Prevention of fructose-induced hypertension by dietary vitamins

Vasdev, Sudesh; Longerich, L; Gill, Vicki

doi:10.1016/j.clinbiochem.2003.09.003

Cited by 42 publications

(42 citation statements)

References 99 publications

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“…Measurement of DNA content in the cells also allowed us to demonstrate that the fructose stimulation did not result in proliferation or death of the HK-2 cells. Fructose feeding has been reported to result in hyperuricemia (33,34); however, this was not detected in the present study. Because hyperuricemia is greatest 50 -200 min after after fructose consumption (5), this effect may be missed in fasting samples.…”

Section: Discussioncontrasting

confidence: 94%

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Fructose, but not dextrose, accelerates the progression of chronic kidney disease

Gersch

Mu²,

Cirillo³

et al. 2007

American Journal of Physiology-Renal Physiology

187

145

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The metabolic syndrome has recently been recognized as a risk factor for kidney disease, but the mechanisms mediating this risk remain unclear. High fructose consumption by animals produces a model of the metabolic syndrome with hypertension, hyperlipidemia, and insulin resistance. The present study was conducted to test the hypothesis that consumption of a high-fructose diet could accelerate the progression of chronic kidney disease. Three groups of 14 male Sprague-Dawley rats were pair fed a specialized diet containing 60% fructose (FRU) or 60% dextrose (DEX) or standard rat chow (CON). After the animals were fed their assigned diet for 6 wk, five-sixths nephrectomy was performed, and the assigned diet was continued for 11 wk. Proteinuria was significantly increased and creatinine clearance was decreased in the FRU group compared with the CON and DEX groups, and blood urea nitrogen was higher in the FRU group than in the CON and DEX groups. Kidneys from the FRU group were markedly larger than kidneys from the CON and DEX groups. Glomerular sclerosis, tubular atrophy, tubular dilatation, and cellular infiltration appeared markedly worse in kidneys from the FRU group than in kidneys from the DEX and CON groups. Monocyte chemoattractant protein-1 (MCP-1) was measured in renal tissue homogenate and found to be increased in the FRU group. In vitro studies were conducted to determine the mechanism for increased renal MCP-1, and fructose stimulation of proximal tubular cells resulted in production of MCP-1. In conclusion, consumption of a high-fructose diet greatly accelerates progression of chronic kidney disease in the rat remnant kidney model. metabolic syndrome; high-fructose corn syrup; monocyte chemoattractant protein-1

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Section: Discussioncontrasting

confidence: 94%

“…A model commonly used in the literature to study the metabolic syndrome is fructose feeding. Rats that consume a highfructose diet for 6 wk develop insulin resistance (11,15), dyslipidemia (2,8,21,22,29,37), hypertension (14,15,33), and hyperuricemia (27,30). Fructose feeding in mice has been shown to lead to the development of obesity as well (18).…”

mentioning

confidence: 99%

Fructose, but not dextrose, accelerates the progression of chronic kidney disease

Gersch

Mu²,

Cirillo³

et al. 2007

American Journal of Physiology-Renal Physiology

187

145

View full text Add to dashboard Cite

show abstract

“…Aldehydes are able to react nonenzymatically with sulfhydryl groups of protein, thus altering their function. Of interest, aldehydes can impair the function of L-type calcium channels, and this may possibly lead to an increased intracellular calcium concentration in vascular smooth muscle, and to an increase of vascular resistance (231). Furthermore, it has been suspected by some investigators that hypertension may rather be related to deficiency in magnesium or copper of experimental high-fructose diets rather than to fructose feeding per se (37,79).…”

Section: F High Blood Pressurementioning

confidence: 99%

Metabolic Effects of Fructose and the Worldwide Increase in Obesity

Tappy

Lê

2010

Physiological Reviews

1,032

899

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While virtually absent in our diet a few hundred years ago, fructose has now become a major constituent of our modern diet. Our main sources of fructose are sucrose from beet or cane, high fructose corn syrup, fruits, and honey. Fructose has the same chemical formula as glucose (C6H12O6), but its metabolism differs markedly from that of glucose due to its almost complete hepatic extraction and rapid hepatic conversion into glucose, glycogen, lactate, and fat. Fructose was initially thought to be advisable for patients with diabetes due to its low glycemic index. However, chronically high consumption of fructose in rodents leads to hepatic and extrahepatic insulin resistance, obesity, type 2 diabetes mellitus, and high blood pressure. The evidence is less compelling in humans, but high fructose intake has indeed been shown to cause dyslipidemia and to impair hepatic insulin sensitivity. Hepatic de novo lipogenesis and lipotoxicity, oxidative stress, and hyperuricemia have all been proposed as mechanisms responsible for these adverse metabolic effects of fructose. Although there is compelling evidence that very high fructose intake can have deleterious metabolic effects in humans as in rodents, the role of fructose in the development of the current epidemic of metabolic disorders remains controversial. Epidemiological studies show growing evidence that consumption of sweetened beverages (containing either sucrose or a mixture of glucose and fructose) is associated with a high energy intake, increased body weight, and the occurrence of metabolic and cardiovascular disorders. There is, however, no unequivocal evidence that fructose intake at moderate doses is directly related with adverse metabolic effects. There has also been much concern that consumption of free fructose, as provided in high fructose corn syrup, may cause more adverse effects than consumption of fructose consumed with sucrose. There is, however, no direct evidence for more serious metabolic consequences of high fructose corn syrup versus sucrose consumption.

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“…31 Sucrose-fed rats were found to have increased norepinephrine turnover in their hearts, 32 pancreas and liver, 33 suggesting enhanced sympathetic activation in these organs. Several reports suggest that chronic fructose feeding may lead to hypertension in rats [34][35][36][37] and dogs, 22 and to nocturnal hypertension in mice. 38 However, other studies, using 24-h recordings rather than tail cuff techniques to 41,42 that seems to be related to activation of the renin-angiotensin system and stimulation of sympathetic activity.…”

Section: Refined Sugar and Cardiovascular Diseasesmentioning

confidence: 99%

Sugary drinks in the pathogenesis of obesity and cardiovascular diseases

Dulloo

2008

Int J Obes

114

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Soft drink overconsumption is now considered to be a major public health concern with implications for cardiovascular diseases. This follows a number of studies performed in animals suggesting that chronic consumption of refined sugars can contribute to metabolic and cardiovascular dysregulation. In particular, the monosaccharide fructose has been attracting increasing attention as the more harmful sugar component in terms of weight gain and metabolic disturbances. High-fructose corn syrup is gradually replacing sucrose as the main sweetener in soft drinks and has been blamed as a potential contributor to the current high prevalence of obesity. There is also considerable evidence that fructose, rather than glucose, is the more damaging sugar component in terms of cardiovascular risk. This review focuses on the potential role of sugar drinks, particularly the fructose component, in the pathogenesis of obesity and cardiovascular diseases.

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Prevention of fructose-induced hypertension by dietary vitamins

Cited by 42 publications

References 99 publications

Fructose, but not dextrose, accelerates the progression of chronic kidney disease

Fructose, but not dextrose, accelerates the progression of chronic kidney disease

Metabolic Effects of Fructose and the Worldwide Increase in Obesity

Sugary drinks in the pathogenesis of obesity and cardiovascular diseases

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