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Biomedical subjects

S Reiser

Publications and source records attributed to S Reiser.

At least 55 records · Page 3Linked to original sources
PubMed1985

Effects of fructose feeding on lipid parameters in obese and lean, diabetic and nondiabetic Zucker rats.

Effects of fructose feeding in moderate amounts on lipid metabolism of obese versus lean, and diabetic versus nondiabetic Zucker rats, were studied. Forty pairs of male lean and obese animals were assigned to two dietary groups, fructose and glucose. For each diet, one-half of lean and obese animals were injected with streptozotocin intraperitoneally (i.p.) to induce diabetes, and the other half were injected with buffer i.p. as a nondiabetic control group. After 9 wk of feeding, animals were fasted overnight, decapitated and exsanguinated. Organs were removed and weighed. Blood glucose, insulin, lactic acid, triglycerides, cholesterol, total liver lipids and urinary glucose were determined. Hyperphagia was observed in obese, non-diabetic and lean-diabetic animals. Streptozotocin injection drastically reduced insulin levels, and produced an impairment of growth, hyperglycemia, glucosuria, polydipsia and polyuria. Fructose feeding increased organ weights in kidney, liver and retroperitoneal adipose tissue, regardless of diabetic state. However, lactic acid levels were lower in fructose-fed groups than glucose-fed groups. In obese rats serum triglyceride levels were also lower in fructose-fed groups than in glucose-fed groups. Serum cholesterol was not affected by fructose feeding. The results indicated that fructose feeding did not produce hyperlipemia and lactic acidosis in the blood circulation in Zucker rats. However, fructose feeding did not improve glucose intolerance in diabetic animals, rather fructose feeding produced hyperinsulinemia in nondiabetic, obese animals.

Animals↗
PubMed1985

Effects of different dietary carbohydrates on hepatic enzymes of copper-deficient rats.

The present study was undertaken to measure the activities of several hepatic enzymes of regulatory importance in the pathways of lipogenesis and gluconeogenesis in rats fed diets marginally deficient in copper (1.2 micrograms Cu/g of diet) and containing either fructose, glucose, or starch as the carbohydrate sources. Although all copper-deficient rats exhibited the characteristic signs of copper deficiency, they were more pronounced in rats fed the diet containing fructose. Except for the activity of phosphoenolpyruvate carboxykinase which was unaffected either by copper deficiency or by the type of dietary carbohydrate, the hepatic activities of glucose-6-phosphate dehydrogenase, malic enzyme, L-alpha-glycerophosphate dehydrogenase and fructose 1,6-diphosphatase were unaffected by copper deficiency but were affected by the type of carbohydrate in the diet. Fructose produced the greatest increase in enzymatic activities, whereas starch produced the least activity and glucose induced an intermediate effect. These results indicate that the deleterious effects of a fructose diet deficient in copper on biochemical and physiological indices could not be due to an immediate metabolite of fructose. However, the involvement of a subsequent metabolite of fructose in the mechanism of copper utilization and/or requirement cannot be excluded.

Animals↗
PubMed1985

Effect of dietary sugars on metabolic risk factors associated with heart disease.

The results from studies in which the effects of the extended feeding of sugars such as sucrose and fructose as compared to starch and other glucose-based carbohydrates on metabolic risk factors associated with heart disease have been reviewed. In general, the feeding of the sugars as compared to starch produced undesirable changes in metabolic risk factors such as blood triglycerides, total cholesterol and its lipoprotein distribution, insulin and uric acid. Other dietary components (e.g., saturated fat) can magnify the adverse metabolic effects of the sugars. A finite segment of the population characterized by high levels of triglycerides and insulin may be at a substantially higher risk than is the general population from the present level of intake of sucrose or fructose.

Animals↗
PubMed1984

Effect of dietary carbohydrates and copper status on blood pressure of rats.

