Site of enhanced insulin sensitivity in exercise-trained rats at rest

Mondon, Carl E.; Dolkas, C. B.; Reaven, Gerald M.

doi:10.1152/ajpendo.1980.239.3.e169

Cited by 99 publications

(109 citation statements)

References 25 publications

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“…5 ' 6 Sprague-Dawley rats become insulin resistant, hyperinsulinemic, and hypertrigryceridemic when fed a fructose-enriched diet, 7 - 8 and the fact that this dietary manipulation also leads to an increase in blood pressure 8 lends further support to the possibility that insulin resistance and hyperinsulinemia may play a role in the genesis of high blood pressure. Furthermore, we have shown that exercise training of rats, which enhances insulin sensitivity 9 and reduces fructose-induced hyperinsulinemia, 10 also attenuates the increase in blood pressure seen in fructose-fed rats.…”

Section: W E Have Recently Speculated That Resistancementioning

confidence: 85%

Somatostatin inhibition of fructose-induced hypertension.

1989

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The role of insulin resistance and byperinsulinemia in the etiology of fructose-induced hypertension was studied in male Sprague-Dawley rats. Rats consumed a fructose-enriched diet (containing 66% of total calories as fructose) for 11 days and were infused continuously during the last 7 days with either a somatostatin analogue or vehicle. At the end of this period, rats receiving the somatostatin analogue had a lower plasma insulin concentration (52±4 vs. 70±6 /iunits/ml, /><0.01) and a lower blood pressure (133±2 vs. 150±2 mm Hg) than did the rats infused with the control solution. In addition, the increase in plasma triglyceride concentration in response to the fructose-enriched diet was significantly attenuated (p<0.001) in the rats infused with somatostatin. These data provide further support that the increase in blood pressure that occurs when normal rats are fed a high fructose diet is dependent on the ability of this intervention to cause insulin resistance and hyperinsulinemia. and the hyperinsulinemia appears to be associated with resistance to insulin-stimulated glucose uptake.5 ' 6 Sprague-Dawley rats become insulin resistant, hyperinsulinemic, and hypertrigryceridemic when fed a fructose-enriched diet, 7 -8 and the fact that this dietary manipulation also leads to an increase in blood pressure 8 lends further support to the possibility that insulin resistance and hyperinsulinemia may play a role in the genesis of high blood pressure. Furthermore, we have shown that exercise training of rats, which enhances insulin sensitivity 9 and reduces fructose-induced hyperinsulinemia, 10 also attenuates the increase in blood pressure seen in fructose-fed rats. 11The present experiments were initiated to further study the relation between insulin-resistance, hyperinsulinemia, and hypertension in fructosefed rats and were based on the use of somatostatin Received September 1, 1988; accepted February 14, 1989. to suppress insulin secretion by /3 cells in pancreatic islets. We reasoned that the infusion of somatostatin would suppress the hyperinsulinemia that normally results when rats are fed a fructoseenriched diet, 7 -8 -10 ' 11 and if elevated plasma insulin concentrations play a role in fructose-induced hypertension, this intervention would also ameliorate the rise in blood pressure that occurs when rats eat a high fructose diet. The results indicated that this prediction was borne out, providing further support for the view that insulin plays a role in the regulation of blood pressure in rats with fructose-induced hypertension. Materials and Methods General ProtocolMale Sprague-Dawley rats (Simonsen Laboratories, Gilroy, California), initially weighing 160-180 g, were used for all experiments. Before dietary manipulation, all rats were fed standard rat chow (Wayne Lab Blox, Allied Mills, Chicago, Illinois) containing 60% vegetable starch, 11% fat, and 29% protein and were maintained on a 12-hour light/dark (6:00 AM-6:00 PM) cycle. In addition, rats were acclimated to the procedure of blood pressure measure...

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Section: W E Have Recently Speculated That Resistancementioning

confidence: 85%

Somatostatin inhibition of fructose-induced hypertension.

1989

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“…21 -23 On the other hand, exercise training in rats has repeatedly been reported to be associated with an enhanced insulin sensitivity. 24,25 We recently reported that exercise training in OVX rats results in an improvement of the insulin-resistant condition without any reduction in body weight. 7 From the present data, it may be suggested that a reduction in body fat contributes to the exercise training-induced improvement in insulin sensitivity in OVX rats.…”

Section: Body Composition In Ovariectomized Trained Ratsmentioning

confidence: 99%

Effects of physical training on body composition and organ weights in ovariectomized and hyperestrogenic rats

