A sucrose-rich diet (SRD) causes hyper- triglyceridemia in nonpregnant rats. To determine whether... more A sucrose-rich diet (SRD) causes hyper- triglyceridemia in nonpregnant rats. To determine whether a 3RD further enhances gestational hypertri- glyceridemia, female rats were divided into the follow ing two groups: 1) rats fed a SRD (63 g sucrose/100 g), and 2) rats that received the same diet except that the sucrose was replaced by an equal amount of corn- starch
The present work was designed to assess the possible benefits of (7% w/w) dietary fish oil in rev... more The present work was designed to assess the possible benefits of (7% w/w) dietary fish oil in reversing the morphological and metabolic changes present in the adipose tissue of rats fed an SRD for a long time. With this purpose, in the epididymal fat tissue, we investigated the effect of dietary fish oil upon: i) the number, size and distribution of cells, ii) the basal and stimulated lipolysis, iii) the lipoprotein lipase (LPL) and the glucose 6-phosphate dehydrogenase activities, and iv) the antilipolytic action of insulin. The study was conducted on rats fed an SRD during 120 days with fish oil being isocaloric substituted for corn oil for 90-120 days in half the animals. Permanent hypertriglyceridemia, insulin resistance and abnormal glucose homeostasis were present in the rats before the source of fat in the diet was replaced. The major new findings of this study are the following: i) Dietary fish oil markedly reduced the fat pads mass, the hypertrophy of fat cells and improved the altered cell size distribution. ii) The presence of fish oil in the diet corrected the inhibitory effect of high sucrose diet upon the antilipolytic action of insulin, reduced the "in vitro" enhanced basal lipolysis and normalized isoproterenol-stimulated lipolysis. Fat pads lipoprotein lipase activity decreased reaching values similar to those observed in age-matched controls fed a control diet (CD). These effects were not accompanied by any change in rat body weight. All these data suggest that the dyslipemic rats fed a moderate amount of dietary fish oil constitute a useful animal model to study diet-regulated insulin action.
Rats fed on a sucrose-rich diet (SRD) (63 % ) up to 30 weeks develop stable hypertriglyceridemia,... more Rats fed on a sucrose-rich diet (SRD) (63 % ) up to 30 weeks develop stable hypertriglyceridemia, impaired glucose tolerance and insulin insensitivity. At present only scarce and non-systematic information is available concerning the possible reversion of these metabolic derangements by nutritional or metabolic interventions. The present study was designed to investigate the effect of the isocaloric substitution of sucrose for starch (during 15 weeks) on lipid and glucose metabolisms in rats in which a well-established hypertriglyceridemia and glucose intolerance were present before the amount of sucrose (63% ) was partially (33% ) or totally (0% ) replaced by an isocaloric amount of starch. Our findings show that: i) when the amount of fructose (sucrose moieties) is partially replaced by starch (from 33 to 18% of the total calories) most of its undesirable effects on lipid metabolism are still present and no significant improvement in glucose regulation is noticed; ii) hypertriglyceridemia and glucose intolerance can be completely reversed, without detectable changes in circulating insulin levels, by shifting completely to starch as the source of carbohydrate in the diet. Moreover, when sucrose was removed from the diet, it took 7 weeks for plasma triglyceride levels to become completely normal while plasma free fatty acids and glucose levels needed twice that time. These findings suggest that manipulation of dietary fructose may play a role in the management of lipid disorders associated with glucose intolerance and insulin resistance.
Biochimica Et Biophysica Acta (bba) - Lipids and Lipid Metabolism, 1996
The aim of this study was to investigate the relationship between the lipid-lowering effects of f... more The aim of this study was to investigate the relationship between the lipid-lowering effects of fish oils and concomitant consequences on glucose tolerance and insulin sensitivity in an experimental animal model of hypertriglyceridemia induced by high sucrose intake. To achieve this goal, male Wistar rats were fed a semi-synthetic sucrose rich diet (SRD) (w/w: 62.3% sucrose, 8% corn oil, 17% protein) for 90 days. At the time, a well established and permanent hypertriglyceridemia accompanied by glucose intolerance was present. After that, one half of the animals continued on the SRD up to 120 days. The other half received an SRD in which the source of fat was substituted by cod liver oil (w/w 7% CLO plus 1% corn oil) from day 90 to 120 (SRD + CLO). Control rats were fed a semi-synthetic diet (CD) (w/w: 62.5% corn starch, 8% corn oil, 17% protein) throughout the 120 days experimental period. Results obtained after the experimental period show that the hypertriglyceridemia and glucose intolerance ensuing long term feeding normal rats with a sucrose-rich diet could be completely reversed mediating no change in circulating insulin levels by shifting the source of fat in the diet from corn oil to cod liver oil. These findings suggest that manipulation of dietary fats may play a role in the management of the lipid disorders associated with glucose intolerance and insulin resistance.