Copper deficiency was induced in rats by feeding diets containing either 62% starch, fructose or glucose deficient in copper for 6 weeks. All copper deficient rats, regardless of the dietary carbohydrate, exhibited decreased ceruloplasmin activity and decreased serum copper concentrations. Rats fed the fructose diet exhibited a more severe copper deficiency as compared to rats fed either starch or glucose. The increased severity of the deficiency was characterized by reduced body weight, serum copper concentration and hematocrit. In all rats fed the copper adequate diets, blood pressure was unaffected by the type of dietary carbohydrate. Significantly reduced systolic blood pressure was evident only in rats fed the fructose diet deficient in copper. When comparing the three carbohydrate diets, the physiological and biochemical lesions induced by copper deprivation could be magnified by feeding fructose.

Animals↗
PubMed1984

The interaction of type of dietary carbohydrates with copper deficiency.

The present study was designed to determine if the more severe copper deficiency in rats fed sucrose and fructose, as compared to starch, is due to a specific effect of the fructose or to a nonspecific effect of any simple carbohydrate. Seventy weanling male rats were fed, for 9 wk, copper-deficient diets or copper-supplemented diets containing either 62% starch, fructose, or glucose. Decreased hematocrit, serum copper, and ceruloplasmin concentrations but increased heart and liver weights, total liver lipid, and hepatic iron concentrations were found in all copper-deficient rats regardless of the dietary carbohydrate. Feeding rats the high glucose diet decreased plasma albumin and liver glycogen but increased blood urea nitrogen when compared to rats fed starch. However, rats fed fructose generally exhibited a more severe copper deficiency as compared to rats fed either starch or glucose. The severity was characterized by lower (p less than 0.05) body weight, liver glycogen, hematocrit, serum copper, and albumin. Conversely, liver and heart weights, blood urea nitrogen, and plasma glutamic oxaloacetic transaminase were higher (p less than 0.05). Plasma cholesterol was increased by copper deficiency only in rats fed fructose or glucose. During the study, 17 of the 40 rats fed copper-deficient diets died; 66% of those fed fructose, 26% fed glucose, and 30% fed starch. These results suggest that the fructose moiety of sucrose is responsible for the increased severity of copper deficiency in rats fed sucrose as compared to starch.

Animals↗
PubMed1984

Seasonal variation in plasma glucose and hormone levels in adult men and women.

Twenty-nine men and women collected diet records for 1 yr. Fasting blood samples were collected four times during the year so that each season of the year was represented. An oral glucose tolerance test was given in the spring and in the fall. Regardless of season men consumed significantly more kilocalories, carbohydrate, sugar, and starch than did the women. Men consumed more simple sugars in the fall than in the spring. No seasonal effect was observed for calories, total carbohydrate, or starch intake. Fasting glucose and insulin were higher in the fall than in the spring. Summed insulin levels after the oral glucose tolerance were significantly different by age and season. Summed insulin levels were significantly higher in older than younger subjects; men and older subjects had higher levels in the spring than in the fall. Fasting levels of thyroxine, free thyroxine, triiodothyronine, and glucagon varied significantly with the season. A significant sex by season interaction was observed in the thyroid hormones. It appears that seasonal variation as well as diurnal variation should be considered in evaluating hormone levels.

Adult↗
PubMed1984

Impairment of glucose tolerance in copper-deficient rats: dependency on the type of dietary carbohydrate.

Copper deficiency was induced in weanling rats in order to study the possible interaction between the types of dietary carbohydrate and copper deficiency on glucose tolerance. Weanling male rats were fed copper-deficient or copper-supplemented diets containing either 62% starch, fructose or glucose. During week 5 the fructose portion of the copper-deficient diet was replaced (20 rats) by starch (10 rats) or glucose (10 rats). During the 9th week, an oral glucose tolerance test weas performed. Copper deficiency was associated with impaired glucose tolerance characterized by increased blood glucose and decreased insulin levels only in copper-deficient rats fed the monosaccharides fructose or glucose but not the polysaccharide starch. Changing the dietary carbohydrates in the copper-deficient diet from fructose to starch increased insulin levels and decreased blood glucose in response to the glycemic stress when compared to rats continuously fed fructose. Although both glucose and fructose feeding impaired the glucose tolerance, fructose was more diabetogenic. This could be demonstrated by some improvements in glucose tolerance when the copper-deficient rats were switched from the fructose to the glucose diet. The data indicate that copper deficiency per se does not impair glucose tolerance.

