Opposite lipemic response of Wistar rats and C57BL/6 mice to dietary glucose or fructose supplementation

Barbosa, Cristina Rosa; Albuquerque, Edilma M V; Faria, Eliana Cotta de; Oliveira, Helena; Castilho, Lísias Nogueira

doi:10.1590/s0100-879x2007000300007

Cited by 17 publications

(14 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…These differences are attributable mainly to differences among experimental protocols, such as (1) the variability in the composition of diets; (2) different forms of fructose administration, such as in the diet [23] or water [24]; (3) duration of dietary treatments, from weeks [24] to months [15]; (4) use of different rodent models [15,23]; and different age of animals, i.e., young [17,23] or adults [24]. To minimize these biases, in the present study we compared several biochemical, physiological, histological and biometric parameters of newly weaned young rats and adult rats submitted to the FRU and FAT diets, i.e., those that are most often used to induce disturbances related to MS. Taken together, our data revealed that FRU diet for adult rats and FAT diet for young rats are the best nutritional interventions to induce MS in rats and differently change the lipid metabolism and the ectopic fat deposition in the liver and kidney in rats of different ages.…”

Section: Discussionmentioning

confidence: 99%

Age-dependent effect of high-fructose and high-fat diets on lipid metabolism and lipid accumulation in liver and kidney of rats

et al. 2013

View full text Add to dashboard Cite

BackgroundThe metabolic syndrome (MS) is characterized by variable coexistence of metabolic and pathophysiological alterations which are important risk factors for developing of type II diabetes and/or cardiovascular diseases. Increased of MS patients in worldwide has stimulated the development of experimental models. However, it is still challenging to find an dietetic model that most closely approximates human MS and, in addition, is not yet fully established the effect of different diets of MS in lipid metabolism in rats of different ages. The aim of this study was to evaluate the effect of different diets of MS in lipid metabolism and ectopic fat deposition and define the most appropriate diet for inducing the characteristic disturbances of the human MS in rats of different ages.MethodsYoung (4 weeks old) and adult rats (12 weeks old) were given a high-fat (FAT) or high-fructose diet (FRU) for 13 weeks and biochemical, physiological, histological and biometric parameters were evaluated.ResultsIn young rats, the FAT diet induced increased mean blood pressure (MAP) and heart rate (HR), body weight after 6 to 10 weeks, and in the 13th week, increased the liver, mesenteric, retroperitoneal and epididymal fat weights, fasting glucose, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and reduced HDL cholesterol; and also induced non-alcoholic fatty liver disease (NAFLD) and renal inflammatory infiltrates. In adult rats, the FRU diet induced transient elevations of MAP and HR in the 6th week, and, at 13 weeks, increased fasting glucose, triglycerides, total cholesterol, AST and ALT; increased liver, kidneys and retroperitoneal fat weights; and induced macrovesicular and microvesicular NAFLD, the presence of fat cells in the kidney, glomerular sclerosis, and liver and kidney inflammation. Additionally, the FAT and FRU diets induced, respectively, increases in liver glycogen in adults and young rats.ConclusionsOur data show that FRU diet in adult rats causes biggest change on metabolism of serum lipids and lipid accumulation in liver and kidney, while the FAT diet in young rats induces elevation of MAP and HR and higher increased visceral lipid stores, constituting the best nutritional interventions to induce MS in rats.

show abstract

Section: Discussionmentioning

confidence: 99%

Age-dependent effect of high-fructose and high-fat diets on lipid metabolism and lipid accumulation in liver and kidney of rats

et al. 2013

View full text Add to dashboard Cite

show abstract

“…A elevação nas concentrações de triglicérides constatada no presente trabalho é quase unanimidade, nos mais diferentes estudos (3,(9)(10)(11)13,15,16,22,25,28,34) ; em alguns destes, tais modificações foram igualmente observadas no fígado (13,36) . Altos níveis de triglicérides séricos são descritos como conseqü-ência da ingestão de frutose (28) , uma vez que esta é mais lipogênica que a glicose (3) .…”

Section: Discussionunclassified

“…A maioria dos trabalhos (7,(9)(10)(11)(12)(13)(14)(15)(16) analisa a influência da elevada ingestão de frutose somente em parâmetros de repouso. Porém, o exercício físico é um componente importante na prevenção e no tratamento da síndrome; foi demonstrado que o nível de capacidade aeróbia apresenta relação inversa com o risco de desenvolver essa doença (17) .…”

