adipose tissue browning 1917-P Alpha cell 1053-P, 2851-PO Abnormal glycorgulation 1492-P Adipose tissue inflammation 99-OR Alpha glucosidase inhibitors 2628-PO Aboriginal 1535-P Adipose tissue insulin resistance 2104-P Alpha lipoic acid 592-P, 2923-PO Acabose 2626-PO Adipose tissue restriction 1856-P Alpha-1-microglobulin 2375-PO Academics 1349-P Adipose tissue secretion 2095-P Alpha-glucosidase inhibitor 2150-P Acanthosis nigricans 2677-PO Adiposity 2042-P Alphatc1-9 2286-P Acarbose 2150-P Administrative claims 1426-P Alternative splicing 1759-P ACC2 1776-P Administrative database 1268-P, 2306-PO Alzheimer’s disease 595-P, 600-P, 1181-P Access to food 755-P Admission glucose 2766-PO Ambulatory blood pressure 550-P ACCORD 207-OR, 709-P, 1065-P Admission hyperglycemia 478-P American indian 1666-P, 2465-PO Accuracy 391-P, 873-P, 874-P, 899-P, 904-P Admissions avoidance 1248-P Amino acid 1125-P, 1451-P ACE gene insertion/deletion polymorphism Adolescents 82-OR, 734-P, 789-P, 790-P, 791-P, Ammonia 1916-P 2331-PO 824-P, 827-P, 835-P, 847-P, 1291-P, 1293-P, AMPK 34-OR, 36-OR, 253-OR, 254-OR, 1050-P, ACE2 719-P, 2291-P 1307-P, 1314-P, 1324-P, 1327-P, 1337-P, 1342-P, 1814-P, 1815-P, 1876-P, 1893-P, 1895-P, 1916-P, Acetyl coa inhibition 636-P 1349-P, 1352-P, 2407-PO, 2504-PO, 2673-PO, 1940-P, 1941-P, 1966-P, 2050-P Acetylation 28-OR 2874-PO Amputation 118-OR, 120-OR, 672-P, 672-P, 2437-PO, Acetylcholine receptor 2283-P Adrenergic signaling 1810-P 2439-PO Acetyl-coa carboxylase (ACC) β 519-P Adults 842-P, 808-P Amygdala 2053-P Actin 1756-P Advanced diabetic nephropathy 548-P Amylin 2167-P Actin cytoskeleton 2075-P Advanced glycation end products 57-OR, 104-OR, Amyloid 300-OR Action potential 599-P 205-OR, 426-P, 1208-P, 1333-P, 1348-P, 1920-P, Anabolic metabolism 616-P Active comparator 238-OR 1937-P, 2409-PO, 2738-PO Ancestry 86-OR, 1540-P Acute complications 2788-PO Advanced practice nurse 318-OR Androgen receptor 2226-P Acute coronary syndrome 349-OR, 459-P, 478-P, Advanced type 2 diabetes 70-OR Angiogenesis 576-P, 610-P, 668-P, 668-P, 1726-P, 1253-P, 1415-P Adverse event 275-OR 2077-P, 2469-PO Acute inflammatory response 1627-P Adverse outcomes 1270-P Angiogrography 2436-PO Acute insulin response 1652-P Aerobic exercise 216-OR, 1890-P Angiotensin 1-7 1964-P Acute phase reactants 421-P Africa 1485-P, 2786-PO Angiotensin II 1854-P, 2910-PO Acute stroke 2711-PO African american 217-OR, 322-OR, 2099-P Angiotensin receptor blocker 1804-P ADAM17 and ACE2 shedding 2367-PO African american women 182-OR, 706-P Animal model 2843-PO, 2922-PO Adaptive control 2582-PO AG average