Animals↗
PubMed1984

The severity of copper deficiency in rats is determined by the type of dietary carbohydrate.

The purpose of this investigation was to study the interaction between copper and dietary carbohydrates on clinical and enzymatic indices associated with copper deficiency. Copper deficiency was produced in rats by feeding diets adequate in all nutrients including selenium and chromium, but marginal in copper (1.2 micrograms/g diet) containing 62% of either starch, fructose, or glucose. During the fifth week, the fructose of the copper-deficient diet (20 rats) was replaced by either starch (10 rats) or by glucose (10 rats). The experiment was terminated after 11 weeks. Copper deficiency in rats fed fructose significantly lowered body weight and hematocrit, but increased liver weight, blood urea nitrogen, ammonia, cholesterol, and triglycerides when compared to rats fed starch or glucose. The copper metalloenzyme, superoxide dismutase, the selenoenzyme, glutathione peroxidase, and hepatic ATP were decreased in the copper-deficient rats fed fructose as compared to copper-deficient rats fed starch or glucose. These results indicate that fructose may be the dietary component which has a deleterious effect on copper and selenium status. Changing the type of dietary carbohydrate in copper-deficient rats from fructose to either starch or glucose ameliorated the severity of the deficiency. The protective effects were more pronounced with starch than with glucose.

Adenosine Triphosphate↗
PubMed1983

Effects of a combination of common snack foods on some risk factors in heart disease and diabetes in rats.

Rats were fed ad libitum diets containing a combination of commonly consumed highly palatable snack foods, a commercial stock diet, or had access to both diets for 10-11 weeks. Rats fed snack foods only had elevations in risk factors associated with heart disease and/or diabetes including serum cholesterol, insulin response to glucose, and serum glucose. Triglyceride levels were not affected by diet. Removable fat pad weights (perirenal and epididymal) were greater in rats fed snack foods than in rats fed only stock diet, even though total body weights were less. Liver glucose 6-phosphate dehydrogenase activity was not affected by diet, but malic enzyme activity was greater in rats fed snack foods only than in the other two groups. These results indicate that some risk factors associated with heart disease and/or diabetes can be elevated by feeding a diet containing commonly consumed snack foods.

Adipose Tissue↗
PubMed1983

Blood lipid distribution of hyperinsulinemic men consuming three levels of fructose.

Twelve carbohydrate-sensitive men selected due to their abnormally high insulin responses to a sucrose load and 12 men with normal insulin responses were fed diets containing 0, 7.5, and 15% fructose for 5 wk each in a cross-over design. The diets contained 43% total carbohydrate, 42% fat, and 15% protein. Initial fasting total cholesterol and low-density lipoprotein cholesterol were higher in the hyperinsulinemic men than in the controls. Diastolic blood pressure was not affected by diet, but systolic blood pressure was slightly higher after the men consumed the 0% fructose diet. Free fatty acids were not different. Total plasma cholesterol and low-density lipoprotein cholesterol were higher after the men consumed 7.5 and 15% fructose than when they consumed the 0% fructose diet. Plasma triglyceride increased significantly as fructose in the diets of the hyperinsulinemics increased, but was not affected in the controls. These changes in blood lipids are associated with heart disease.

Blood Pressure↗
PubMed1983

Role of dietary fructose in the enhancement of mortality and biochemical changes associated with copper deficiency in rats.