Shinoda

2002

Int J Obes

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OBJECTIVE:To investigate whether regular endurance-type exercise can benefit rats submitted to a model of ovariectomy (OVX)-induced obesity with or without estrogen replacement. SUBJECTS: OVX Sprague-Dawley rats were compared to an ovariectomized-estradiol-treated group (OVXE2) and a Shamoperated (Sham) group. Each of these groups were subdivided into a sedentary and a treadmill-trained (8 wk) group. DESIGN AND MEASUREMENTS: An experimental study in which various parameters, including fat depots, blood lipids and several organ weights were measured. RESULTS: Plasma levels of 17b-estradiol and uterus weights were significantly (P < 0.05) lower in OVX compared to Sham and significantly (P < 0.01) higher in OVXE2 (hyperestrogenic) compared to Sham rats. Body weights were significantly (P < 0.01) different among groups, in the following decreasing order: OVX, Sham and OVXE2. The average daily food intake and food efficiency were significantly (P < 0.01) increased in OVX compared to Sham, whereas estradiol treatment diminished this effect (P < 0.01). Exercise training did not alter any of the above-mentioned variables in any of the three estrogen groups. Mesenteric and subcutaneous fat weights were significantly (P < 0.01) increased by OVX. This increase was abolished by estrogen replacement or by exercise training. Exercise training also decreased fat weights in OVXE2 and Sham rats. OVX resulted in a decrease in the weights of several other tissues (femur, heart, lungs, liver and adrenal glands) while hyperestrogenic replacement resulted in an increase in weight of all measured tissues. Aside from fat depots, exercise training did not affect any of the tissue weights with the exception for an increase in the weight of the plantaris muscle and adrenal glands and a decrease in lung weight in all three estrogen groups. CONCLUSION: In OVX animals, exercise training may bring about positive changes in body composition (ie reduction in fat weights) despite an ovariectomy-induced increase in body weight.

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“…4 - 7 Based on these findings, we raised the possibility that the changes in insulin action and concentration noted in fructose-fed rats with hypertension may play a role in the pathogenesis of the elevated blood pressure seen in this situation. In this context, we have previously demonstrated that insulin-stimulated glucose uptake is enhanced in exercise-trained rats 8 and that the hyperinsulinemia associated with feeding rats a high fructose diet is 130 HYPERTENSION VOL 12, No 2, AUGUST 1988 were placed individually in exercise wheel cages (Wahman, Timonium, MD, USA) and allowed to run at their own pace. The cages, as supplied by the manufacturer, consist of a rotating wheel cage (with the number of revolutions/day recorded by a cyclometer attached to the wheel axis) plus an adjoining feed cage.…”

Section: Exercise Training Insulin Resistance • Hyperinsulinemiamentioning

confidence: 99%

“…In this context, we have previously demonstrated that insulin-stimulated glucose uptake is enhanced in exercise-trained rats 8 and that the hyperinsulinemia associated with feeding rats a high fructose diet is attenuated if rats are allowed to run spontaneously.…”

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Attenuation of fructose-induced hypertension in rats by exercise training.

Reaven¹,

Ho²,

Hoffman³

1988

Hypertension

141

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SUMMARY This study was initiated to see if the insulin resistance, hyperinsulinemia, and hypertension that follow feeding nonnotensive Sprague-Dawley rats a fructose-rich diet could be prevented by letting rats run spontaneously in exercise wheel cages. Blood pressure in sedentary rats increased from (mean ± SEM) 125 ± 2 to 148 ± 3 mm Hg in response to 2 weeks of a high fructose diet, and this increment was significantly (p < 0.001) attenuated in exercising rats (from 121 ± 1 to 131 ± 2 mm Hg). In addition, mean (±SEM) plasma insulin concentration was lower in fructose-fed rats allowed to run spontaneously (44 ± 2 vs 62 ± 5 /xU/ml; p < 0.01). Finally, resistance to insulin-stimulated glucose uptake was assessed by determining the steady state plasma glucose response to a continuous glucose and exogenous Insulin infusion during a period in which endogenous insulin secretion was suppressed. The results of these studies indicated that the mean ( ± SEM) steady state plasma glucose concentration was significantly lower in the exercise-trained rats (127 ± 5 vs 168 ± 6 mg/dl; p < 0.001), despite tbe fact that the steady state plasma insulin levels were also lower in rats allowed to run spontaneously (75 ± 4 vs 90 ± 5 ftU/ml; p < 0.05). Thus, the ability of exercise-trained rats to stimulate glucose disposal was enhanced as compared with that of sedentary rats fed the same fructose-rich diet. These data demonstrate that the insulin resistance, hyperinsulinemia, and hypertension produced hi nonnotensive rats by feeding them a high fructose diet can be attenuated if rats are allowed to run spontaneously. I N a previous report we found that hypertension can be produced by feeding a high fructose diet to normal rats.1 Fructose-fed rats also develop resistance to insulin-stimulated glucose uptake and hyperinsulinemia, 1 -3 phenomena that have recently been identified as occurring in patients with hypertension.4 -7 Based on these findings, we raised the possibility that the changes in insulin action and concentration noted in fructose-fed rats with hypertension may play a role in the pathogenesis of the elevated blood pressure seen in this situation. In this context, we have previously demonstrated that insulin-stimulated glucose uptake is enhanced in exercise-trained rats 8 and that the hyperinsulinemia associated with feeding rats a high fructose diet is attenuated if rats are allowed to run spontaneously. 9Thus, in the present report, we tested the hypothesis that insulin resistance and hyperinsulinemia are involved in the development of hypertension in fructose-fed rats by comparing the effects of fructoserich diets on both insulin metabolism and blood pressure in sedentary rats with those seen in rats allowed to exercise spontaneously in running wheels. Materials and Methods General ProtocolMale Sprague-Dawley rats (Harlan, Indianapolis, IN, USA) were used for all experiments. The rats were approximately 6 weeks old and weighed approximately 150 g when the study was started. Prior to any manipulation of diet or level of ...

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Site of enhanced insulin sensitivity in exercise-trained rats at rest

Cited by 99 publications

References 25 publications

Somatostatin inhibition of fructose-induced hypertension.

Somatostatin inhibition of fructose-induced hypertension.

Effects of physical training on body composition and organ weights in ovariectomized and hyperestrogenic rats

Attenuation of fructose-induced hypertension in rats by exercise training.

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