glucose 2542-PO Ankle-brachial index 119-OR, 588-P Adaptive optics 154-OR Age 92-OR, 560-P, 625-P, 962-P, 1208-P, 1210-P, ANRIL 449-P ADCY5 1635-P 1397-P, 1519-P, 1597-P, 2415-PO Ansiscope 2402-PO Addition study 2721-PO AGE reader 1519-P Anti CD3 antibody 1705-P Additivity 909-P Age related macular degeneration 2409-PO Antibiotic eradication 192-OR OR-Oral P-Poster PO-Published Only A755 Antibody 1687-P Audit impact 2671-PO 2213-P, 2235-P, 2263-P, 2263-P, 2266-P, Anticancer agent 2767-PO Autoantibodies 128-OR, 1611-P, 1839-P 2271-P,2278-P, 2282-P, 2292-P, 2294-P, 2294B-P, Antidiabetic medication 209-OR Autoantigen 1700-P 2520-PO, 2823-PO, 2851-PO, 2968-PO Antihyperglycemic agents 1030-P Autoimmune 246-OR, 1626-P Beta cell apoptosis 199-OR, 336-OR, 2162-P, 2171-P Anti-inflammation 377-OR, 1678-P, 1703-P, 2052-P Autoimmune regulator (AIRE) 1692-P Beta cell biology 2244-P Anti-obesity 2052-P Autoimmunity 19-OR, 282-OR, 1207-P, 1475-P, Beta cell compensation 2219-P Anti-oxidant 1078-P, 1740-P, 2170-P, 2977-PO 1714-P, 2166-P, 2431-PO Beta cell dysfunction 335-OR, 1578-P, 1832-P Antioxidant enzyme defense 607-P Autoislets 362-OR Beta cell function 80-OR, 163-OR, 199-OR, Antipsychotic 150-OR, 317-OR, 2138-P Automated insulin delivery 228-OR 427-P,954-P, 981-P, 1028-P, 1117-P, 1138-P, SUBJECT INDEX Anxa1 2967-PO Automatic messages 867-P 1292-P, 1292-P, 1402-P, 1402-P, 1462-P, 1492-P, Anxiety 775-P, 787-P, 844-P Automatic suspension 974-P 1547-P, 1688-P, 1825-P, 1828-P, 1829-P, 1835-P, Aortic stiffness 1413-P, 2328-PO Autonomic neuropathy 53-OR, 131-OR, 593-P, 1838-P, 1842-P, 2153-P, 2185-P, 2228-P, 2284-P, Apnea hypopnea index 1302-P 2395-PO 2697-PO, 2717-PO,2847-PO Apo a-I 2249-P Autophagy 60-OR, 512-P, 539-P, 1784-P, 1801-P, Beta cell mass 44-OR, 46-OR, 195-OR, 341-OR, Apoe polymorphism 637-P 1864-P, 1915-P, 2178-P, 2183-P, 2336-PO, 2803-PO 2258-P, 2915-PO Apolipoprotein A-I 303-OR Autoreactive T cells 288-OR Beta cell preservation 2572-PO Apolipoprotein B 355-OR, 659-P, 2422-PO Avanafil 585-P Beta cell proliferation 46-OR, 1686-P, 2193-P, Apoptosis 203-OR, 288-OR, 492-P, 502-P, 590-P, Avandamet 2639-PO 2200-P 1795-P, 2093-P, 2165-P, 2170-P, 2172-P, 2176-P, Average plasma glucose 2532-PO Beta cell protection 110-OR, 338-OR 2187-P, 2292-P Azelnidipine 1204-P Beta cell regeneration 1729-P, 2040-P, 2634-PO, Appetite regulation 2106-P B lymphocyte 291-OR 2642-PO, 2966-PO APPL1 2182-P B12 1062-P, 1068-P Beta cell rest 2236-P Appointment adherence 1240-P B7.
Recommended publications
  • Mir-338-3P Functions As a Tumor Suppressor in Gastric Cancer by Targeting PTP1B

