Naslov
Dexamethasone reversed insulin resistance induced by hyperglycemia in cultured hepatocytes

Autori
Roša, Jagoda ; Roša Josip

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Izvornik
CONTROL OF METABOLISM AND INSULIN ACTION / Assimacopoulos-Jannet, F ; Tappy, L - Ženeva : Universite de Geneve, Universite de Lausanne, 1999

Skup
European Association for the Study of Diabetes (EASD) Study Group

Mjesto i datum
Ženeva, Švicarska, 09.10.1997. - 11.10.1997

Vrsta sudjelovanja
Poster

Vrsta recenzije
Međunarodna recenzija

Ključne riječi
dexamethasone; hepatocytes; hyperglycemia; insulin resistance

Sažetak
Studies were performed to test the specific effect of hyperglycemia on the reported decrese in liver glycogen in the diabetes and the contribution of hyperglycemia to insulin resistance in cultured hepatocytes isolated from the normal rats. We cultured normal rat hepatocytes in a serum-free medium, containing high glucose concentration (27,8 mmol/l) with or without insulin (0.08 umol/l) and with or without dexamethasone (1umol)or with both hormones for 24h and 72h. The initial glycogen content was 1.05+-0.13 umol/mg protein. Hyperglycemia for 24h did not affect the ability of cells to accumulate glycogen in response to glucose and we have a continous deposition of glycogen up to 1.86+-0.17 umol/mg protein. Glycogen deposition with insulin in comparison with that of glucose induced glycogenesis was without significant difference. However, basal 14C-glucose incorporation into glycogen was 12.18+-0.73 umol/mg protein and we have parallel increased glucose turnover, since the insulin-stimulated 14C-glucose incorporation into glycogen was higher (21.63+-3 umol/mg protein). Hyperglycemia for 72h led to 3-fold reduction of basal 14C-incorporation into glycogen (3.99+-0.3 umol/mg protein) and also led to glycogen mobilisation and glycogen content was degraded to low level (0.2+-0.07 umol/mg protein). despute presence of insulin glycogen content was mobilased. Insulin was not able to increase basal 14C-glucose incorporation. Furthemore, dexamethasone was mandatory for preserved insulin effect during 72h hyperglycemia.With dexamethasone after 24h hyperglycemia insulin -stimulated glucose incorporaton was 45.42+-7.27 umol/mg protein/h and after 72h was 57.94+-5 umol/mg protein/h. With dexamethasone insulin was essential to stimulate glycogen synthesis and glycogen concentration was 3.75+-0.33 umol/mg protein after 3 day. dexamethasone, on the other hand was not able to preserve glucose effectiveness. In conclusion, chronic hyperglycemia (72h) led to a significant decrese in glucose effectiveness on hepatic glycogen metabolismand could induce hepatic insulin resistance. Dexamethasone oppose this glucotoxic effect of hyperglycmia on insulin action and we have in vitro normalisation of the insulin-stimulated glycogen deposition and 14C-glucose incorporation into glycogen, but there was not in vitro reversal the ability of glucose itself to promote glycogen deposition.

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti

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