Apoprotein C-III deficiency markedly stimulates triglyceride secretion in vivo: comparison with apoprotein E
Autor: | Toshihiro Takahashi, Tetsu Ebara, Mitsuru Adachi, Hiroto Tajima, Tsutomu Hirano, Shigenobu Saito |
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Rok vydání: | 2001 |
Předmět: |
Blood Glucose
Apolipoprotein E medicine.medical_specialty Physiology Ratón Endocrinology Diabetes and Metabolism Detergents Stimulation Biology Polyethylene Glycols Mice chemistry.chemical_compound Apolipoproteins E In vivo Physiology (medical) Internal medicine medicine Animals Insulin Secretion Obesity Apolipoproteins C Triglycerides Aurothioglucose Hypertriglyceridemia Mice Knockout Apolipoprotein C-III Triglyceride Homozygote Metabolic disorder medicine.disease Mice Inbred C57BL Cholesterol Endocrinology chemistry lipids (amino acids peptides and proteins) |
Zdroj: | American Journal of Physiology-Endocrinology and Metabolism. 281:E665-E669 |
ISSN: | 1522-1555 0193-1849 |
Popis: | Apoprotein (apo) C-III plays an important role in the development of hypertriglyceridemia by inhibiting triglyceride (TG) removal. However, the effect of apo C-III on TG production remains unclear. We measured TG secretion rate (TGSR) in apo C-III gene-disrupted (apo C-III-null) mice to investigate the influence of this protein on TG turnover. TGSR measured by the Triton WR-1339 method was increased twofold in these mice compared with wild-type (WT) mice. Obesity was induced by the injection of gold-thioglucose (GTG), which made the WT mice hypertriglyceridemic due to a threefold increase of TGSR. However, GTG-induced obesity failed to increase TG in apo C-III-null mice, although TGSR was increased 10-fold, suggesting substantial stimulation of TG removal. Apo E-null mice were severely hypercholesterolemic but were not hypertriglyceridemic, and TGSR was rather decreased. GTG-induced obesity made these mice hypertriglyceridemic because of TG overproduction to an extent similar to that seen in WT mice. These results suggest that apo C-III deficiency potently enhances TG turnover, especially when TG production is stimulated, and that apo E deficiency is not always rate limiting for TG production. |
Databáze: | OpenAIRE |
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