Ingrid Kathrin Hals
Bakgrunn og aktiviteter
Vitenskapelig, faglig og kunstnerisk arbeid
Et utvalg av nyere tidsskriftspublikasjoner, kunstneriske produksjoner, bok, inklusiv bokdeler og rapport-del. Se alle publikasjoner i databasen
Tidsskriftspublikasjoner
- (2019) Treatment of latent autoimmune diabetes in adults: What is best?. Current diabetes reviews. vol. 15 (3).
- (2019) Investigating optimal β-cell-preserving treatment in latent autoimmune diabetes in adults: Results from a 21-month randomized trial. Diabetes, obesity and metabolism. vol. 21 (10).
- (2018) Metabolic outcomes in adults born preterm with very low birthweight or small for gestational age at term: A cohort study. Journal of Clinical Endocrinology and Metabolism. vol. 103 (12).
- (2017) Hyperoxia reduces insulin release and induces mitochondrial dysfunction with possible implications for hyperoxic treatment of neonates. Physiological Reports. vol. 5 (19).
- (2016) Culture at low glucose up-regulates mitochondrial function in pancreatic β cells with accompanying effects on viability. Islets. vol. 8 (6).
- (2015) Mitochondrial respiration in insulin-producing β-cells: General characteristics and adaptive effects of hypoxia. PLOS ONE.
- (2013) Reduced availability of glucose during culture attenuates hypoxia-induced reduction in cellular viability and function in pancreatic beta cells. Diabetologia. vol. 56.
- (2013) Acute hypoxia impacts similarly on encapsulated and non-encapsulated human pancreatic islets. Diabetologia. vol. 56.
- (2013) Alginate Microencapsulation of Human Islets Does Not Increase Susceptibility to Acute Hypoxia. Experimental Diabetes Research. vol. 2013.
- (2013) Preconditioning with Associated Blocking of Ca2+ Inflow Alleviates Hypoxia-Induced Damage to Pancreatic beta-Cells. PLOS ONE. vol. 8 (7).
- (2012) Marked over expression of uncoupling protein-2 in beta cells exerts minor effects on mitochondrial metabolism. Biochemical and Biophysical Research Communications - BBRC. vol. 423 (2).
- (2012) Diabetes reduces beta-cell mitochondria and induces distinct morphological abnormalities, which are reproducible by high glucose in vitro with attendant dysfunction. Islets. vol. 4 (3).
- (2010) Marked, but not moderate induction of uncoupling protein 2 enhances selected aspects of beta cell mitochondrial metabolism and decreases susceptibility to toxicity. Diabetologia. vol. 53.
- (2010) Six Months of Diazoxide Treatment at Bedtime in Newly Diagnosed Subjects With Type 1 Diabetes Does Not Influence Parameters of beta-Cell Function and Autoimmunity but Improves Glycemic Control. Diabetes Care. vol. 33 (3).
- (2010) Facilitation of fatty acid uptake by CD36 in insulin-producing cells reduces fatty-acid-induced insulin secretion and glucose regulation of fatty acid oxidation. Biochimica et Biophysica Acta - Molecular and Cell Biology of Lipids. vol. 1801 (2).
- (2007) Moderate over expression of UCP-2 in beta cells reduces ROS formation and protects against H2O2-but not cytokine-induced toxicity and aggravates toxicity due to NO. Diabetologia. vol. 50.
- (2007) Over-expression of CD36 in insulin producing cells reduces fatty-acidinduced insulin secretion and glucose-regulation of fatty-acid oxidation. Diabetologia. vol. 50.
- (2002) Induction of UCP-2 mRNA in beta cells is stimulated by oxidation of fatty acids but not by nutrient oversupply. Endocrinology. vol. 143.
- (2001) Uncoupling protein 2 participates in cellular defense against oxidative stress in clonal beta cells. Biochemical and Biophysical Research Communications - BBRC. vol. 282.