Rats were fed copper deficient (0.9 microgram/g) or copper-supplemented diets in which the carbohydrate was either starch, sucrose, or fructose (62% by weight) for 7 wk. Regardless of the nature of the carbohydrate, copper deficiency decreased blood ceruloplasmin activity, hepatic copper and ATP levels, and increased plasma cholesterol and triglycerides. Copper deficiency in rats fed sucrose or fructose, but not those fed starch, significantly lowered blood hematocrit, Hb, and albumin and significantly increased heart and liver weight and the glucose response to a glycemic stress. Hepatic copper level was significantly lower in copper-deficient rats fed sucrose or fructose than in those fed starch. Fasting blood glucose, cholesterol, and triglyceride levels were significantly higher in copper deficient rats fed fructose than in those fed starch. During the study 14 copper-deficient rats died, one of 10 fed starch, six of 20 fed sucrose, and seven of 20 fed fructose. Death was apparently the result of rupture of the heart in the region of the apex. These results indicate that fructose-containing carbohydrates as compared to starch markedly increase the severity of copper deficiency in rats. Whether this effect is due to differences in the nature of the simple carbohydrate (fructose versus glucose) or to molecular size (simple versus complex carbohydrate) remains to be established.

Animals↗
PubMed1983

Effect of chronic hyperinsulinism on metabolic parameters and histopathology in rats fed sucrose or starch.

The purpose of this study was to determine the effects of chronic hyperinsulinism on metabolic risk factors and on the histopathologic changes in the heart and aorta of rats fed sucrose or starch diets for 8 months. Hyperinsulinism was attained by the subcutaneous implantation of osmotically driven minipumps partially coated with paraffin so as to deliver 3 units/day of porcine insulin for up to 4 weeks. Control rats were implanted with pumps containing 1.6% glycerol. There were initially 12 rats each in four groups of rats; sucrose-insulin, sucrose-control, starch-insulin, starch-control. Nonfasted blood insulin levels obtained every 3 weeks from the tail vein averaged 553, 156, 426, and 107 microU/ml in sucrose-insulin, sucrose-control, starch-insulin, and starch-control rats, respectively. Sucrose-fed rats had greater body weight, deposited more body fat, and had higher levels of nonfasting insulin and glucose and 6-hour fasted triglyceride than did starch-fed rats. Rats receiving insulin had greater body weight and removable fat weight, higher levels of nonfasting and fasting insulin and lower level of nonfasting glucose than did rats not receiving insulin. Neither hyperinsulinism nor the type of dietary carbohydrate significantly affected the amount of blood cholesterol. Histopathology of the heart and aorta revealed no unique changes above those commonly observed in laboratory rats as a function of age.

Animals↗
PubMed1983

Effect of copper deficiency on metabolism and mortality in rats fed sucrose or starch diets.

Copper deficiency was induced in rats by feeding sucrose or starch diets deficient in copper. Copper-deprived rats fed either diet exhibited decreased plasma ceruloplasmin concentration and increased plasma cholesterol. Glucose homeostasis and utilization was impaired both in vivo and in vitro. Oral glucose tolerance was impaired, insulin binding decreased, and CO2 formation and lipogenesis from [U-14C]glucose were decreased. Feeding sucrose but not starch diets deficient in copper magnified the copper deficiency and resulted in 60% mortality. Although both deficient diets contained the same concentration of copper, the hepatic copper concentration of rats fed sucrose was reduced nearly threefold compared to rats fed starch. Reduced epididymal fat pad, increased liver weight, reduced blood hemoglobin and a marked hypertrophy of the heart with gross deformities as well as histopathologic changes were noted only in those rats fed the copper-deficient sucrose diet. The biochemical lesions induced by deprivation of copper can be suppressed by feeding diets containing starch or can be magnified by high sucrose intake.

Adipose Tissue↗
PubMed1983

Effects of dietary fructose on plasma glucose and hormone responses in normal and hyperinsulinemic men.

Twelve men with abnormally high insulin responses to a sucrose load and 12 normal men were fed diets containing 0, 7.5, or 15% of the calories as fructose for 5 weeks each. The diets contained approximately 43% of the calories as total carbohydrate, 42% as fat and 15% as protein. Mean insulin responses of the hyperinsulinemic men were initially 235% of control responses. Plasma glucose concentrations 1 hour after the sucrose load were significantly higher in hyperinsulinemic men than in controls. There were no initial differences between the two groups in glucagon or gastric inhibitory polypeptide (GIP) responses. Consumption of 7.5 and 15% Fructose diets increased fasting plasma glucose and GIP responses in both groups. Consumption of the 15% fructose diet resulted in significantly higher insulin and glucose responses than consumption of the other two diets. These results indicate that moderate levels of dietary fructose can produce undesirable changes in glucose metabolism of both normal and hyperinsulinemic men.