Section: Introductionunclassified

Capacidade aeróbia de ratos alimentados com dieta rica em frutose

Moura

Cambri

Quadros

et al. 2008

Rev Bras Med Esporte

View full text Add to dashboard Cite

Introdução: Evidências apontam que a ingestão exacerbada de frutose pode desencadear distúrbios característicos da síndrome metabólica. Objetivos: Analisar os efeitos da ingestão de dieta rica em frutose sobre aspectos metabólicos de ratos da linhagem Wistar. Adicionalmente, verificar a capacidade aeróbia através da identificação da máxima fase estável de lactato (MFEL). Métodos: Dezesseis ratos foram separados em dois grupos de oito animais: a) controle, alimentados com dieta balanceada, e b) frutose, alimentados com dieta rica em frutose. Foram analisadas a tolerância à glicose (área sob a curva de glicose durante teste de tolerância à glicose), sensibilidade à insulina (taxa de remoção da glicose sérica após sobrecarga exógena de insulina), perfil lipídico sérico e concentração de lactato sanguíneo [lac]s durante exercício na intensidade da MFEL. Resultados: Teste t não pareado (p < 0,05) revelou diferença para a tolerância à glicose e triglicérides, porém não houve diferença na sensibilidade à insulina e na [lac]s. Anova one way com post hoc de Newman-Keuls (p < 0,05) revelou diferença para a cinética da glicose durante o teste de tolerância, mas não para a cinética do lactato durante exercício na MSSL. Conclusão: As alterações fisiológicas provocadas pela dieta rica em frutose e inerentes à síndrome metabólica não prejudicam a capacidade aeróbia de ratos.Palavras-chave: máxima fase estável de lactato, síndrome metabólica, exercício. ABSTRACTIntroduction: Evidence points that exacerbated ingestion of fructose may trigger disturbs characteristic of the metabolic syndrome. Objectives: To analyze the effects of a fructose rich diet on metabolic aspects of Wistar lineage rats. Additionally, to verify the aerobic capacity, through the identification of the maximal lactate steady state (MSSL). Procedures: Sixteen rats were separated in two groups of eight animals: a) Control, fed a balanced diet, and b) fructose, fed a fructose-rich diet. The glucose tolerance, (area under serum glucose during a glucose tolerance test), insulin sensibility (glucose disappearance rate after exogenous insulin administration), serum lipid profile and blood lactate concentration [lac]b during exercise at MSSL intensity, have been analyzed. Results: Non-paired t test (p<0.05) revealed difference between groups in the area under the curve of glucose and serum triglycerides, no difference in insulin sensibility or in [lac]b was detected, though. One-way ANOVA with Newman Keuls post hoc revealed difference in the glucose kinetics during tolerance test, but not in the lactate kinetics during the MSSL. Conclusion: The physiological alterations promoted by fructose-rich diet and intrinsic to the metabolic syndrome do not harm the aerobic capacity of rats.

show abstract

“…On the other hand, fructose supplementation has been extensively studied in rodents, especially in rats, and has been shown to promote insulin resistance and inflammation [14,15]. Few mice studies suggest that the metabolic response towards high fructose diets provides discrepant results concerning the effect on body weight, glucose and lipid homeostasis [38][39][40]. Messier et al [39] have shown that the combination of HF diet and fructose supplementation in mice leads to increased weight gain and impairments in blood glucose regulation, but this combination model has not been extensively studied.…”

Section: Page 16 Of 42mentioning

confidence: 99%

Coenzyme Q10 supplementation lowers hepatic oxidative stress and inflammation associated with diet-induced obesity in mice

Sohet

Neyrinck

Pachikian

et al. 2009

Biochemical Pharmacology

145

View full text Add to dashboard Cite

Please cite this article as: Sohet FM, Neyrinck AM, Pachikian BD, de Backer FC, Bindels LB, Niklowitz P, Menke T, Cani PD, Delzenne NM, Coenzyme Q10 supplementation lowers hepatic oxidative stress and inflammation associated with diet-induced obesity in mice, Biochemical Pharmacology (2008Pharmacology ( ), doi:10.1016Pharmacology ( /j.bcp.2009 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Aims:The aim of the study is to investigate the effect of the antioxidant coenzyme Q10 (CoQ10) on hepatic metabolic and inflammatory disorders associated with diet-induced obesity and glucose intolerance.Methods: C57bl6/j mice were fed for 8 weeks, either a control diet (CT) or a high fat diet plus 21% fructose in the drinking water (HFF). CoQ10 supplementation was performed in this later condition (HFFQ).Results HFF mice exhibit increased energy consumption, fat mass development, fasting glycemia and insulinemia and impaired glucose tolerance. HFF treatment promoted the expression of genes involved in reactive oxygen species production (NADPH oxidase), inflammation (CRP, STAMP-2) and metabolism (CPT1) in the liver. CoQ10 supplementation decreased the global hepatic mRNA expression of inflammatory and metabolic stresses markers without changing obesity and tissue lipid peroxides compared to HFF mice. HFF diets paradoxically decreased TBARS (reflecting lipid peroxides) levels in liver, muscle and adipose tissue versus CT group, an effect related to vitamin E content of the diet. Conclusion:In conclusion, HFF model promotes glucose intolerance and obesity by a mechanism independent on the level of tissue peroxides. CoQ10 tends to decrease hepatic stress gene expression, independently of any modulation of lipid peroxidation, which is classically considered as its most relevant effect.

show abstract

Opposite lipemic response of Wistar rats and C57BL/6 mice to dietary glucose or fructose supplementation

Cited by 17 publications

References 37 publications

Age-dependent effect of high-fructose and high-fat diets on lipid metabolism and lipid accumulation in liver and kidney of rats

Age-dependent effect of high-fructose and high-fat diets on lipid metabolism and lipid accumulation in liver and kidney of rats

Capacidade aeróbia de ratos alimentados com dieta rica em frutose

Coenzyme Q10 supplementation lowers hepatic oxidative stress and inflammation associated with diet-induced obesity in mice

Contact Info

Product

Resources

About