Effects of physical training on serum and pituitary growth hormone contents in diabetic rats (original) (raw)
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Effects of swimming training on bone mass and the GH/IGF-1 axis in diabetic rats
Growth Hormone & IGF Research, 2006
The influence of moderate physical training on serum growth hormone (GH), insulin-like growth factor-1 (IGF-1) and binding protein (IGFBP-3) in experimental diabetic rats was investigated. Male Wistar rats were divided into 4 groups, sedentary control (SC), trained control (TC), sedentary diabetic (SD) and trained diabetic (TD). Experimental diabetes was induced of Alloxan (35mg/b.w.) The training program consisted by swimming 5 days/week, 1 h/day, supporting a load of 2.5% b.w., during 6 weeks. Then, the rats were sacrificed and blood was collected for determinations of serum glucose, insulin, GH, IGF-1 and IGFBP-3. Samples of liver were used to evaluate glycogen, protein and DNA contents. The results were analyzed by ANOVA, and Bonferroni test and the significance level was set at 2.5%. Diabetes decreased serum GH, IGF-1, IGFBP-3 and liver glycogen stores in SD group. Physical training promoted increase in serum IGF-1 in both TC and TD groups (SC=82±15; TC=103±13; SD=77±16; TD=112± 29 ng/ml) and liver glycogen store in TD group when compared to SD (SC=5.2±1.2; TC= 6.2±1; SD=2±0.5; TD=5±1.8 mg/100mg). Therefore, physical training contributes to the increase in liver glycogen content and to rise of insulin-like growth factor level in diabetic rats. It was concluded that moderate physical training promotes important adaptations related to GH-IGF-1 axis in diabetic organisms.
Long-term physical training increases liver IGF-I in diabetic rats
Growth Hormone & IGF Research, 2009
Diabetes reduces the serum levels of insulin-like growth factor-I (IGF-I) and physical training may prevent this reduction. Almost all circulating IGF-I is produced and secreted by the liver. To examine the influence of moderate physical training on liver IGF-1 levels in diabetes, male Wistar rats were given a single dose of alloxan (30 mg/kg b.w.) to induce diabetes and then randomly allocated to sedentary or trained groups. The training protocol consisted of a 1 h swimming session/day, five days/week for eight weeks with a load corresponding to 5% of the body weight. These two groups were compared with sedentary or trained non-diabetic rats (controls). A subcutaneous insulin tolerance test (ITT) was performed at the 6th week of experiment. At the end of the training period, the rats in all groups were sacrificed and blood was collected for the quantification of hematocrit and serum glucose, insulin, triglycerides, albumin, GH and IGF-1. Skeletal muscle and hepatic glycogen levels and hepatic triglyceride, protein, DNA and IGF-I concentrations were also determined. Diabetes reduced the serum insulin, GH and IGF-I concentrations, and the hepatic protein/DNA ratio and IGF-I concentrations, but increased serum glucose and triglyceride levels. Serum glucose removal during ITT was increased in the trained diabetic animals compared to sedentary control. Physical training reduced the serum glucose and triglyceride levels but increased the muscle glycogen content and restored the hepatic protein/DNA ratio and serum and hepatic IGF-I in diabetic rats. In conclusion, long-term chronic exercise improved the metabolic state and attenuated the reduction in serum and hepatic IGF-I concentrations caused by diabetes.
Effect of Growth Hormone Suppression on Exercise Training and Growth Responses in Young Rats
Pediatric Research, 1994
Exercise training improves maximal oxygen uptake and endurance times in adult human beings and other animals. The mechanism of this improvement results in part from anabolic effects of exercise and may be mediated by growth hormone (GH). Little is known about the role of GH in the adaptation to exercise in younger, stilldeveloping organisms. To examine this role, we began a 4wk treadmill exercise training protocol in 14-d-old female rats. GH was suppressed by passive immunization with anti-GH releasing hormone antisera. There were four experimental groups: I) GH-control (normal GH secretory capacity), untrained (n = 21); 2) GH-suppressed, untrained (n = 13); 3) GH-control, trained (n = 14); and 4) GHsuppressed; trained (n = 11). At the end of the training period, maximal oxygen uptake and treadmill endurance running time were measured. Serum GH and IGF-I were assessed using RIA, and whole hind limb musculature succinate dehydrogenase (an indicator of mitochondria1 function) was measured with standard fluorometric technique. Body weight gain was markedly reduced in GHsuppressed rats (mean, 54% of GH-controls in untrained rats and 55% in trained; p < 0.05). No apparent effect of training on linear growth was observed. As expected, serum IGF-I was markedly reduced by GH suppression, but no exercise-induced increase occurred in IGF-I as a result of training in either the GH-control or GH-suppressed rats. In GH-control rats, maximal oxygen uptake and succinate dehydrogenase were 69% and 25% greater, respectively, in trained compared with untrained rats (p < 0.05). Despite GH inhibition, similar increases were found in the trained GH-suppressed rats (68% greater than controls for maximal oxygen uptake and 34% for succinate dehydrogenase, p < 0.05). Thus, marked improvement in cardiorespiratory function occurs with training in young female rats even when normal pituitary GH function is suppressed.