    Mir-338-3P Functions As a Tumor Suppressor in Gastric Cancer by Targeting PTP1B

    Sun et al. Cell Death and Disease DOI 10.1038/s41419-018-0611-0 Cell Death & Disease ARTICLE Open Access miR-338-3p functions as a tumor suppressor in gastric cancer by targeting PTP1B Feng Sun1, Mengchao Yu2,JingYu2, Zhijian Liu1,XinyanZhou2,YanqingLiu2, Xiaolong Ge3,HaidongGao2, Mei Li4, Xiaohong Jiang2,SongLiu1,XiChen2 and Wenxian Guan 1 Abstract Gastric cancer (GC) is one of the most common malignant tumors and peritoneal metastasis is the primary cause for advanced GC’s mortality. Protein-tyrosine phosphatase 1B (PTP1B) functions as an oncogene and involves in carcinogenesis and cancer dissemination. However, the function and regulation of PTP1B in GC remain poorly understood. In this study, we found that PTP1B was upregulated in GC tissues and overexpression of PTP1B in vitro promoted cell migration and prevented apoptosis. Then, we predicted that PTP1B was a target of miR-338-3p and we revealed an inverse correlation between miR-338-3p levels and PTP1B protein levels in GC tissues. Next, we verified that PTP1B was inhibited by miR-338-3p via direct targeting to its 3′-untranslated regions. Moreover, overexpression of miR-338-3p in vitro attenuated GC cell migration and promoted apoptosis, and these effects could be partially reversed by reintroduction of PTP1B. Finally, we established an orthotopic xenograft model and a peritoneal dissemination model of GC to demonstrate that miR-338-3p restrained tumor growth and dissemination in vivo by targeting PTP1B. Taken together, our results highlight that PTP1B is an oncogene and is negatively regulated by miR- 1234567890():,; 1234567890():,; 338-3p in GC, which may provide new insights into novel molecular therapeutic targets for GC.
  • The Antidiabetic Drug Lobeglitazone Has the Potential to Inhibit PTP1B T Activity ⁎ Ruth F

    The Antidiabetic Drug Lobeglitazone Has the Potential to Inhibit PTP1B T Activity ⁎ Ruth F

    Bioorganic Chemistry 100 (2020) 103927 Contents lists available at ScienceDirect Bioorganic Chemistry journal homepage: www.elsevier.com/locate/bioorg The antidiabetic drug lobeglitazone has the potential to inhibit PTP1B T activity ⁎ Ruth F. Rochaa, Tiago Rodriguesc, Angela C.O. Menegattia,b, , Gonçalo J.L. Bernardesc,d, Hernán Terenzia a Centro de Biologia Molecular Estrutural, Departamento de Bioquímica, Universidade Federal de Santa Catarina, Campus Trindade, 88040-900 Florianópolis, SC, Brazil b Universidade Federal do Piauí, CPCE, 64900-000 Bom Jesus, PI, Brazil c Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Avenida Professor Egas Moniz, 1649-028 Lisbon, Portugal d Department of Chemistry, University of Cambridge, Lensfield Road, CB2 1EW Cambridge, UK ARTICLE INFO ABSTRACT Keywords: Protein tyrosine phosphatase 1B (PTP1B) is considered a potential therapeutic target for the treatment of type 2 Thiazolidinediones diabetes mellitus (T2DM), since this enzyme plays a significant role to down-regulate insulin and leptin sig- Lobeglitazone nalling and its over expression has been implicated in the development of insulin resistance, T2DM and obesity. PPAR-γ Some thiazolidinediones (TZD) derivatives have been reported as promising PTP1B inhibitors with anti hy- PTP1B perglycemic effects. Recently, lobeglitazone, a new TZD, was described as an antidiabetic drug that targetsthe Non-competitive inhibitors PPAR-γ (peroxisome γ proliferator-activated receptor) pathway, but no information on its effects on PTP1B have been reported to date. We investigated the effects of lobeglitazone on PTP1B activity in vitro. Surprisingly, lobeglitazone led to moderate inhibition on PTP1B (IC50 42.8 ± 3.8 µM) activity and to a non-competitive reversible mechanism of action.
  • Trace Amine-Associated Receptor 1 Activation Regulates Glucose-Dependent