A sucrose-rich diet (SRD) causes hyper- triglyceridemia in nonpregnant rats. To determine whether... more A sucrose-rich diet (SRD) causes hyper- triglyceridemia in nonpregnant rats. To determine whether a 3RD further enhances gestational hypertri- glyceridemia, female rats were divided into the follow ing two groups: 1) rats fed a SRD (63 g sucrose/100 g), and 2) rats that received the same diet except that the sucrose was replaced by an equal amount of corn- starch
The present work was designed to assess the possible benefits of (7% w/w) dietary fish oil in rev... more The present work was designed to assess the possible benefits of (7% w/w) dietary fish oil in reversing the morphological and metabolic changes present in the adipose tissue of rats fed an SRD for a long time. With this purpose, in the epididymal fat tissue, we investigated the effect of dietary fish oil upon: i) the number, size and distribution of cells, ii) the basal and stimulated lipolysis, iii) the lipoprotein lipase (LPL) and the glucose 6-phosphate dehydrogenase activities, and iv) the antilipolytic action of insulin. The study was conducted on rats fed an SRD during 120 days with fish oil being isocaloric substituted for corn oil for 90-120 days in half the animals. Permanent hypertriglyceridemia, insulin resistance and abnormal glucose homeostasis were present in the rats before the source of fat in the diet was replaced. The major new findings of this study are the following: i) Dietary fish oil markedly reduced the fat pads mass, the hypertrophy of fat cells and improved the altered cell size distribution. ii) The presence of fish oil in the diet corrected the inhibitory effect of high sucrose diet upon the antilipolytic action of insulin, reduced the "in vitro" enhanced basal lipolysis and normalized isoproterenol-stimulated lipolysis. Fat pads lipoprotein lipase activity decreased reaching values similar to those observed in age-matched controls fed a control diet (CD). These effects were not accompanied by any change in rat body weight. All these data suggest that the dyslipemic rats fed a moderate amount of dietary fish oil constitute a useful animal model to study diet-regulated insulin action.
Rats fed on a sucrose-rich diet (SRD) (63 % ) up to 30 weeks develop stable hypertriglyceridemia,... more Rats fed on a sucrose-rich diet (SRD) (63 % ) up to 30 weeks develop stable hypertriglyceridemia, impaired glucose tolerance and insulin insensitivity. At present only scarce and non-systematic information is available concerning the possible reversion of these metabolic derangements by nutritional or metabolic interventions. The present study was designed to investigate the effect of the isocaloric substitution of sucrose for starch (during 15 weeks) on lipid and glucose metabolisms in rats in which a well-established hypertriglyceridemia and glucose intolerance were present before the amount of sucrose (63% ) was partially (33% ) or totally (0% ) replaced by an isocaloric amount of starch. Our findings show that: i) when the amount of fructose (sucrose moieties) is partially replaced by starch (from 33 to 18% of the total calories) most of its undesirable effects on lipid metabolism are still present and no significant improvement in glucose regulation is noticed; ii) hypertriglyceridemia and glucose intolerance can be completely reversed, without detectable changes in circulating insulin levels, by shifting completely to starch as the source of carbohydrate in the diet. Moreover, when sucrose was removed from the diet, it took 7 weeks for plasma triglyceride levels to become completely normal while plasma free fatty acids and glucose levels needed twice that time. These findings suggest that manipulation of dietary fructose may play a role in the management of lipid disorders associated with glucose intolerance and insulin resistance.
Biochimica Et Biophysica Acta (bba) - Lipids and Lipid Metabolism, 1996
The aim of this study was to investigate the relationship between the lipid-lowering effects of f... more The aim of this study was to investigate the relationship between the lipid-lowering effects of fish oils and concomitant consequences on glucose tolerance and insulin sensitivity in an experimental animal model of hypertriglyceridemia induced by high sucrose intake. To achieve this goal, male Wistar rats were fed a semi-synthetic sucrose rich diet (SRD) (w/w: 62.3% sucrose, 8% corn oil, 17% protein) for 90 days. At the time, a well established and permanent hypertriglyceridemia accompanied by glucose intolerance was present. After that, one half of the animals continued on the SRD up to 120 days. The other half received an SRD in which the source of fat was substituted by cod liver oil (w/w 7% CLO plus 1% corn oil) from day 90 to 120 (SRD + CLO). Control rats were fed a semi-synthetic diet (CD) (w/w: 62.5% corn starch, 8% corn oil, 17% protein) throughout the 120 days experimental period. Results obtained after the experimental period show that the hypertriglyceridemia and glucose intolerance ensuing long term feeding normal rats with a sucrose-rich diet could be completely reversed mediating no change in circulating insulin levels by shifting the source of fat in the diet from corn oil to cod liver oil. These findings suggest that manipulation of dietary fats may play a role in the management of the lipid disorders associated with glucose intolerance and insulin resistance.
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