Triglyceridemia, Glucoregulation, and Blood Pressure in Various Rat Strains

Vrána, A.; Kazdová, Ludmila; Dobešová, Z; Kuneš, Jaroslav; Křen, Vladimı́r; Bı́lá, V; Stolba, P; Klimeš, I

doi:10.1111/j.1749-6632.1993.tb35692.x

Cited by 40 publications

(40 citation statements)

References 12 publications

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“…The variability in responses could be due to the differences in experimental design: administration of fructose diet at an earlier age than in our experiment (6,18,26), higher fructose percentile than in our experiment (6,14,25), or presence of sucrose in the diet (35). In addition, variability to fructose feeding has been observed with different rat strains (7,39) and among identical rat strains supplied by different vendors (27,35).…”

Section: Discussionmentioning

confidence: 68%

Fructose-induced leptin resistance exacerbates weight gain in response to subsequent high-fat feeding

Shapiro¹,

Mu²,

Roncal³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

273

217

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RJ, Scarpace PJ. Fructose-induced leptin resistance exacerbates weight gain in response to subsequent high-fat feeding. Am J Physiol Regul Integr Comp Physiol 295: R1370 -R1375, 2008. First published August 13, 2008 doi:10.1152/ajpregu.00195.2008.-It has been suggested that increased fructose intake is associated with obesity. We hypothesized that chronic fructose consumption causes leptin resistance, which subsequently may promote the development of obesity in response to a high-fat diet. Sprague-Dawley rats were fed a fructose-free control or 60% fructose diet for 6 mo and then tested for leptin resistance. Half of the rats in each group were then switched to high-fat diet for 2 wk, while the other half continued on their respective diets. Chronic fructose consumption caused leptin resistance, while serum leptin levels, weight, and adiposity were the same as in control rats that were leptin responsive. Intraperitoneal leptin injections reduced 24-h food intake in the fructose-free group (73.7 Ϯ 6.3 vs. 58.1 Ϯ 8 kcal, P ϭ 0.02) but had no effect in fructose-fed rats (71.2 Ϯ 6.6 vs. 72.4 Ϯ 6.4 kcal, P ϭ 0.9). Absence of anorexic response to intraperitoneal leptin injection was associated with 25.7% decrease in hypothalamic signal transducer and activator of transcription 3 phosphorylation in the high-fructose-fed rats compared with controls (P ϭ 0.015). Subsequent exposure of the fructose-mediated, leptin-resistant rats to a high-fat diet led to exacerbated weight gain (50.2 Ϯ 2 g) compared with correspondingly fed leptin-responsive animals that were pretreated with the fructose-free diet (30.4 Ϯ 5.8 g, P ϭ 0.012). Our data indicate that chronic fructose consumption induces leptin resistance prior to body weight, adiposity, serum leptin, insulin, or glucose increases, and this fructose-induced leptin resistance accelerates highfat induced obesity.

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Section: Discussionmentioning

confidence: 68%

Fructose-induced leptin resistance exacerbates weight gain in response to subsequent high-fat feeding

Shapiro¹,

Mu²,

Roncal³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

273

217

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“…Both fibratesFagonists of peroxisome proliferator-activated receptor alpha (PPARa)Fand retinoidsFpanagonists of the retinoic acid receptors RAR and RXRFwere commonly shown to influence triglyceridemia through changing the expression of apolipoprotein C-III (ApoC-III) gene. 6,7 This gene alone as well as the whole ApoA-I/C-III/A-IV cluster (and most recently its new member, ApoA-V) were associated with dyslipidemia in human populations and animal models 3,8 and were also suggested as putative candidates for hypertriglyceridemia in a genetic model of insulin resistance syndrome, polydactylous (PD/Cub) rat strain [9][10][11][12][13][14] (http:// www.img.cas.cz/fb/, Table 1). Therefore, we examined the effect of fenofibrate and isotretinoin administration on metabolic profile, insulin sensitivity and lipolysis in tissues and the expression of ApoC-III and one of its proposed upstream regulatory genes, hepatocyte nuclear factor-4 (Hnf-4), in the PD/Cub rat strain.…”

