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Titolo:
Genotoxicity and diabetic embryopathy: Impaired expression of developmental control genes as a cause of defective morphogenesis
Autore:
Chang, TI; Loeken, MR;
Indirizzi:
Harvard Univ, Sch Med, Dept Med, Joslin Diabet Ctr,Sect Mol Biol, Boston, MA 02215 USA Harvard Univ Boston MA USA 02215 Ctr,Sect Mol Biol, Boston, MA 02215 USA
Titolo Testata:
SEMINARS IN REPRODUCTIVE ENDOCRINOLOGY
fascicolo: 2, volume: 17, anno: 1999,
pagine: 153 - 165
SICI:
0734-8630(1999)17:2<153:GADEIE>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROGRAMMED CELL-DEATH; PROTEIN-KINASE-C; TUMOR ALVEOLAR RHABDOMYOSARCOMA; FUEL-MEDIATED TERATOGENESIS; CULTURED RAT CONCEPTUS; MOUSE EMBRYOS; CONGENITAL-MALFORMATIONS; SUPEROXIDE-DISMUTASE; OXIDATIVE STRESS; DNA-REPLICATION;
Keywords:
embryo; diabetes; glucose; neural tube; apoptosis; Pax-3;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
156
Recensione:
Indirizzi per estratti:
Indirizzo: Loeken, MR Harvard Univ, Sch Med, Dept Med, Joslin Diabet Ctr,Sect Mol Biol, 1 JoslinPl, Boston, MA 02215 USA Harvard Univ 1 Joslin Pl Boston MA USA 02215 ston, MA 02215 USA
Citazione:
T.I. Chang e M.R. Loeken, "Genotoxicity and diabetic embryopathy: Impaired expression of developmental control genes as a cause of defective morphogenesis", SEM REP END, 17(2), 1999, pp. 153-165

Abstract

Since the advent of insulin therapy for diabetes mellitus, the survival ofmothers with diabetes prior to pergnancy and their offspring has greatly improved. Nevertheless, the observation that the earliest stages of organogenesis can be! impaired in the offspring of women with diabetes raises the question of how abnormal fuel metabolism disturbs embryogenesis. Research into this process has been made possible in recent years by advances in molecular biology which makes it possible to study gene expression in early embryos, and by the availability of genetically engineered mutant mouse strains. Using these approaches, a model is emerging in which elevated glucose, bydisturbing expression of genes which regulate embryonic development and cell cycle progression, causes premature cell death of emerging organ structures, thereby causing defective morphogenesis. Investigation into the signaling mechanisms by which excess glucose metabolism exhibits toxic effects onembryo gene expression will explain how diabetic embryopathy occurs on a molecular and cellular level, as well as increase our understanding of the role of metabolic homeostasis in proper embryonic development.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 15:49:56