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Titolo:
TNF alpha and leptin inhibit basal and glucose-stimulated insulin secretion and gene transcription in the HIT-T15 pancreatic cells
Autore:
Tsiotra, PC; Tsigos, C; Raptis, SA;
Indirizzi:
Hellen Natl Diabet Ctr, Athens 10675, Greece Hellen Natl Diabet Ctr Athens Greece 10675 bet Ctr, Athens 10675, Greece Univ Athens, Res Inst, Propedeut Dept Internal Med 2, Athens, Greece Univ Athens Athens Greece Propedeut Dept Internal Med 2, Athens, Greece Univ Athens, Ctr Diabet, Propedeut Dept Internal Med 2, Athens, Greece Univ Athens Athens Greece Propedeut Dept Internal Med 2, Athens, Greece
Titolo Testata:
INTERNATIONAL JOURNAL OF OBESITY
fascicolo: 7, volume: 25, anno: 2001,
pagine: 1018 - 1026
SICI:
0307-0565(200107)25:7<1018:TAALIB>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; BETA-CELLS; TYROSINE PHOSPHORYLATION; ADIPOSE-TISSUE; ISLET FUNCTION; MESSENGER-RNA; NITRIC-OXIDE; LINE INS-1; OBESE GENE; OB/OB MICE;
Keywords:
pancreatic beta cell line; glucose; tumor necrosis factor alpha; leptin; insulin secretion; preproinsulin transcription;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
50
Recensione:
Indirizzi per estratti:
Indirizzo: Tsigos, C Hellen Natl Diabet Ctr, 3 Ploutarchou St, Athens 10675, Greece Hellen Natl Diabet Ctr 3 Ploutarchou St Athens Greece 10675 ece
Citazione:
P.C. Tsiotra et al., "TNF alpha and leptin inhibit basal and glucose-stimulated insulin secretion and gene transcription in the HIT-T15 pancreatic cells", INT J OBES, 25(7), 2001, pp. 1018-1026

Abstract

BACKGROUND: Tumor necrosis factor alpha (TNF alpha), a cytokine produced at inflammatory sites and in adipose tissue, is known primarily for its detrimental effects on insulin action. There is evidence to suggest that TNF alpha may also influence beta -cell function. Leptin is another adipose tissue-derived hormone that might also act on beta -cells. OBJECTIVE: We explored the independent and combined effects of TNF alpha and leptin upon basal and glucose-stimulated insulin transcription and secretion in the HIT-T15 pancreatic beta cell line. METHODS: Cells were cultured for 40 h in the presence of near-normal basal(7 mM) or high (16.7 mM) glucose and treated with either TNF alpha (1, 10 and 50 ng/ml) or leptin (10, 50 and 100 ng/ml) or both together. Insulin concentrations were measured by radioimmunoassay. Insulin m RNA levels were evaluated by a semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) method, after normalization with beta -actin mRNA. RESULTS: TNF alpha significantly suppressed basal and glucose-stimulated insulin secretion and proinsulin mRNA transcription in a dose-dependent manner, an effect that was more powerful in the presence of high glucose. Leptin also inhibited dose-dependent insulin mRNA and protein at both glucose concentrations, but did not appear to further potentiate the suppressive effects of TNF alphaCONCLUSION: TNF alpha suppresses both basal and glucose-stimulated insulintranscription and secretion in HIT-T15 cells, an effect that is enhanced significantly by high glucose. Leptin also independently inhibits basal and glucose-stimulated insulin secretion and transcription but does not modify TNF alpha effects. These effects might contribute to the abnormalities of glucose metabolism that characterize conditions of increased TNF alpha and/or leptin production.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/01/20 alle ore 03:23:58