Effect of short- and long-term high-fat feeding on autophagy flux and lysosomal activity in rat liver

Title:

Effect of short- and long-term high-fat feeding on autophagy flux and lysosomal activity in rat liver

Creator:

Papáčková, Z., Daňková, H., Páleníčková, E., Ludmila Kazdová, and Monika Cahová

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:61285ea4-c947-4d41-b11a-8fc2fa3e4556
uuid:61285ea4-c947-4d41-b11a-8fc2fa3e4556

Subject:

Fyziologie člověka a srovnávací fyziologie, fyziologie člověka, human physiology, autophagy, lysosomal, liver, lysosomal lipase, biolysis, 14, and 612

Type:

article, články, model:article, and TEXT

Description:

Autophagy-lysosomal pathway is a cellular mechanism ensuring degradation of various macromolecules like proteins or triacylglycerols (TAG). Its disruption is related to many pathological states, including liver steatosis. We compared the effect of short- and long-established steatosis on the intensity of autophagy-lysosomal pathway in rat liver. The experiments were carried out on 3-month old Wistar rats fed standard (SD) or highfat diet for 2 (HF-2) or 10 (HF-10) weeks. HF diet administered animals accumulated an increased amount of TAG in the liver (HF-2→HF-10). Autophagy flux was up-regulated in HF-2 group but nearly inhibited after 10 weeks of HF administration. The expression of autophagy related genes was up-regulated in HF-2 but normal in HF-10. In contrast, total activities of two lysosomal enzymes, lysosomal lipase (LAL) and acid phosphatase, were unaffected in HF-2 but significantly increased in HF-10 groups. mRNA expression of lysosomal enzymes was not affected by the diet. We conclude that in a state of metabolic unbalance (steatosis), autophagy machinery and lysosomal enzymes expression are regulated independently. The accumulation of TAG in the liver is associated with the increase of total LAL activity and protein expression. In contrast, the autophagy response is bi-phasic and after rapid increase it is significantly diminished. This may represent an adaptive mechanism that counteracts the excessive degradation of substrate, i.e. TAG, and eliminate over-production of potentially hazardous lipiddegradation intermediates., Z. Papáčková, ... [et al.]., and Obsahuje seznam literatury

Language:

English

Rights:

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

Source:

Physiological research | 2012 Volume:61 | Number:Suppl 2

Harvested from:

CDK

Metadata only:

false