期刊
JOURNAL OF DIABETES
卷 8, 期 3, 页码 314-323出版社
WILEY
DOI: 10.1111/1753-0407.12293
关键词
apolipoprotein C-III; forkhead box protein O1; hepatic insulin production; hypertriglyceridemia; mice; type 1 diabetes
资金
- American Diabetes Association
- Chinese Shenkang Chronic Disease Prevention Program [2012 SHDC12012303]
BackgroundHypertriglyceridemia is a common lipid disorder that is characterized by elevated plasma levels of triglyceride (TG)-rich particles, such as very low-density lipoprotein (VLDL), in poorly controlled diabetes. The aim of the present study was to determine the potential therapeutic effect of hepatic insulin production on hypertriglyceridemia in mice. MethodsMice were induced diabetic and hypertriglyceridemic by streptozotocin (STZ) treatment. Using an adenovirus-mediated gene transfer approach, we delivered rat preproinsulin cDNA into the liver of diabetic mice and then determined plasma TG metabolism. To investigate the mechanism by which hepatic insulin improves TG metabolism, we determined hepatic expression of apolipoprotein C-III (ApoC-III), a structural moiety and functional inhibitor of VLDL-TG catabolism. ResultsPlasma VLDL-TG levels were markedly elevated in STZ-treated mice, and were accompanied by hyperglycemia and hypertriglyceridemia. These metabolic abnormalities were restored to near normal following hepatic insulin production in insulin vector-treated diabetic mice. In contrast, hypertriglyceridemia and hyperglycemia persisted in control vector-treated diabetic animals. Hepatic ApoC-III expression became deregulated secondary to insulin deficiency, contributing to impaired TG metabolism in diabetic mice. Hepatic insulin production suppressed excessive hepatic ApoC-III production to basal levels. ConclusionHepatic insulin production is efficacious in correcting hypertriglyceridemia associated with insulin deficiency in diabetic mice.
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