Blood Glucose↗
PubMed1983

Serum uric acid, inorganic phosphorus, and glutamic-oxalacetic transaminase and blood pressure in carbohydrate-sensitive adults consuming three different levels of sucrose.

12 men and 12 women, classified as carbohydrate-sensitive on the basis of an exaggerated insulin response to a sucrose load, consumed diets containing either 5, 18, or 33% sucrose in a crossover design. The diets simulated the average American diet and consisted of identical natural and processed foods with the exception of a patty. The patty provided the experimental levels of sucrose; the difference was made up by starch. Each level of sucrose was consumed for a 6-week period. Subject body weights were maintained. Fasting serum uric acid and inorganic phosphorus increased as the level of dietary sucrose increased. Diastolic blood pressure was significantly higher when subjects were on the 33% sucrose diet as compared to the 5 and 18% diets. Serum glutamic-oxalacetic transaminase was not affected by diet. In tolerance tests after a sucrose load (2 g/kg body weight), the uric acid response was higher after the 18 and 33% sucrose diets than after the 5% sucrose diet. Serum inorganic phosphorus, which increased significantly with each level of dietary sucrose, decreased following the sucrose load. These results indicate that carbohydrate-sensitive individuals may be affected adversely by the level of sucrose commonly found in the Westernized diet. Since elevated serum uric acid and blood pressure have been identified as risk factors in degenerative diseases, this study suggests that carbohydrate-sensitive individuals should limit their sucrose consumption.

Adult↗
PubMed1983

Effect of copper or insulin in diabetic copper-deficient rats.

The effects of copper and insulin on lipogenesis and glucose tolerance were studied using diabetic, copper-deficient rats. Diabetes was induced by intraperitoneal injection of 50 mg streptozotocin/kg body weight to rats fed a sucrose-copper deficient diet for 7 weeks. Five days later the rats were injected intraperitoneally with [14C]glucose with either saline, insulin, copper, or copper plus insulin. The disappearance of serum [14C]glucose at 30, 60, and 120 min postinjection and the incorporation of [14C]glucose into lipid of epididymal fat 2 hr after administration were determined. The combined effect of copper and insulin significantly decreased peak blood glucose at 30 min and increased the incorporation of [14C]glucose into lipid in the epididymal fat pad when compared to either copper or insulin alone. The enhancement of glucose utilization may be due to a formation of a more stable complex which will increase insulin binding and/or decrease its degradation.

Adipose Tissue↗
PubMed1982

Moderate diet control in children: the effects on metabolic indicators that predict obesity-related degenerative diseases.

Nine prepubertal obese boys ages 9 1/2 to 12 yr followed moderately restricted diets and moderate exercise routine for 31 wk. Foods were selected from the family's basic diet and the physical activities were tailored to the home environment. This dietary (approximate decrease of 600 kcal/day) and activity (approximate increase of 300 kcal/day) intervention program was sufficient to stop weight gain and normalize key metabolic indices for prediction of atherosclerosis, hypertension, and diabetes. Throughout the treatment period serum lipid responses included significantly lower (p less than 0.05) total cholesterol, low-density lipoprotein-cholesterol and triglycerides. High-density lipoprotein-cholesterol was constant throughout the period. Responses in carbohydrate metabolism included significantly lower (p less than 0.05) fasting insulin and glucose. Insulin and glucose levels were positively correlated with total caloric consumption and insulin was also positively correlated with sucrose consumption (p less than 0.05). Fasting insulin/glucose ratios and glycosylated Hb decreased throughout the treatment period, but serum glucagon levels remained constant. In response to a glucose load, insulin and glucose decreased significantly by wk 31 of treatment. A practical approach for normalizing metabolism in obese male children is presented.

Arteriosclerosis↗