Section: Introductionmentioning

confidence: 99%

Isotretinoin and fenofibrate induce adiposity with distinct effect on metabolic profile in a rat model of the insulin resistance syndrome

et al. 2004

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OBJECTIVE:To investigate the effect of transcription-modulating drugs, fenofibrate and isotretinoin, on metabolic profile, insulin sensitivity of adipose and muscle tissues and gene expression in a genetic model of insulin resistance syndrome, polydactylous rat strain (PD/Cub). DESIGN: Administration of fenofibrate (100 mg/kg/day), isotretinoin (30 mg/kg/day) or vehicle to adult male PD/Cub rats fed standard laboratory chow for 15 days. MEASUREMENTS: Parameters of lipid and carbohydrate metabolismForal glucose tolerance test, serum concentrations of insulin, triglycerides (TG), free fatty acids (FFA), glycerol, total cholesterol (CH); morphometric variables, in vitro insulin sensitivity of adipose and muscle tissues, catecholamine-stimulated lipolysis and the expression of ApoC-III and Hnf-4 genes in liver. RESULTS: Both experimental groups displayed an increase in adiposity with contrasting effects on TG (lowered by fenofibrate and increased by isotretinoin) and gene expression (no change in fibrate-treated rats and increased expression of ApoC-III and Hnf-4 in isotretinoin-treated group). Fenofibrate-treated rats also showed decreased concentrations of FFA and CH with concomitant decrease of catecholamine-induced lipolysis in adipocytes, but also hyperinsulinemia and the highest insulin/ glucose ratio. Isotretinoin increased glycerol concentrations and decreased the insulin sensitivity of peripheral tissues. CONCLUSION: The PD/Cub rat showed a distinct pharmacogenetic reaction to fenofibrate and isotretinoin administration. Several lines of evidence now implicate specific variant(s) of ApoC-III and/or ApoA-V alleles as responsible for the dyslipidemia observed in this genetic model. The PD/Cub strain may also serve as a pharmacogenetic model for dissection of the retinoidinduced hypertriglyceridemia.

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“…Brown Norway rat was transferred from the USA to the Institute of Biology, First Faculty of Medicine in 1964 and since then has been bred by brother ϫ sister mating for more than 70 generations. The metabolic profile of this highly inbred strain has been assessed in several studies (21,22,28) and BN/Cub, compared with several models of insulin resistance and dyslipidemia, was found to be markedly "normometabolic" in terms of carbohydrate and lipid metabolism.…”

Section: Methodsmentioning

confidence: 99%

Rosiglitazone fails to improve hypertriglyceridemia and glucose tolerance in CD36-deficient BN.SHR4 congenic rat strain

Šeda

Kazdová²,

Křenová

et al. 2003

Physiological Genomics

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The favorable metabolic effects of thiazolidinediones are supposedly related to the peroxisome proliferator-activated receptor-γ (PPARγ)-driven changes in lipid metabolism, particularly in free fatty acid (FFA) trafficking. The fatty acid translocase CD36 is one of the proposed PPARγ targets to mediate this action. We assessed the effect of rosiglitazone (RSG, Avandia) administration in two inbred rat strains, BN/Cub and BN.SHR4 congenic strain, differing in 10 cM proximal segment of chromosome 4. Rats were fed high-sucrose diet with or without RSG for 1 wk. In BN.SHR4, which carries defective Cd36 allele of SHR origin, RSG failed to improve glucose tolerance (assessed by the oral glucose tolerance test), did not lower triglyceridemia, nor induced increases in epididymal and retroperitoneal adipose tissue weights and adipose tissue glucose utilization, effects observed in BN/Cub. On the other hand, the RSG-treated BN.SHR4 showed lower concentrations of FFA and substantial increase in glycogen synthesis and glucose oxidation in skeletal muscle. Altogether, these results support involvement of CD36 in RSG action, suggesting this pharmacogenetic interaction may be of particular importance in CD36-deficient humans.

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Triglyceridemia, Glucoregulation, and Blood Pressure in Various Rat Strains

Cited by 40 publications

References 12 publications

Fructose-induced leptin resistance exacerbates weight gain in response to subsequent high-fat feeding

Fructose-induced leptin resistance exacerbates weight gain in response to subsequent high-fat feeding

Isotretinoin and fenofibrate induce adiposity with distinct effect on metabolic profile in a rat model of the insulin resistance syndrome

Rosiglitazone fails to improve hypertriglyceridemia and glucose tolerance in CD36-deficient BN.SHR4 congenic rat strain

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