Effects of exercise training on hippocampus concentrations of insulin and IGF-1 in diabetic rats
Hippocampus, 2009
The present study investigated the role of swimming training on cerebral metabolism and hippocampus concentrations of insulin and IGF-1 in diabetic rats. Wistar rats were divided in sedentary control (SC), trained control (TC), sedentary diabetic (SD), and trained diabetic (TD). Diabetes was induced by Alloxan (35 mg kg−1 b.w.). Training program consisted in swimming 5 days/week, 1 h/day, 8 weeks, supporting a load corresponding to 90% of maximal lactate steady state (MLSS). For MLSS determination, rats were submitted to three sessions of 25-min supporting loads of 4, 5, or 6% of body wt, with intervals of 1 week. Blood samples were collected every 5 min for lactate determination. An acute exercise test (25 min to 90% of MLSS) was done in 7th week to confirm the efficacy of training. All dependent variables were analyzed by one-way analysis of variance (ANOVA) and a significance level of P < 0.05 was used for all comparisons. The Bonferroni test was used for post hoc comparisons. At the end of the training period, rats were sacrificed and sample blood was collected for determinations of serum glucose, insulin, GH, and IGF-1. Samples of gastrocnemius muscle and liver were removed to evaluate glycogen content. Hippocampus was extracted to determinate glycogen, insulin, and IGF-1 contents. Diabetes decreased serum GH, IGF-1, and liver glycogen stores in SD. Diabetes also increased hippocampus glycogen and reduced hippocampus IGF-1 content. Physical training recovered liver and hippocampus glycogen stores and promoted increases in serum IGF-1 in TD group. Physical training restored hippocampus IGF-1 content in diabetic group. It was concluded that in diabetic rats, physical training induces important metabolic and hormonal alterations that areassociated with an improvement in glucose homeostasis and with an increased activity in the systemic and hippocampus IGF-1 peptide. © 2009 Wiley-Liss, Inc.
Moderate physical training increases brain insulin concentrations in experimental diabetic rats
Indian journal of experimental biology, 2008
Insulin is an important modulator of growth and metabolic function in the central nervous system. The aim of this study was to investigate the influence of swimming physical training (at 32 degrees +/- 1 degree C, 1 hr/day, 5 days/week, with an overload equivalent to 5% of the body weight, for 4 weeks) on brain insulin concentrations in alloxan induced type 1 diabetic rats. Training attenuated hyperglycemia but had no effect on insulinemia in diabetic rats. Hematocrit and blood albumin values remained without changes. Brain insulin did not change in diabetic rats. However, physical training increased the concentration in both control and diabetic rats. It is concluded that in the present experimental conditions, diabetes had no influence on brain insulin, however moderate physical training increased the hormone in both control and diabetic animals.
Journal of diabetes and metabolic disorders, 2011
Normal 0 false false false MicrosoftInternetExplorer4 /* Style Definitions */ table.MsoNormalTable {mso-style-name:"Table Normal"; mso-tstyle-rowband-size:0; mso-tstyle-colband-size:0; mso-style-noshow:yes; mso-style-parent:""; mso-padding-alt:0cm 5.4pt 0cm 5.4pt; mso-para-margin:0cm; mso-para-margin-bottom:.0001pt; mso-pagination:widow-orphan; font-size:10.0pt; font-family:"Times New Roman"; mso-ansi-language:#0400; mso-fareast-language:#0400; mso-bidi-language:#0400;} Background: The aim of this study was to determine possible relationship between changes induced by exercise in serum concentrations of growth hormone and insulin with IGF-1 system components over time in trained and untrained individuals. Methods: Nineteen healthy men among physical education students as trained group and 15 healthy men among non-physical education students as untrained group voluntarily participated in this study. The subjects randomly were divided into experimental (t...
Growth Hormone & Igf Research, 2009
Objective: The aim of this study was to analyze the association between glucose infusion during intermittent physical exercise and its metabolic effects on rats. Design: Forty male rats were divided into eight groups based on training (intermittent), exercise and carbohydrate intake (glucose 20%): TEC (trained exercised with carbohydrate), TES (trained exercised without carbohydrate), TNC (trained non-exercised with carbohydrate), TNS (trained non-exercised without carbohydrate), UEC (untrained exercised with carbohydrate), UES (untrained exercised without carbohydrate), UNC (untrained non-exercised with carbohydrate) and UNS (untrained non-exercised without carbohydrate). The training and/or exercise protocol consisted of the rats running on a treadmill for 1 min above the lactate threshold, or running below the lactate threshold for 30 s, intermittently for 30 min. Blood was analyzed for glycemia, lactate and IGF-1. Muscle and liver glycogen were measured (T2). Results: Glycemia was found to be different in T2 compared to T1 in the TEC, TNC, UEC and UNC groups. Lactate was higher in T2 than in T1, but remained within the lactate threshold. Glycogen showed higher concentrations in the trained groups and, whether trained or not, in the supplemented groups. IGF-1 levels were higher in exercised rats independent of supplementation or glycogen levels. Trained rats showed lower IGF-1 when exercising than did the untrained animals. Conclusions: We conclude that intermittent exercise is beneficial in preventing a trained lactate pool, and that, in association with glucose supplementation, intermittent exercise will be efficient both in preventing a trained lactate pool and in maintaining sufficient glycemia levels. Exercise raises IGF-1 levels, whereas training inverts this relationship.
