Very-low-density lipoprotein triglyceride kinetics in acute and chronic carbohydrate-fed rats

Hirano, Takehiro; Mamo, John; Poapst, M.; Steiner, George

doi:10.1152/ajpendo.1988.255.3.e236

Cited by 13 publications

(17 citation statements)

References 4 publications

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“…Fructose feeding causes overproduction of TG in the liver (25) and a defect in TG catabolism due to altered composition and nature of very-low-density lipoprotein particles (26). Olmesartan remarkably suppressed TGSR without affecting LPL concentration in fructose-fed rats.…”

Section: Discussionmentioning

confidence: 99%

Olmesartan Medoxomil, an Angiotensin II Receptor Blocker Ameliorates Insulin Resistance and Decreases Triglyceride Production in Fructose-Fed Rats

et al. 2004

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Section: Discussionmentioning

confidence: 99%

Olmesartan Medoxomil, an Angiotensin II Receptor Blocker Ameliorates Insulin Resistance and Decreases Triglyceride Production in Fructose-Fed Rats

et al. 2004

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“…Nevertheless, most published studies in rats or mice did not show an inhibitory effect of thiazolidinediones on VLDL secretion, thereby concluding that the lowering of plasma TG resulted in total or in part from increased VLDL clearance (22,24,25). Unlike the fructose-fed hamster and insulin resistant humans, the rodent models used in the latter studies display impaired plasma TG clearance as the major mechanism of their hypertriglyceridemia when they become insulin-resistant (8). This perhaps explains the discrepancy between our results and those of the latter studies.…”

Section: Discussionmentioning

confidence: 99%

“…These animal models may not, however, be ideal for the study of human lipoprotein disorders because, unlike humans, their livers secrete both apoB48 and apoB100-containing VLDL, and they do not necessarily develop VLDL oversecretion as the basis for their hypertriglyceridemia (8,9). Unlike livers from rat or mouse, the liver of the golden Syrian hamster secretes only apoB100-containing VLDL, and its lipoprotein metabolism more closely resembles that of humans (10).…”

mentioning

confidence: 99%

Ameliorated Hepatic Insulin Resistance Is Associated with Normalization of Microsomal Triglyceride Transfer Protein Expression and Reduction in Very Low Density Lipoprotein Assembly and Secretion in the Fructose-fed Hamster

Carpentier¹,

Taghibiglou²,

Leung³

et al. 2002

Journal of Biological Chemistry

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To determine whether reduction of insulin resistance could ameliorate fructose-induced very low density lipoprotein (VLDL) oversecretion and to explore the mechanism of this effect, fructose-fed hamsters received placebo or rosiglitazone for 3 weeks. Rosiglitazone treatment led to normalization of the blunted insulinmediated suppression of the glucose production rate and to a ϳ2-fold increase in whole body insulin-mediated glucose disappearance rate (p < 0.001). Rosiglitazone ameliorated the defect in hepatocyte insulin-stimulated tyrosine phosphorylation of the insulin receptor, IRS-1, and IRS-2 and the reduced protein mass of IRS-1 and IRS-2 induced by fructose feeding. Protein-tyrosine phosphatase 1B levels were increased with fructose feeding and were markedly reduced by rosiglitazone. Rosiglitazone treatment led to a ϳ50% reduction of VLDL secretion rates (p < 0.05) in vivo and ex vivo. VLDL clearance assessed directly in vivo was not significantly different in the FR (fructose-fed ؉ rosiglitazone-treated) versus F (fructose-fed ؉ placebo-treated) hamsters, although there was a trend toward a lower clearance with rosiglitazone. Enhanced stability of nascent apolipoprotein B (apoB) in fructose-fed hepatocytes was evident, and rosiglitazone treatment resulted in a significant reduction in apoB stability. The increase in intracellular mass of microsomal triglyceride transfer protein seen with fructose feeding was reduced by treatment with rosiglitazone. In conclusion, improvement of hepatic insulin signaling with rosiglitazone, a peroxisome proliferator-activated receptor ␥ agonist, is associated with reduced hepatic VLDL assembly and secretion due to reduced intracellular apoB stability.The typical dyslipidemia of insulin-resistant states and Type 2 diabetes consists of hypertriglyceridemia due to VLDL 1 overproduction, low high density lipoprotein cholesterol, and small dense low density lipoprotein particles (1). Elevated plasma free fatty acid (FFA) flux from peripheral and intra-abdominal adipose tissue depots due to resistance to the insulin antilipolytic and esterification effect in adipose tissue is felt to play an important role in driving VLDL assembly and secretion in insulin resistant states (2-4). Nevertheless, previous studies in humans suggest that insulin also has an important direct effect on the liver in controlling VLDL secretion (5-7).Rat and mouse models of insulin resistance and type 2 diabetes have provided important insights into the molecular mechanisms of insulin resistance. These animal models may not, however, be ideal for the study of human lipoprotein disorders because, unlike humans, their livers secrete both apoB48 and apoB100-containing VLDL, and they do not necessarily develop VLDL oversecretion as the basis for their hypertriglyceridemia (8, 9). Unlike livers from rat or mouse, the liver of the golden Syrian hamster secretes only apoB100-containing VLDL, and its lipoprotein metabolism more closely resembles that of humans (10). We have shown that insulin resistance in the fru...

