The reduction of dietary sucrose improves dyslipidemia, adiposity, and insulin secretion in an insulin-resistant rat model

Fortino, María Alejandra; Lombardo, Yolanda B.; Chicco, Adriana

doi:10.1016/j.nut.2007.04.007

Cited by 16 publications

(15 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Aside from total energy intake, dietary variety reveals different metabolic patterns depending on the source of energy. High-fat (HF) and high-carbohydrate (HC) intakes were shown to contribute to syndromes such as hyperlipidemia and glucose intolerance [1][2][3]. Frequent disruption of energy balance due to excessive energy intake causes hypertrophy and hyperplasia of fat cells, and this positive balance also induces insulin resistance in the liver [4].…”

Section: Introductionmentioning

confidence: 99%

High-Carbohydrate Diet Selectively Induces Tumor Necrosis Factor-α Production in Mice Liver

et al. 2010

View full text Add to dashboard Cite

Obesity may represent a state of chronic low-grade inflammation associated with infiltration of adipose tissue by inflammatory cells. Tumor necrosis factor-α (TNF-α) and monocyte chemoattractant protein-1 (MCP-1/JE), two important inflammatory cytokines, have been shown to be regulated according to changes in body adiposity. In this study on Swiss mice, we compared the influences of long-term high-carbohydrate (HC) or high-fat (HF) diet on adiposity, glucose tolerance, and secretion of TNF-α and MCP-1/JE by adipose tissue and liver. For 8 weeks, male Swiss mice (7-8 weeks) were fed either standard laboratory rodent diet (control group), HC diet (64% carbohydrate, 19% protein, and 11% fat), or HF diet (45% carbohydrate, 17% protein, and 38% fat), with the latter two diets having no fiber. Oral glucose tolerance test, triacylglycerol (TAG) plasma concentration, and systemic or tissue levels of the two proinflammatory cytokines were determined. Body weight increased by approximately 20% in mice fed the experimental diets compared with mice fed the control diet. Systemically, the hypercaloric diets induced hyperglycemia with impairment in glucose tolerance, elevated circulating TAG levels, and increased plasma concentrations of TNF-α and MCP-1/JE. In the target organs (adipose tissue and liver), both diets increased MCP-1/JE levels. However, the HC diet, but not the HF diet, was able to increase TNF-α concentration in the liver. These results have shown that the nature of nutrients influences the type of proinflammatory cytokines in target organs and may contribute to the comorbidities of obesity.

show abstract

Section: Introductionmentioning

confidence: 99%

High-Carbohydrate Diet Selectively Induces Tumor Necrosis Factor-α Production in Mice Liver

et al. 2010

View full text Add to dashboard Cite

show abstract

“…Previous studies have demonstrated that rats fed a sucrose-rich diet (SRD) exhibited impaired insulin activity and hypertriglyceridemia; this model of insulin resistance induced by an environmental factor is probably accompanied by fatty liver disease [9][10][11] .…”

mentioning

confidence: 99%

Circulating Very-Low-Density Lipoprotein Characteristics Resulting from Fatty Liver in an Insulin Resistance Rat Model

Zago¹,

Lucero²,

Macri

et al. 2010

Ann Nutr Metab

View full text Add to dashboard Cite

The close association between nonalcoholic fatty liver and insulin resistance is now widely recognized. While the former is characterized by excessive intrahepatic triglyceride accumulation, the latter induces overproduction of very-low-density lipoprotein (VLDL) particles. It has not been well elucidated whether these apparently opposite mechanisms impact on VLDL characteristics or not. The aim of the present study was to evaluate the VLDL secretion and features resulting from insulin resistance and fatty liver in rats fed a sucrose-rich diet (SRD, i.e. addition of sucrose to drinking water during 12 weeks). No differences in calorie intake were observed in comparison to controls. Both groups showed similar weight gains throughout the treatment period. However, SRD rats showed an increased proportion of body fat as assessed by X-ray absorptiometry, increased visceral obesity, liver weight and fat accumulation in the liver (p < 0.04). Histological study revealed moderate micro- and macrovesicular steatosis. Fasting insulin, triglyceride and free fatty acid (FFA) levels increased while VLDLs decreased in SRD rats (p < 0.05). The chemical composition of VLDLs of SRD rats showed a higher percentage of triglycerides, and the VLDL triglyceride/protein ratio, an estimator of lipoprotein size, suggests that VLDL particles of SRD rats are larger than those of controls (p < 0.0005). FFA levels correlated with VLDL triglycerides (r = 0.49, p = 0.03) and liver fat content correlated with plasma triglycerides (r = 0.65), VLDL triglycerides (r = 0.55) and triglyceride/protein ratio (r = 0.52, p < 0.02). The VLDL secretion rate assay showed an increase in SRD rats (p < 0.02), confirming an overproduction despite liver fat accumulation. Our findings are consistent with an insulin resistance development model in which hepatic lipid content would constitute an important determinant of a triglyceride-rich, large-particle VLDL secretion; both features would increase its atherogenic potential.

