Lipasin / betatrophin is differentially expressed in liver and white adipose tissue without association with insulin resistance in Wistar and Goto-Kakizaki rats

Title:

Lipasin / betatrophin is differentially expressed in liver and white adipose tissue without association with insulin resistance in Wistar and Goto-Kakizaki rats

Creator:

Monika Cahová, David Habart, Olejár, T., Zuzana Berková, Zuzana Papáčková, Daňková, H., Alena Lodererová, Marie Heczková, and František Saudek

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:c5584b0c-398f-4bfa-8749-226f52be3e79
uuid:c5584b0c-398f-4bfa-8749-226f52be3e79
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, inzulinová rezistence, játra, tuková tkáň, insulin resistance, liver, adipose tissue, Lipasin / betatrophin, Goto-Kakizaki, 14, and 612

Type:

article, články, journal articles, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

Lipasin is a recently identified lipokine expressed predominantly in liver and in adipose tissue. It was linked to insulin resistance in mice and to type 1 and type 2 diabetes (T1D, T2D) in humans. No metabolic studies concerning lipasin were performed yet in rats. Therefore, we used rat model of T2D and insulin resistance, Goto-Kakizaki (GK) rats, to determine changes of lipasin expression in liver and in white adipose tissue (WAT) over 52 weeks in the relation to glucose tolerance, peripheral tissue insulin sensitivity and adiposity. GK rats were grossly glucose intolerant since the age of 6 weeks and developed peripheral insulin resistance at the age of 20 weeks. Expression of lipasin in the liver did not differ between GK and Wistar rats, declining with age, and it was not related to hepatic triacylglycerol content. In WAT, the lipasin expression was significantly higher in Wistar rats where it correlated positively with adiposity. No such correlation was found in GK rats. In conclusion, lipasin expression was associated neither with a mild age-related insulin resistance (Wistar), nor with severe genetically-based insulin resistance (GK)., M. Cahová, D. Habart, T. Olejár, Z. Berková, Z. Papáčková, H. Daňková, A. Lodererova, M. Heczková, F. Saudek., and Obsahuje bibliografii

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Source:

Physiological research | 2017 Volume:66 | Number:2

Harvested from:

CDK

Metadata only:

false