Khosrow Adeli,
Volume 2, Issue 2 (6-2003)
Abstract
Insulin resistant states are emerging rapidly and lots of efforts have gone into understanding their pathogenesis and major metabolic consequences. Hypertriglyceridemia, a major complication of this metabolic syndrome, seems to be caused by overproduction of lipoproteins (LPs) containing apo B that are rich in triglycerides.
Some in vitro and in vivo models have been introduced so as to understand mechanisms governing lipid metabolism in insulin resistance states. Human and animal studies have suggested a key role for overproduction of VLDL in hypertriglyceridemia and dyslipidemic states.
Recently, we have employed a diet-induced animal model of insulin resistance (hamster fed with fructose) in our laboratory in order to examine the relationship among development of insulin resistant state, impaired metabolism of LPs and overproduction of LPs containing apo B. These experiments have indicated that insulin resistant states occur along with overproduction of VLDL containing apoB105 from liver and enteral LPs rich in apo B 48. In insulin resistant states, decreased metabolic signaling to liver and intestine seems to play a critical role in overproduction of LPs. We have also been recognized a number of intracellular factors which may regulate VLDL production.
This article reviews recent advances in the area the hypothesis indicating that a complex interaction exist between increased free fatty acids flow from peripheral tissues to the liver and intestine (caused by hyperinsulinemia) and prolonged lipogenesis has also been expounded.
Parvaneh Yavari, Fereydoun Siassi, Mahmoud Jalali, Kazem Mohammad, Bagher Larijani, Ali Keshavarz, Maryam Chamari,
Volume 5, Issue 1 (8-2005)
Abstract
Background: Lipoprotein abnormalities have been identified among the several risk factors that could account for increases the risk of CVD in diabetes. Abnormal status of B-group and antioxidant vitamins in diabetes may illustrate the benefits of these vitamins supplementation on modification of lipid profiles.
Methods: As a randomized double blind placebo controlled clinical trial, 110 type 2 diabetic patients were randomly assigned to one of the five treatment groups and received one of the following supplements per day for a period of 2 months: 1) B-group vitamins including B2 (10 mg), B6 (10mg), B12 (200µg) and Folate (1000µg) 2) B-group vitamins and vitamin E (100mg) 3) B-group vitamins and vitamin C (200mg) 4) B-group vitamins, vitamins E (100mg) and C (200mg) and 5) placebo. Fasting blood samples at the beginning and at the end of 2 months trial were collected and analyzed for cholesterol, triglyceride, apolipoproteins A1 and B (apo A1 & B), vitamin E, folate, vitamin B12 in serum and vitamin C in whole blood. Differences in baselines models. Covariates and changes in variables during study were adjusted by analysis of covariance using general linear.
Results: No significant changes were found in mean serum apolipoproteins levels after 2 months of supplementation. Vitamin E variation showed significant positive correlation with variation in apo A1 (P=0.003) and apo B (P<0.001). In multiple regression analysis, serum vitamin E levels were an independent and important predictor of serum apoA1 and B levels (P=0.002 and P<0.001, respectively). Serum vitamin B12 variation was important predictor of serum apo B levels (P<0.05).
Conclusion: Serum vitamin E level is a good predictor of serum apo A1 and B levels. Further increases in dose of vitamin supplements and intervention period are recommended for obtaining the desirable modifications.