    Trace Amine-Associated Receptor 1 Activation Regulates Glucose-Dependent

    Trace amine-associated receptor 1 activation regulates glucose-dependent insulin secretion in pancreatic beta cells in vitro by ©Arun Kumar A thesis submitted to the School of Graduate Studies in partial fulfillment of the requirements for the degree of Master of Science Department of Biochemistry, Faculty of Science Memorial University of Newfoundland FEBRUARY 2021 St. John’s, Newfoundland and Labrador i Abstract Trace amines are a group of endogenous monoamines which exert their action through a family of G protein-coupled receptors known as trace amine-associated receptors (TAARs). TAAR1 has been reported to regulate insulin secretion from pancreatic beta cells in vitro and in vivo. This study investigates the mechanism(s) by which TAAR1 regulates insulin secretion. The insulin secreting rat INS-1E -cell line was used for the study. Cells were pre-starved (30 minutes) and then incubated with varying concentrations of glucose (2.5 – 20 mM) or KCl (3.6 – 60 mM) for 2 hours in the absence or presence of various concentrations of the selective TAAR1 agonist RO5256390. Secreted insulin per well was quantified using ELISA and normalized to the total protein content of individual cultures. RO5256390 significantly (P < 0.0001) increased glucose- stimulated insulin secretion in a dose-dependent manner, with no effect on KCl-stimulated insulin secretion. Affymetrix-microarray data analysis identified genes (Gnas, Gng7, Gngt1, Gria2, Cacna1e, Kcnj8, and Kcnj11) whose expression was associated with changes in TAAR1 in response to changes in insulin secretion in pancreatic beta cell function. The identified potential links to TAAR1 supports the regulation of glucose-stimulated insulin secretion through KATP ion channels.
  • Edinburgh Research Explorer

    Edinburgh Research Explorer

    Edinburgh Research Explorer International Union of Basic and Clinical Pharmacology. LXXXVIII. G protein-coupled receptor list Citation for published version: Davenport, AP, Alexander, SPH, Sharman, JL, Pawson, AJ, Benson, HE, Monaghan, AE, Liew, WC, Mpamhanga, CP, Bonner, TI, Neubig, RR, Pin, JP, Spedding, M & Harmar, AJ 2013, 'International Union of Basic and Clinical Pharmacology. LXXXVIII. G protein-coupled receptor list: recommendations for new pairings with cognate ligands', Pharmacological reviews, vol. 65, no. 3, pp. 967-86. https://doi.org/10.1124/pr.112.007179 Digital Object Identifier (DOI): 10.1124/pr.112.007179 Link: Link to publication record in Edinburgh Research Explorer Document Version: Publisher's PDF, also known as Version of record Published In: Pharmacological reviews Publisher Rights Statement: U.S. Government work not protected by U.S. copyright General rights Copyright for the publications made accessible via the Edinburgh Research Explorer is retained by the author(s) and / or other copyright owners and it is a condition of accessing these publications that users recognise and abide by the legal requirements associated with these rights. Take down policy The University of Edinburgh has made every reasonable effort to ensure that Edinburgh Research Explorer content complies with UK legislation. If you believe that the public display of this file breaches copyright please contact [email protected] providing details, and we will remove access to the work immediately and investigate your claim. Download date: 02. Oct. 2021 1521-0081/65/3/967–986$25.00 http://dx.doi.org/10.1124/pr.112.007179 PHARMACOLOGICAL REVIEWS Pharmacol Rev 65:967–986, July 2013 U.S.
  • Dualism of Peroxisome Proliferator-Activated Receptor Α/Γ: a Potent Clincher in Insulin Resistance

    Dualism of Peroxisome Proliferator-Activated Receptor Α/Γ: a Potent Clincher in Insulin Resistance

    AEGAEUM JOURNAL ISSN NO: 0776-3808 Dualism of Peroxisome Proliferator-Activated Receptor α/γ: A Potent Clincher in Insulin Resistance Mr. Ravikumar R. Thakar1 and Dr. Nilesh J. Patel1* 1Faculty of Pharmacy, Shree S. K. Patel College of Pharmaceutical Education & Research, Ganpat University, Gujarat, India. [email protected] Abstract: Diabetes mellitus is clinical syndrome which is signalised by augmenting level of sugar in blood stream, which produced through lacking of insulin level and defective insulin activity or both. As per worldwide epidemiology data suggested that the numbers of people with T2DM living in developing countries is increasing with 80% of people with T2DM. Peroxisome proliferator-activated receptors are a family of ligand-activated transcription factors; modulate the expression of many genes. PPARs have three isoforms namely PPARα, PPARβ/δ and PPARγ that play a central role in regulating glucose, lipid and cholesterol metabolism where imbalance can lead to obesity, T2DM and CV ailments. It have pathogenic role in diabetes. PPARα is regulates the metabolism of lipids, carbohydrates, and amino acids, activated by ligands such as polyunsaturated fatty acids, and drugs used as Lipid lowering agents. PPAR β/δ could envision as a therapeutic option for the correction of diabetes and a variety of inflammatory conditions. PPARγ is well categorized, an element of the PPARs, also pharmacological effective as an insulin resistance lowering agents, are used as a remedy for insulin resistance integrated with type- 2 diabetes mellitus. There are mechanistic role of PPARα, PPARβ/δ and PPARγ in diabetes mellitus and insulin resistance. From mechanistic way, it revealed that dual PPAR-α/γ agonist play important role in regulating both lipids as well as glycemic levels with essential safety issues.
  • Combination Treatment with Pioglitazone and Fenofibrate

