Search published articles


Showing 2 results for Moazami

Mahtab Moazami, Babisan Askari,
Volume 12, Issue 4 (Jul-Aug 2018)
Abstract

ABSTRACT
           Background and Objectives: Inactivity, obesity and hormone disorders can lead to various diseases in obese and non-athletic individuals. The objective of this study was to investigate effects of six months of aerobic exercise on serum levels of insulin, growth hormone (GH) and insulin-like growth hormone 1 (IGF-1) in sedentary obese women.
           Methods: In  this quasi-experimental  study, 15  inactive,  obese  (body mass index >30) women aged 37-47 years were selected from employees of the Ferdowsi University in Mashhad (Iran), via purposive and available sampling. The participants were randomly divided into an experimental group (n=10) and a control (n=5) group. The experimental group performed 60 minutes of aerobic exercise at 55-65% of heart rate reserve, three sessions a week, for six months. Serum GH, IGF-1 and insulin levels were measured in both groups before the first training session and after the last training session. The Shapiro–Wilk test and the Levene's test were used to assess normal distribution of data and homogeneity of variance, respectively. Independent and dependent t-tests were used to compare between-group and within-group differences at significance of 0.05. All statistical analyses were performed using the SPSS software (version 18).
           Results: Serum concentrations of IGF-1 and insulin reduced significantly following the six-month aerobic exercise program. In addition, the exercise training caused an insignificant increase in GH levels.
           Conclusion: Our proposed aerobic exercise protocol significantly reduces IGF-1 level, which is closely related to the incidence of atherosclerosis, breast cancer, and colon cancer. The significant decline in insulin secretion following the six-month aerobic exercise program may provide more amounts of nutrients for muscle glucose metabolism.
           Keywords: Growth hormone, Insulin, Insulin-like growth factor 1, Exercise.

Mohtaram Yazdanian, Mahtab Moazami, Mohammad Shabani, Sadegh Cheragh Birjandi,
Volume 13, Issue 6 (Nov-Dec 2019)
Abstract

ABSTRACT
              Background and Objectives: Cerebral ischemia causes irreversible structural and functional damage in certain areas of the brain, especially in the hippocampus. The aim of this study was to examine effects of exercise preconditioning on neuronal cell death and expression of neurotrophin-4 (NT-4) and tropomyosin receptor kinase B (TrkB) in the hippocampal CA1 region following transient global cerebral ischemia/reperfusion in rat.
              Methods: Twenty-one male Wistar rats (weighing 250-300 g) were randomly divided into three groups (control+healthy, control+ischemia and exercise+ischemia). The rats in the exercise group ran on a treadmill five sessions a week for eight weeks. Ischemia was induced by occlusion of both common carotid arteries for 45 minutes. Cresyl violet staining was performed to assess cell death, and real-time PCR was carried out to evaluate expression of NT-4 and TrkB.
              Results: Cerebral ischemia was associated with significant neuronal death in the hippocampal CA1 region (P<0.05). Exercise significantly decreased the ischemia-induced cell death (P<0.05). NT-4 expression was significantly lower in the control+ischemia group and in the exercise+ischemia group compared to the control+healthy group (P<0.05), but there was no significant difference between the control+ischemia group and the exercise+ischemia group in terms of NT-4 expression (P˃0.05). Moreover, TrkB expression did not differ significantly between the groups (P˃0.05).
              Conclusion: When used as a preconditioning stimulant before the induction of cerebral ischemia, exercise could have neuroprotective effects against cerebral ischemia-induced cell death, but it has no significant effect on NT-4 and TrkB expression.
              Keywords: Exercise Preconditioning, Ischemia/Reperfusion, NT-4, TrkB, Cell death.
ABSTRACT
              Background and Objectives: Cerebral ischemia causes irreversible structural and functional damage in certain areas of the brain, especially in the hippocampus. The aim of this study was to examine effects of exercise preconditioning on neuronal cell death and expression of neurotrophin-4 (NT-4) and tropomyosin receptor kinase B (TrkB) in the hippocampal CA1 region following transient global cerebral ischemia/reperfusion in rat.
              Methods: Twenty-one male Wistar rats (weighing 250-300 g) were randomly divided into three groups (control+healthy, control+ischemia and exercise+ischemia). The rats in the exercise group ran on a treadmill five sessions a week for eight weeks. Ischemia was induced by occlusion of both common carotid arteries for 45 minutes. Cresyl violet staining was performed to assess cell death, and real-time PCR was carried out to evaluate expression of NT-4 and TrkB.
              Results: Cerebral ischemia was associated with significant neuronal death in the hippocampal CA1 region (P<0.05). Exercise significantly decreased the ischemia-induced cell death (P<0.05). NT-4 expression was significantly lower in the control+ischemia group and in the exercise+ischemia group compared to the control+healthy group (P<0.05), but there was no significant difference between the control+ischemia group and the exercise+ischemia group in terms of NT-4 expression (P˃0.05). Moreover, TrkB expression did not differ significantly between the groups (P˃0.05).
              Conclusion: When used as a preconditioning stimulant before the induction of cerebral ischemia, exercise could have neuroprotective effects against cerebral ischemia-induced cell death, but it has no significant effect on NT-4 and TrkB expression.
              Keywords: Exercise Preconditioning, Ischemia/Reperfusion, NT-4, TrkB, Cell death.


Page 1 from 1     

© 2007 All Rights Reserved | Medical Laboratory Journal

Creative Commons License
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.