Chronic sucrose ingestion induces mild hypertension and tachycardia in rats.

Buñag, Ruben D.; Tomita, Tatsuo; Sasaki, Susumu

doi:10.1161/01.hyp.5.2.218

Cited by 88 publications

(46 citation statements)

References 36 publications

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“…The carbohydrate in the AIN-76A diet is two-thirds sucrose and one-third corn starch, whereas the carbohydrate source in the grain diet is primarily starch. Because sucrose-feeding to Dahl saltsensitive rats, 6,8,9 SHRs, 7 and Sprague Dawley rats [21][22][23] leads to an increase in arterial blood pressure, we expected to observe that the diet with wheat flour substituted for sucrose would normalize blood pressure in the SS/Mcw rats. The lack of any difference in the disease phenotypes between the rats fed these 2 diets indicates that the carbohydrate source does not affect the degree of hypertension or renal disease in the Dahl SS/Mcw rat.…”

Section: Discussionmentioning

confidence: 99%

Dietary Protein Source Determines the Degree of Hypertension and Renal Disease in the Dahl Salt-Sensitive Rat

2005

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Abstract-Previous studies demonstrated that a whole-grain diet attenuated sodium-dependent hypertension and renal disease in Dahl salt-sensitive rats from the colony at the Medical College of Wisconsin (Dahl SS/Mcw rats) compared with rats maintained on a purified AIN-76A diet. The present experiments determined which component(s) of the grain diet prevented renal and cardiovascular disease. Male SS/Mcw rats were maintained on isocaloric diets identical to AIN-76A, except the source of protein (wheat gluten for casein), carbohydrate (wheat flour for sucrose), or fat (soybean oil for corn oil) was substituted in separate diets. Rats were maintained on the different diets from weaning and studied after 3 weeks on a high-salt (4.0% NaCl) diet. Substitution of the carbohydrate in the diet did not affect body weight, arterial pressure, or renal disease. Replacement of casein with wheat gluten significantly reduced body weight (258Ϯ7 versus 353Ϯ3 grams), mean arterial pressure (133Ϯ2 versus 153Ϯ2 mm Hg), and albumin excretion (9Ϯ1 versus 50Ϯ7 mg/d) to levels of rats fed the whole-grain diet (nϭ7 to 16/group). Replacement of the fat in the diet increased arterial pressure without affecting body weight or albumin excretion. Key Words: hypertension, sodium-dependent Ⅲ rats Ⅲ blood pressure Ⅲ diet T he composition and quantity of dietary nutrients can have profound effects on arterial blood pressure. In humans, increased consumption of food containing cholesterol, saturated fats, or carbohydrates is associated with an elevation of arterial blood pressure, whereas a high-protein diet is linked to a decrease in blood pressure. [1][2][3][4] Experimental studies have also examined the influence of changes in dietary protein, fat, and carbohydrates on arterial blood pressure in animal models. The development of hypertension is accelerated in genetic models of hypertension depending on the source and composition of dietary protein, 5 carbohydrates, 6 -9 and fat. 9,10 These clinical and experimental results indicate that different components of the diet, independent of sodium chloride content, can have a profound influence on the long-term level of arterial blood pressure.Studies from our laboratory demonstrated that sodiumsensitive changes in blood pressure and kidney disease in inbred Dahl salt-sensitive rats from the colony at the Medical College of Wisconsin (Dahl SS/Mcw rats) were modified depending on the chow fed to the rats. Rats fed chow formulated following the guidelines established by the American Institute of Nutrition in 1976 (AIN-76A) 11,12 had a greater degree of sodium-dependent hypertension and renal disease in comparison to rats fed a diet derived largely from grain products. 13 The AIN-76A and the grain diet (Teklad 3075S) are composed of approximately the same percentage of protein, carbohydrates, and fat. Differences between the 2 diets, however, include the source of protein (casein in the AIN-76A versus corn and wheat protein in the grain diet), carbohydrates (sucrose and corn starch in AIN-76A versus cor...