    Combination Treatment with Pioglitazone and Fenofibrate

    179 Combination treatment with pioglitazone and fenofibrate attenuates pioglitazone-mediated acceleration of bone loss in ovariectomized rats Rana Samadfam, Malaika Awori, Agnes Be´nardeau1, Frieder Bauss2, Elena Sebokova1, Matthew Wright1 and Susan Y Smith Charles River Laboratories, 22022 Transcanadienne, Senneville, Montre´al, Que´bec, Canada H9X 3R3 1F. Hoffmann-La Roche AG, Basel, CH-4070 Switzerland 2Roche Diagnostics GmbH, Penzberg, DE-82377 Germany (Correspondence should be addressed to S Y Smith; Email: [email protected]) Abstract Peroxisome proliferator-activated receptor (PPAR) g ago- mineral content (w45%) and bone mineral density (BMD; nists, such as pioglitazone (Pio), improve glycemia and lipid w60%) at the lumbar spine. Similar effects of treatments were profile but are associated with bone loss and fracture risk. Data observed at the femur, most notably at sites rich in trabecular regarding bone effects of PPARa agonists (including bone. At the proximal tibial metaphysis, concomitant fenofibrate (Feno)) are limited, although animal studies treatment with PioCFeno prevented Pio exacerbation of suggest that Feno may increase bone mass. This study ovariectomy-induced loss of trabecular bone, resulting in investigated the effects of a 13-week oral combination BMD values in the PioCFeno group comparable to OVX treatment with Pio (10 mg/kg per day)CFeno (25 mg/kg controls. Discontinuation of Pio or Feno treatment of per day) on body composition and bone mass parameters OVX rats was associated with partial reversal of effects on compared with Pio or Feno alone in adult ovariectomized bone loss or bone mass gain, respectively, while values in the (OVX) rats, with a 4-week bone depletion period, followed PioCFeno group remained comparable to OVX controls.
  • Comparative Transcriptional Network Modeling of Three PPAR-A/C Co-Agonists Reveals Distinct Metabolic Gene Signatures in Primary Human Hepatocytes

    Comparative Transcriptional Network Modeling of Three PPAR-A/C Co-Agonists Reveals Distinct Metabolic Gene Signatures in Primary Human Hepatocytes

    Comparative Transcriptional Network Modeling of Three PPAR-a/c Co-Agonists Reveals Distinct Metabolic Gene Signatures in Primary Human Hepatocytes Rene´e Deehan1, Pia Maerz-Weiss2, Natalie L. Catlett1, Guido Steiner2, Ben Wong1, Matthew B. Wright2*, Gil Blander1¤a, Keith O. Elliston1¤b, William Ladd1, Maria Bobadilla2, Jacques Mizrahi2, Carolina Haefliger2, Alan Edgar{2 1 Selventa, Cambridge, Massachusetts, United States of America, 2 F. Hoffmann-La Roche AG, Basel, Switzerland Abstract Aims: To compare the molecular and biologic signatures of a balanced dual peroxisome proliferator-activated receptor (PPAR)-a/c agonist, aleglitazar, with tesaglitazar (a dual PPAR-a/c agonist) or a combination of pioglitazone (Pio; PPAR-c agonist) and fenofibrate (Feno; PPAR-a agonist) in human hepatocytes. Methods and Results: Gene expression microarray profiles were obtained from primary human hepatocytes treated with EC50-aligned low, medium and high concentrations of the three treatments. A systems biology approach, Causal Network Modeling, was used to model the data to infer upstream molecular mechanisms that may explain the observed changes in gene expression. Aleglitazar, tesaglitazar and Pio/Feno each induced unique transcriptional signatures, despite comparable core PPAR signaling. Although all treatments inferred qualitatively similar PPAR-a signaling, aleglitazar was inferred to have greater effects on high- and low-density lipoprotein cholesterol levels than tesaglitazar and Pio/Feno, due to a greater number of gene expression changes in pathways related to high-density and low-density lipoprotein metabolism. Distinct transcriptional and biologic signatures were also inferred for stress responses, which appeared to be less affected by aleglitazar than the comparators. In particular, Pio/Feno was inferred to increase NFE2L2 activity, a key component of the stress response pathway, while aleglitazar had no significant effect.
  • Corporate Presentation June 2019 Disclaimer

