Research Topics
| Emma HeartSummaryAffiliation: Marine Biological Laboratory Country: USA Publications
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Detail Information
Publications
Glucose-dependent increase in mitochondrial membrane potential, but not cytoplasmic calcium, correlates with insulin secretion in single islet cellsEmma Heart
Department of Medicine, Obesity Research Center, Boston University School of Medicine, Boston, MA 02118, USA
Am J Physiol Endocrinol Metab 290:E143-E148. 2006....
Role for malic enzyme, pyruvate carboxylation, and mitochondrial malate import in glucose-stimulated insulin secretionEmma Heart
BioCurrents Research Center, Marine Biological Laboratory, 7 MBL St, Lillie 219, Woods Hole, MA 02543, USA
Am J Physiol Endocrinol Metab 296:E1354-62. 2009..These data suggest that although ME1 overexpression augments anaplerosis and GSIS in INS-1 832/13 cells, it is not likely involved in MSSIS and GSIS in pancreatic islets...
Rhythm of the beta-cell oscillator is not governed by a single regulator: multiple systems contribute to oscillatory behaviorEmma Heart
BioCurrents Research Center, Molecular Physiology Program, Marine Biological Laboratory, Woods Hole, Massachusetts 02543, USA
Am J Physiol Endocrinol Metab 292:E1295-300. 2007..This supports the hypothesis that a high-fat environment might contribute to loss of regular oscillatory pattern in diabetic subjects, acting, at least in part, at the level of the single beta-cell...
Plasma membrane electron transport in pancreatic ?-cells is mediated in part by NQO1Joshua P Gray
United States Coast Guard Academy, New London, Connecticut, USA
Am J Physiol Endocrinol Metab 301:E113-21. 2011..We propose a model for the role of PMET as a regulator of glycolytic flux and an important component of the metabolic machinery in ?-cells...
The level of menadione redox-cycling in pancreatic ?-cells is proportional to the glucose concentration: role of NADH and consequences for insulin secretionEmma Heart
Cellular Dynamics Program, Marine Biological Laboratory, Woods Hole, MA 02543, United States
Toxicol Appl Pharmacol 258:216-25. 2012..These data may explain the apparent dichotomy between the stimulatory and inhibitory effects of H(2)O(2) and menadione on insulin secretion...
beta-Cell mitochondria exhibit membrane potential heterogeneity that can be altered by stimulatory or toxic fuel levelsJakob D Wikstrom
Tufts University, Department of Pharmacology and Experimental Therapeutics, 136 Harrison Ave, Boston, MA 02111, USA
Diabetes 56:2569-78. 2007..This study offers insight into the different metabolic states of beta-cell mitochondria...
Ca2+, NAD(P)H and membrane potential changes in pancreatic beta-cells by methyl succinate: comparison with glucoseEmma Heart
Obesity Research Center, Evans Department of Medicine, Boston University School of Medicine, Boston, MA 02118, USA
Biochem J 403:197-205. 2007..The data are consistent with the common intermediates being pyruvate, cytosolic NADPH or both, and suggest that cytosolic NADPH production could account for the more rapid onset of MeS-induced secretion compared with glucose stimulation...
Synchronizing Ca2+ and cAMP oscillations in pancreatic beta-cells: a role for glucose metabolism and GLP-1 receptors? Focus on "regulation of cAMP dynamics by Ca2+ and G protein-coupled receptors in the pancreatic beta-cell: a computational approach&George G Holz
Am J Physiol Cell Physiol 294:C4-6. 2008
Insulin-like and non-insulin-like selenium actions in 3T3-L1 adipocytesEmma Heart
Department of Physiology and Biophysics, Keck School of Medicine, University of Southern California, Los Angeles, California 90089-9142, USA
J Cell Biochem 88:719-31. 2003..In summary, selenium stimulates glucose transport and antilipolysis in a PI3K-dependent manner, but independent of insulin receptor activation. Selenium exerts both insulin-like and non-insulin-like actions in cells...
Glucose transport by osmotic shock and vanadate is impaired by glucosamineEmma Heart
Department of Physiology and Biophysics, University of Southern California, Los Angeles, California 90089-9142, USA
Biochem Biophys Res Commun 292:308-11. 2002..These data suggest that an Akt-independent mechanism is operative in glucosamine-induced insulin resistance and glucosamine impairs glucose transport stimulated by various stimuli involving and not involving Akt activation...