show abstract

“…Serum levels of these enzymes are related to multiple components of MS 8 . Several studies have demonstrated the induction of NAFLD in rats by diets with large amounts of simple carbohydrates 17,18 . However, few are focused on dietary manipulation for effective reversal of metabolic damage generated by these diets 17 .…”

Section: Introductionmentioning

confidence: 99%

“…Consumption of simple carbohydrates such as sucrose and fructose has increased steadily over the last 20 years 17 . The excess of glucose or fructose causes the synthesis of triacylglycerols that will accumulate in the liver.…”

Section: Introductionmentioning

confidence: 99%

“…This accumulation is the cause of NAFLD 1,5 . Rats fed a diet high in simple carbohydrates (SC) developed dyslipidemia, weight gain, visceral adiposity and reduced insulin sensitivity 17 . Axen et al 19 also reported higher levels of triglycerides in obese mice fed with SC compared to those fed a high-fat diet and, similarly, another study indicated that by replacing fat with carbohydrates the diet contributes to weight gain 20 .…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Fructose and NAFLD: metabolic implications and models of induction in rats

Castro¹,

Cardoso²,

Vannucchi³

et al. 2011

Acta Cir. Bras.

View full text Add to dashboard Cite

PURPOSE:The increase in fructose consumption is paralleled by a higher incidence of obesity worldwide. This monosaccharide is linked to metabolic syndrome, being associated with hypertriglyceridemia, hypertension, insulin resistance and diabetes mellitus. It is metabolized principally in the liver, where it can be converted into fatty acids, which are stored in the form of triglycerides leading to NAFLD. Several models of NAFLD use diets high in simple carbohydrates. Thus, this study aimed to describe the major metabolic changes caused by excessive consumption of fructose in humans and animals and to present liver abnormalities resulting from high intakes of fructose in different periods of consumption and experimental designs in Wistar rats. METHODS: Two groups of rats were fasted for 48 hours and reefed for 24 or 48 hours with a diet containing 63% fructose. Another group of rats was fed an diet with 63% fructose for 90 days. RESULTS: Refeeding for 24 hours caused accumulation of large amounts of fat, compromising 100% of the hepatocytes. The amount of liver fat in animals refed for 48 hours decreased, remaining mostly in zone 2 (medium-zonal). In liver plates of Wistar rats fed 63% fructose for 45, 60 and 90 days it's possible to see that there is an increase in hepatocytes with fat accumulation according to the increased time; hepatic steatosis, however, is mild, compromising about 20% of the hepatocytes. CONCLUSIONS: Fructose is highly lipogenic, however the induction of chronic models in NAFLD requires long periods of treatment. The acute supply for 24 or 48 hours, fasted rats can cause big changes, liver steatosis with macrovesicular in all lobular zones. Key words: Fructose. Fatty Liver. Diet. Rats. RESUMO OBJETIVO:O aumento do consumo de frutose é concomitante a maior incidência mundial de obesidade. Este monossacarídeo está relacionado à Síndrome Metabólica, sendo vinculado à hipertrigliceridemia, hipertensão arterial, resistência à insulina e diabetes mellitus. É metabolizada principalmente no fígado, onde pode ser convertida em ácidos graxos, os quais serão estocados na forma de trigligérides ocasionando a esteatose hepática não alcoólica (NAFLD). Vários modelos de NAFLD utilizam dietas ricas em carboidratos simples. Desta forma, este trabalho teve como objetivos descrever as principais alterações metabólicas causadas pelo consumo excessivo de frutose em humanos e em animais e apresentar as alterações hepáticas decorrentes da alta ingestão de frutose em diferentes períodos de consumo e desenhos experimentais em ratos Wistar. MÉTODOS: Dois grupos de ratos Wistar foram mantidos em jejum durante 48 horas e realimentados por 24 ou 48 horas com dieta contendo 63% de frutose. Outro grupo de ratos Wistar foi alimentado com 63% de frutose durante 90 dias. RESULTADOS: A realimentação por 24 horas provocou acúmulo de grande quantidade de gordura. A quantidade de gordura hepática nos animais realimentados por 48 horas diminuiu, mantendo-se principalmente nas zona 2 (medio-zonal). Em fígados de ratos Wi...

show abstract

The reduction of dietary sucrose improves dyslipidemia, adiposity, and insulin secretion in an insulin-resistant rat model

Cited by 16 publications

References 32 publications

High-Carbohydrate Diet Selectively Induces Tumor Necrosis Factor-α Production in Mice Liver

High-Carbohydrate Diet Selectively Induces Tumor Necrosis Factor-α Production in Mice Liver

Circulating Very-Low-Density Lipoprotein Characteristics Resulting from Fatty Liver in an Insulin Resistance Rat Model

Fructose and NAFLD: metabolic implications and models of induction in rats

Contact Info

Product

Resources

About