    Corporate Presentation June 2019 Disclaimer

    Corporate Presentation June 2019 Disclaimer Some of the statements contained in this presentation constitute forward-looking statements. Statements that are not historical facts are forward-looking statements. Forward-looking statements generally can be identified by the use of forward-looking terminology such as “may”, “will”, “expect”, “intend”, “estimate”, “anticipate”, “believe”, “continue” or similar terminology. These statements are based on the Company’s current strategy, plans, objectives, assumptions, estimates and projections. Investors should therefore not place undue reliance on those statements. The Company makes no representation, warranty or prediction that the results anticipated by such forward- looking statements will be achieved, and such forward-looking statements represent, in each case, only one of many possible scenarios and should not be viewed as the most likely or standard scenario. Forward-looking statements speak only as of the date that they are made and the Company does not undertake to update any forward-looking statements in light of new information or future events. Forward-looking statements involve inherent risks and uncertainties. The Company cautions that a number of important factors could cause actual results to differ materially from those contained in any forward-looking statement. 2 Well Diversified Mid-to-Late Stage Metabolic Pipeline for Large Market Opportunities Global partnerships secured for late stage clinical program in type 2 diabetes • Imeglimin: First in class oral drug candidate targeting
  • Mechanism of Satellite Cell Regulation by Myokines

    Mechanism of Satellite Cell Regulation by Myokines

    J Phys Fitness Sports Med, 6 (5): 311-316 (2017) DOI: 10.7600/jpfsm.6.311 JPFSM: Review Article Mechanism of satellite cell regulation by myokines Yasuro Furuichi* and Nobuharu L. Fujii Department of Health Promotion Sciences, Graduate School of Human Health Sciences, Tokyo Metropolitan University, 1-1 Minami-Osawa, Hachioji, Tokyo 193-0397, Japan Received: July 19, 2017 / Accepted: August 7, 2017 Abstract Skeletal muscle stem cells, known as satellite cells, participate in postnatal skeletal muscle growth, regeneration, and hypertrophy. They are quiescent in the resting state, but are activated after muscle injury, and subsequently replicate and fuse into existing myofibers. The behavior of satellite cells during muscle regeneration is regulated by extrinsic factors, such as the extracellular matrix, mechanical stimuli, and soluble factors. Myokines, muscle-derived secretory factors, are important regulators of satellite cell activation, proliferation, and differen- tiation. It is well known that muscle injury induces the release of various growth factors from myofibers, and these growth factors affect satellite cells. It has recently been shown that myo- kines secreted from myofibers without cell damage also regulate satellite cell functions. Here, we summarize myokines with known roles in the regulation of satellite cells and the mecha- nism underlying this regulatory process. Keywords : secretion, myogenesis, muscle regeneration regulation, but there are also molecules related to muscle Introduction regeneration or plasticity. In this review, we introduce the Skeletal muscle is a unique tissue that has a remarkable reported myokines involved in the regulation of satellite ability to regenerate after injury. In response to tissue cell behavior and its molecular mechanism.
  • Negotiating Gender and Spirituality in Literary Representations of Rastafari

