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J Cell Mol Med. 2019 Jun 20. doi: 10.1111/jcmm.14504. [Epub ahead of print]

Hepatic functional and pathological changes of type 1 diabetic mice in growing and maturation time.

Jiang S1,2, Tang X2,3, Wang K1,2, Liang Y1,2, Qian Y1, Lu C1, Cai L2,4.

Author information

1
Department of Pediatrics, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou Medical University, Wenzhou, China.
2
Department of Pediatrics, Pediatric Research Institute, University of Louisville School of Medicine, Louisville, Kentucky.
3
The Center of Cardiovascular Disorders, The First Hospital of Jilin University, Changchun, China.
4
Department of Pharmacology and Toxicology, University of Louisville School of Medicine, Louisville, Kentucky.

Abstract

To detect the changes in the liver function in both male and female OVE26 mice from young to adults for better understanding of type 1 diabetes-induced hepatic changes, OVE26 mice and wild-type FVB mice were raised in the same environment without any intervention, and then killed at 4, 12, 24 and 36 weeks for examining liver's general properties, including pathogenic and molecular changes. The influence of diabetes on the bodyweight of male and female mice was different. Both male and female OVE26 mice did not obtain serious liver injury or non-alcoholic fatty liver disease, manifested by mild elevation of plasma alanine transaminase, and less liver lipid content along with significantly suppressed lipid synthesis. Uncontrolled diabetes also did not cause hepatic glycogen accumulation in OVE26 mice after 4 weeks. Oxidative stress test showed no change in lipid peroxidation, but increased protein oxidation. Changed endoplasmic reticulum stress and apoptosis along with increased antioxidant capacity was observed in OVE26 mice. In conclusion, uncontrolled type 1 diabetes did not cause hepatic lipid deposition most likely because of reduced lipids synthesis in response to insulin deficiency. Enhanced antioxidant capacity might not only prevent the occurrence of severe acute liver injury but also the self-renewal, leading to liver dysfunction.

KEYWORDS:

early life; gender; lipids; liver; type 1 diabetes

PMID:
31222979
DOI:
10.1111/jcmm.14504
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