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Section: Discussionmentioning

confidence: 99%

Dietary Protein Source Determines the Degree of Hypertension and Renal Disease in the Dahl Salt-Sensitive Rat

2005

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“…Rats who had their drinking water replaced with an 8% sucrose solution developed hypertension and tachycardia that was evident within a week and was not related to weight gain. 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.…”

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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“…Sympathetic activity, as measured by direct recordings of hypothalamic and ganglionic activity, is enhanced, 33 which in turn may cause further impairment of insulin sensitivity. 34 However, it is doubtful that sustained hypertension can be explained by this mechanism alone.…”

Section: Fructose-feeding and Hypertension Mechanismsmentioning

confidence: 99%

High-fructose feeding elicits insulin resistance, hyperinsulinism, and hypertension in normal mongrel dogs.

1994

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To determine whether chronic high-fructose feeding causes insulin resistance and hypertension in normal dogs, we fed 10 male dogs a normosodic diet containing 60% of the calories as fructose for 20 to 28 days; a control group of 8 dogs was fed a similar diet containing dextrose instead of fructose. In the fructose-fed group, (1) fasting triglyceridemia increased from 35.3±0.63 to 91.9±11.55 mg/dL after 25 days (f <.001); (2) fasting insulinemia increased from 19.0±1.9 to 58.9±7.22 iU/mL after 25 days (P<.001); (3) insulin resistance, which was estimated by steady-state glycemia during an insulin suppression test, increased from 105.8±21.5 to 187.8±32.6 mg/dL after 15 days (/ > <.001), whereas steady-state insulinemia did not change; (4) mean arterial pressure increased from 100.4±1.6 to 122.6±2.3 mm Hg after 28 days (P<.0l); and (5) cumulative sodium balance was increased on days 7 through 11 (111.60±4.44 mEq on day 8, P<.01), returning to T here is overwhelming epidemiologic evidence that insulin resistance and hyperinsulinemia are strongly associated with hypertension. 1 A constellation of cardiovascular risk factors fostered by insulin resistance, including alterations in the circulating lipidic profile (such as hypertrigryceridemia and hypercholesterolemia with high low-density lipoprotein and low high-density lipoprotein cholesterol), atherosclerosis, and hypertension, has been described and conventionally called "syndrome X." 2 The frequent association between non-insulin-dependent diabetes mellitus, obesity, and hypertension has been tentatively ascribed to the presence of insulin resistance. -3 However, a marked impairment in insulin action has also been demonstrated in nonobese, nondiabetic essential hypertensive subjects. 4 Insulin resistance and hypertension have been induced in rodents by chronic high-sucrose or highfructose feeding. 5 These models have provided important information regarding the biochemical mechanisms responsible for the impairment of insulin activity. normal for the rest of the experiment. All these parameters were similar between the fructose-fed and dextrose-fed groups before the diets were started and remained constant in the dextrose-fed group. Neither group showed any change in body weight, fasting plasma glucose, atrial natriuretic factor, or endothelin-1 levels. We conclude that chronic high-fructose feeding elicits hypertriglyceridemia, insulin resistance, hyperinsulinemia, hypertension, and a transient sodium retention in dogs without fostering fasting hyperglycemia or weight gain. Endothelin and atrial natriuretic factor do not appear to play a role in the development of hypertension in this model. However, despite these advances, the pathogenic mechanisms that relate insulin resistance to hypertension remain undefined. Most of our knowledge about the homeostatic mechanisms responsible for coupling the renal excretion of sodium to the control of blood volume and blood pressure has been obtained in dogs 7 ; however, to date there have been no available nonobese, ...

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Chronic sucrose ingestion induces mild hypertension and tachycardia in rats.

Cited by 88 publications

References 36 publications

Dietary Protein Source Determines the Degree of Hypertension and Renal Disease in the Dahl Salt-Sensitive Rat

Dietary Protein Source Determines the Degree of Hypertension and Renal Disease in the Dahl Salt-Sensitive Rat

Sugary drinks in the pathogenesis of obesity and cardiovascular diseases

High-fructose feeding elicits insulin resistance, hyperinsulinism, and hypertension in normal mongrel dogs.

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