    Negotiating Gender and Spirituality in Literary Representations of Rastafari

    Negotiating Gender and Spirituality in Literary Representations of Rastafari Annika McPherson Abstract: While the male focus of early literary representations of Rastafari tends to emphasize the movement’s emergence, goals or specific religious practices, more recent depictions of Rasta women in narrative fiction raise important questions not only regarding the discussion of gender relations in Rastafari, but also regarding the functions of literary representations of the movement. This article outlines a dialogical ‘reasoning’ between the different negotiations of gender in novels with Rastafarian protagonists and suggests that the characters’ individual spiritual journeys are key to understanding these negotiations within the gender framework of Rastafarian decolonial practices. Male-centred Literary Representations of Rastafari Since the 1970s, especially, ‘roots’ reggae and ‘dub’ or performance poetry have frequently been discussed as to their relations to the Rastafari movement – not only based on their lyrical content, but often by reference to the artists or poets themselves. Compared to these genres, the representation of Rastafari in narrative fiction has received less attention to date. Furthermore, such references often appear to serve rather descriptive functions, e.g. as to the movement’s philosophy or linguistic practices. The early depiction of Rastafari in Roger Mais’s “morality play” Brother Man (1954), for example, has been noted for its favourable representation of the movement in comparison to the press coverage of
  • Scientific Evidence of Diets for Weight Loss

    Scientific Evidence of Diets for Weight Loss

    Nutrition 69 (2020) 110549 Contents lists available at ScienceDirect Nutrition journal homepage: www.nutritionjrnl.com Scientific evidence of diets for weight loss: Different macronutrient composition, intermittent fasting, and popular diets Rachel Freire Ph.D. * Mucosal Immunology and Biology Research Center and Center for Celiac Research and Treatment, Department of Pediatrics, Massachusetts General Hospital, and Harvard Medical School, Boston, Massachusetts, USA ARTICLE INFO ABSTRACT Article History: New dietary strategies have been created to treat overweight and obesity and have become popular and widely adopted. Nonetheless, they are mainly based on personal impressions and reports published in books and magazines, rather than on scientific evidence. Animal models and human clinical trials have been Keywords: employed to study changes in body composition and metabolic outcomes to determine the most effective Obesity diet. However, the studies present many limitations and should be carefully analyzed. The aim of this review Weight-loss was to discuss the scientific evidence of three categories of diets for weight loss. There is no one most effec- Popular diets tive diet to promote weight loss. In the short term, high-protein, low-carbohydrate diets and intermittent Fasting Macronutrient fasting are suggested to promote greater weight loss and could be adopted as a jumpstart. However, owing to adverse effects, caution is required. In the long term, current evidence indicates that different diets pro- moted similar weight loss and adherence to diets will predict their success. Finally, it is fundamental to adopt a diet that creates a negative energy balance and focuses on good food quality to promote health. © 2019 Elsevier Inc.
  • Metabolite Sensing Gpcrs: Promising Therapeutic Targets for Cancer Treatment?

    Metabolite Sensing Gpcrs: Promising Therapeutic Targets for Cancer Treatment?

    cells Review Metabolite Sensing GPCRs: Promising Therapeutic Targets for Cancer Treatment? Jesús Cosín-Roger 1,*, Dolores Ortiz-Masia 2 , Maria Dolores Barrachina 3 and Sara Calatayud 3 1 Hospital Dr. Peset, Fundación para la Investigación Sanitaria y Biomédica de la Comunitat Valenciana, FISABIO, 46017 Valencia, Spain 2 Departament of Medicine, Faculty of Medicine, University of Valencia, 46010 Valencia, Spain; [email protected] 3 Departament of Pharmacology and CIBER, Faculty of Medicine, University of Valencia, 46010 Valencia, Spain; [email protected] (M.D.B.); [email protected] (S.C.) * Correspondence: [email protected]; Tel.: +34-963851234 Received: 30 September 2020; Accepted: 21 October 2020; Published: 23 October 2020 Abstract: G-protein-coupled receptors constitute the most diverse and largest receptor family in the human genome, with approximately 800 different members identified. Given the well-known metabolic alterations in cancer development, we will focus specifically in the 19 G-protein-coupled receptors (GPCRs), which can be selectively activated by metabolites. These metabolite sensing GPCRs control crucial processes, such as cell proliferation, differentiation, migration, and survival after their activation. In the present review, we will describe the main functions of these metabolite sensing GPCRs and shed light on the benefits of their potential use as possible pharmacological targets for cancer treatment. Keywords: G-protein-coupled receptor; metabolite sensing GPCR; cancer 1. Introduction G-protein-coupled receptors (GPCRs) are characterized by a seven-transmembrane configuration, constitute the largest and most ubiquitous family of plasma membrane receptors, and regulate virtually all known physiological processes in humans [1,2]. This family includes almost one thousand genes that were initially classified on the basis of sequence homology into six classes (A–F), where classes D and E were not found in vertebrates [3].