Transcriptional regulation of the apoC-III gene by insulin in diabetic mice: correlation with changes in plasma triglyceride levels.
Why the study?
Does insulin treatment reduce apoC-III transcriptional activity in diabetic mice and HepG2 cells?
Population
Streptozotocin-treated mouse model of insulin-dependent diabetes mellitus (IDDM) and HepG2 cells
Comparison
Insulin treatment vs Insulin-deficient diabetic state (untreated)
Design
Preclinical
Authors
Discussion
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Member takes
Implication
May explain insulin's triglyceride effects in diabetes models; hypothesis-generating for apoC-III mechanisms, pending human studies.
Structured PICO
Does insulin treatment reduce apoC-III transcriptional activity in diabetic mice and HepG2 cells?
P
Population
Streptozotocin-treated mouse model of insulin-dependent diabetes mellitus (IDDM) and HepG2 cells
I
Intervention
Insulin treatment
C
Comparator
Insulin-deficient diabetic state (untreated)
O
Outcome
Hepatic apoC-III mRNA levels and transcriptional activitysurrogate
Insulin down-regulates apoC-III transcription, suggesting that insulin deficiency in IDDM leads to apoC-III overexpression, which may contribute to hypertriglyceridemia.
Cite This Study
Chen et al. (1994) studied this question.