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“…TG secretion rate (TGSR) in vivo may also be determined by injecting radiolabeled VLDL-TG, or a precursor of TG such as glycerol , and determining the turnover rate of VLDL-TG under steady-state conditions (4-6) . There have been several reports (7)(8)(9), including work from our laboratory (10) , that have indicated that calculated TGSR may differ substantially depending on which method is employed. Few studies have examined the relationship of TGSR derived by the tracer or the triton methods .…”

Section: Discussionmentioning

confidence: 99%

Comparison of the Isotopical Tracer and the Triton WR 1339 Methods for Triglyceride Kinetics in Carbohydrate-fed Rats

Hirano

Mamo

Takahashi

1990

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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SummaryRadiolabeled tracer [3H] very low density lipoprotein (VLDL)-triglyceride (TG) and non-tracer (Triton WR 1339) methods were used to determine VLDL-TG kinetics in normal rats and in rats given either a 10% glucose or a 10% fructose drinking solution for 16h ad libitum. The carbohydrate-fed rats were hypertriglyceridemic com pared to control animals. VLDL-TG was endogenously prelabeled with [3H] glycerol in control, glucose and fructose-fed rats, and injected into identically treated recipients. Triton WR 1339, a potent inhibitor of VLDL-TG catabolism, was injected into the same animal 30 min after the end of the tracer method to measure TG secretion rate (TGSR). The tracer and non-tracer methods showed that fructose-fed rats had a sig nificantly lower fractional catabolic rate (FCR) than either control or glucose-fed rats. In contrast, glucose-fed rats had a TGSR greater than control without a reduction in FCR. For all treatments, TG concentra tion correlated with FCR for the tracer method and with TGSR for the non-tracer method. There was good correlation of TGSR determined by the tracer and non-tracer method for control rats despite the substantial difference in the absolute values. No such relationship was observed in carbohydrate-fed rats. Control rats were made hypertriglyceridemic by Intralipid infusion. A lower FCR was observed when determined by the tracer method, but this was not observed by the triton method. These results suggest that TG kinetics determined by the tracer and the triton methods cannot be readily correlated, especially in hypertriglyceridemic state. However, the two kinetic studies both suggested that overproduc tion of VLDL-TG in glucose-fed rats and impaired VLDL-TG catabo lism in fructose-fed rats were the primary cause for their hypertriglycer idemic, respectively.

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Very-low-density lipoprotein triglyceride kinetics in acute and chronic carbohydrate-fed rats

Cited by 13 publications

References 4 publications

Olmesartan Medoxomil, an Angiotensin II Receptor Blocker Ameliorates Insulin Resistance and Decreases Triglyceride Production in Fructose-Fed Rats

Olmesartan Medoxomil, an Angiotensin II Receptor Blocker Ameliorates Insulin Resistance and Decreases Triglyceride Production in Fructose-Fed Rats

Ameliorated Hepatic Insulin Resistance Is Associated with Normalization of Microsomal Triglyceride Transfer Protein Expression and Reduction in Very Low Density Lipoprotein Assembly and Secretion in the Fructose-fed Hamster

Comparison of the Isotopical Tracer and the Triton WR 1339 Methods for Triglyceride Kinetics in Carbohydrate-fed Rats

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