Chronic fructose intake accelerates non-alcoholic fatty liver disease in the presence of essential hypertension

Lírio, Layla Mendonça; Forechi, Ludimila; Zanardo, Tadeu Caliman; Batista, Hiago Martins; Meira, Eduardo Frizzera; Nogueira, Breno Valentim; Mill, José Geraldo; Baldo, Marcelo Perim

doi:10.1016/j.jdiacomp.2015.10.008

Cited by 30 publications

(31 citation statements)

References 44 publications

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“…Moreover, dietary protein content was suggested to be a critical determinant of weight gain during ad libitum feeding [20]. This prediabetic animal model presented low food intake, which is enriched in 16.1% protein, and increased fluid intake of sucrose-enriched water, in agreement with previous studies [18]. This means that HSu-treated animals ingested a smaller amount of protein and a greater amount of carbohydrates, which can be translated by higher fat mass and smaller lean mass, which allowed the maintenance of body weight.…”

Section: Discussionsupporting

confidence: 90%

Glucose and Lipid Dysmetabolism in a Rat Model of Prediabetes Induced by a High-Sucrose Diet

Burgeiro¹,

Cerqueira²,

Varela-Rodríguez³

et al. 2017

Preprint

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Glucotoxicity and lipotoxicity are key features of type 2 diabetes mellitus, but their molecular nature during the early stages of the disease remains to be elucidated. We aimed to characterize glucose and lipid metabolism in insulin-target organs (liver, skeletal muscle, and white adipose tissue) in a rat model treated with a high-sucrose (HSu) diet. Two groups of 16-week-old male Wistar rats underwent a 9-week protocol: HSu diet (n = 10)-received 35% of sucrose in drinking water; Control (n = 12)-received vehicle (water). Body weight, food, and beverage consumption were monitored and glucose, insulin, and lipid profiles were measured. Serum and liver triglyceride concentrations, as well as the expression of genes and proteins involved in lipid biosynthesis were assessed. The insulin-stimulated glucose uptake and isoproterenol-stimulated lipolysis were also measured in freshly isolated adipocytes. Even in the absence of obesity, this rat model already presented the main features of prediabetes, with fasting normoglycemia but reduced glucose tolerance, postprandial hyperglycemia, compensatory hyperinsulinemia, as well as decreased insulin sensitivity (resistance) and hypertriglyceridemia. In addition, impaired hepatic function, including altered gluconeogenic and lipogenic pathways, as well as increased expression of acetyl-coenzyme A carboxylase 1 and fatty acid synthase in the liver, were observed, suggesting that liver glucose and lipid dysmetabolism may play a major role at this stage of the disease.

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Section: Discussionsupporting

confidence: 90%

Glucose and Lipid Dysmetabolism in a Rat Model of Prediabetes Induced by a High-Sucrose Diet

Burgeiro¹,

Cerqueira²,

Varela-Rodríguez³

et al. 2017

Preprint

View full text Add to dashboard Cite

show abstract

“…Throughout the 9-week treatment, the HSu-treated group had lower food consumption but higher beverage (35% sucrose) and caloric intake, while maintaining body weight, as previously described [17,18,19]. Similar body weight might have been maintained due to: first, differences in digestion and absorption may have modified the amount of ‘bioavailable’ energy, affecting the actual positive energy balance; second, the composition of weight gain (fat mass and lean mass) might be different, as the energy cost of protein deposition is higher than that of adipose tissue.…”

Section: Discussionsupporting

confidence: 64%

Glucose and Lipid Dysmetabolism in a Rat Model of Prediabetes Induced by a High-Sucrose Diet

et al. 2017

View full text Add to dashboard Cite

Glucotoxicity and lipotoxicity are key features of type 2 diabetes mellitus, but their molecular nature during the early stages of the disease remains to be elucidated. We aimed to characterize glucose and lipid metabolism in insulin-target organs (liver, skeletal muscle, and white adipose tissue) in a rat model treated with a high-sucrose (HSu) diet. Two groups of 16-week-old male Wistar rats underwent a 9-week protocol: HSu diet (n = 10)—received 35% of sucrose in drinking water; Control (n = 12)—received vehicle (water). Body weight, food, and beverage consumption were monitored and glucose, insulin, and lipid profiles were measured. Serum and liver triglyceride concentrations, as well as the expression of genes and proteins involved in lipid biosynthesis were assessed. The insulin-stimulated glucose uptake and isoproterenol-stimulated lipolysis were also measured in freshly isolated adipocytes. Even in the absence of obesity, this rat model already presented the main features of prediabetes, with fasting normoglycemia but reduced glucose tolerance, postprandial hyperglycemia, compensatory hyperinsulinemia, as well as decreased insulin sensitivity (resistance) and hypertriglyceridemia. In addition, impaired hepatic function, including altered gluconeogenic and lipogenic pathways, as well as increased expression of acetyl-coenzyme A carboxylase 1 and fatty acid synthase in the liver, were observed, suggesting that liver glucose and lipid dysmetabolism may play a major role at this stage of the disease.

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“…However its mechanism remains unknown [19, 20]. A minimal consumption of fructose is needed, as previous study showed that 6 weeks of 10% of fructose in drinking water is not sufficient to induce hypertension [16]. In our study, fructose supplementation was not associated with a cardiac hypertrophy as shown by the similar heart weight in FF and C (Table 1).…”

Section: Discussionsupporting

confidence: 53%

Metabolic Syndrome and Hypertension Resulting from Fructose Enriched Diet in Wistar Rats

Dupas

Feray

Goanvec

et al. 2017

BioMed Research International

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Increased sugar consumption, especially fructose, is strongly related to the development of type 2 diabetes (T2D) and metabolic syndrome. The aim of this study was to evaluate long term effects of fructose supplementation on Wistar rats. Three-week-old male rats were randomly divided into 2 groups: control (C; n = 14) and fructose fed (FF; n = 18), with a fructose enriched drink (20–25% w/v fructose in water) for 21 weeks. Systolic blood pressure, fasting glycemia, and bodyweight were regularly measured. Glucose tolerance was evaluated three times using an oral glucose tolerance test. Insulin levels were measured concomitantly and insulin resistance markers were evaluated (HOMA 2-IR, Insulin Sensitivity Index for glycemia (ISI-gly)). Lipids profile was evaluated on plasma. This fructose supplementation resulted in the early induction of hypertension without renal failure (stable theoretical creatinine clearance) and in the progressive development of fasting hyperglycemia and insulin resistance (higher HOMA 2-IR, lower ISI-gly) without modification of glucose tolerance. FF rats presented dyslipidemia (higher plasma triglycerides) and early sign of liver malfunction (higher liver weight). Although abdominal fat weight was increased in FF rats, no significant overweight was found. In Wistar rats, 21 weeks of fructose supplementation induced a metabolic syndrome (hypertension, insulin resistance, and dyslipidemia) but not T2D.

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Chronic fructose intake accelerates non-alcoholic fatty liver disease in the presence of essential hypertension

Cited by 30 publications

References 44 publications

Glucose and Lipid Dysmetabolism in a Rat Model of Prediabetes Induced by a High-Sucrose Diet

Glucose and Lipid Dysmetabolism in a Rat Model of Prediabetes Induced by a High-Sucrose Diet

Glucose and Lipid Dysmetabolism in a Rat Model of Prediabetes Induced by a High-Sucrose Diet

Metabolic Syndrome and Hypertension Resulting from Fructose Enriched Diet in Wistar Rats

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