Hereditary hypertriglyceridemic rat: suitable model of cardiovascular disease and metabolic syndrome?

Title:

Hereditary hypertriglyceridemic rat: suitable model of cardiovascular disease and metabolic syndrome?

Creator:

Zicha, J., Pecháňová, O., Čačányiová, S., Cebová, M. , Kristek , F., Török, J. , Šimko, F., Dobešová, Z. , and Kuneš, J.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:cb28ead5-94d2-410f-93e9-10b22ff4fc8a
uuid:cb28ead5-94d2-410f-93e9-10b22ff4fc8a

Subject:

Hereditary hypertriglyceridemic rat, Insulin resistance, Hypertension, Cardiovascular system, and Metabolic alterations

Type:

article, model:article, and TEXT

Description:

Hypertriglyceridemia and hypertension seem to be very important cardiovascular risk factors. The Prague hereditary hypertriglyceridemic (hHTG) rat was developed as a model of human hypertriglyceridemia. It was demonstrated that these rats are not obese, they are hypertensive and insulin resistant and they have some disturbances in glucose metabolism. Several QTLs were identified for blood pressure, its particular components (dependent on major vasoactive systems) and plasma triglycerides throughout the genome of hHTG rats by using of F2 hybrids strategy. It is evident that hHTG rats are a suitable model for the study of metabolic disturbances in relation to blood pressure as well as for the search of genetic determinants of these abnormalities. Numerous abnormalities of blood pressure regulation as well as alterations in the structure and function of cardiovascular apparatus (heart, conduit and resistance arteries) were found in hHTG rats. A special attention was paid to possible changes in the efficiency of various vasoactive systems such as nitric oxide, renin-angiotensin-aldosterone system and sympathetic nervous system, which seem to contribute substantially to cardiovascular and/or metabolic abnormalities observed in Prague hereditary hypertriglyceridemic rats.

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2006 Volume:55 | Number:Suppl 1

Harvested from:

CDK

Metadata only:

false