Effect of training and growth hormone suppression on insulin-like growth factor I mRNA in young rats
Journal of Applied Physiology, 1994
The growth hormone (GH)-insulin-like growth factor I (IGF-I) axis plays a role in the adaptation to exercise training, but IGF-I gene expression in response to exercise training and GH suppression has not been studied. Twenty female rates underwent a 4-wk treadmill training program begun in the prepubertal period (day 14 of life). In 10 of the training rats, GH production was suppressed by anti-GH-releasing hormone antibodies (GH suppressed). IGF-I mRNA and protein levels were measured in liver and hindlimb skeletal muscle. GH suppression reduced IGF-I mRNA expression in the liver to a much greater extent than in the muscle. In the GH control rats, training induced significant increases in hepatic exon 1-derived IGF-I mRNA (mean increase 30%; P < 0.05) and muscle exon 2-derived mRNA (mean increase 35%; P < 0.05). In the GH-suppressed rats, only muscle exon 1-derived transcripts were significantly increased by training (55%; P < 0.05) and this was associated with a significa...
International Journal of Research in Medical Sciences, 2021
Background: The growth hormone (GH) response to resistance training is altered by many factors including sex steroid concentrations, fitness, intensity of exercise, age, gender, duration of exercise and glycemic state but the exact understanding of the interplay of different exercises to GH levels and its induced physiological adaptations is still obscure. This study aimed to see how resistance exercise affects GH levels and its correlation to plasma glucose levels in healthy non-obese adolescent subjects. Methods: 48 healthy non-obese adolescent subjects, 24 males and 24 females were included in the study. High volume exercise training regimen was used which involved major muscle group of arms, legs and trunk. Pre and post exercise levels of serum GH and random blood sugar were estimated in male and female groups. Results: The mean body mass index (BMI) of male and female groups was 23.22±3.12 kg/m 2 and 20.40±4.49 kg/m 2 , respectively. The post-exercise serum GH levels in male and females increased significantly by 0.54±1.041 ng/ml (p<0.05) and 0.85±1.023 ng/ml (p<0.001) respectively. The random blood sugar levels in males after exercise significantly increased (p<0.05) by 7.16±12.61 mg/dl and in females by 6.20±12.09 mg/dl (p<0.05). There was significant correlation (p<0.05) between increase in serum GH levels and increase in random blood sugar levels in both male and female group. Conclusions: Exercise induced increase in GH and its interplay with serum glucose can be better gained access into via metanalytical/elaborate studies of the major hormones and fuels involved.
IJVST-2019; Vol.11, No.1, 2019
Growth hormone has mitotic and anti-apoptotic effects which may increase proliferation and transformation of cells when it is expressed aberrantly. This study investigated the effects of resistance training and growth hormone injection on circulating IGF-1, IGFBP-3 levels and IGF-1/IGFBP-3 ratio in male Wistar rats. Thirty-two male Wistar rats were randomly assigned to a control group (C, n = 8), a resistance training group (RT, n = 8), a growth hormone injection group (GI, n = 8) and a resistance training + growth hormone injection group (RG, n = 8). The resistance training protocol comprised of climbing a ladder (5 days/week, 3 sets/5 reps) while carrying a weight suspended from the tail. The growth hormone (2 mg/kg/day, 5 days/week) was injected before an exercise session. Serum IGF-1, IGFBP-3 levels, and IGF-1/IGFBP-3 ratio were measured after 8 weeks. One-way ANOVA analysis was used for comparison of serum IGF-1 and IGFBP-3 levels between groups. Serum IGF-1 levels and IGF-1/IGFBP-3 ratio signifi cantly decreased, but serum IGFBP-3 levels showed no significant change in the RT group compared to the C group. Also, both serum IGF-1 and IGFBP-3 levels and IGF-1/IGFBP-3 ratio in GI and RG groups significantly increased compared to the other groups. In conclusion, resistance training decreases serum IGF-1 levels and/or IGF-1/IGFBP-3 ratio in normal condition. On the other hand, the growth hormone injection with and without the resistance training increases serum IGF-1 levels and IGF-1/IGFBP-3 ratio which could be noted as a condition with a higher risk of neoplasm.