Effects of exercise training on hippocampus concentrations of insulin and IGF‐1 in diabetic rats

Gomes, Ricardo José; Oliveira, Camila Aparecida Machado de; Ribeiro, Carla; Mota, Clécia Soares de Alencar; Moura, Leandro Pereira de; Tognoli, Lilian Mari Marcondes Cesar; Leme, José Alexandre Curiacos de Almeida; Luciano, Eliete; Mello, María Alice Rostom de

doi:10.1002/hipo.20636

Cited by 28 publications

(34 citation statements)

References 47 publications

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“…Indeed, changes in neuronal precursor generation, cell survival and incorporation, and increased cell density have all been reported after both voluntary exercise and the imposed moderate physical activity used in our study (68). One recent addition to the armamentarium of beneficial effects induced by physical activity on neuronal function is IGF-1 (24,30,31), and our findings further support the possibility that PA-induced preservation of neuronal IGF-1 expression during IH may underlie components of the beneficial effect of exercise on IH-induced cognitive deficits. Indeed, regular physical activity was associated with overall enhancements in IGF-1 tissue levels, such that the IH-induced reductions in IGF-1 led to preservation of normal levels in PA-IH but markedly low concentrations in NA-IH conditions.…”

Section: Discussionsupporting

confidence: 53%

“…To further assess whether the protective effect of PA may be related to induction of IGF-1 pathways by regular physical activity (24,30,31), immunohistochemistry of the hippocampus for IGF-1 was conducted and showed increased expression of IGF-1 after PA-IH compared with IH-NA rats ( Figure 6A). Of note, IGF-1 expression was circumscribed to neurons (i.e., NeuN-labeled cells), and not in glia (i.e., GFAP-labeled cells; Figure 6B).…”

Section: Resultsmentioning

confidence: 99%

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Physical Activity Attenuates Intermittent Hypoxia-induced Spatial Learning Deficits and Oxidative Stress

Gozal

Nair²,

Goldbart³

2010

Am J Respir Crit Care Med

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Rationale: Exposure to intermittent hypoxia (IH), such as occurs in sleep-disordered breathing, is associated with substantial cognitive impairments, oxidative stress and inflammation, and increased neuronal cell losses in brain regions underlying learning and memory in rats. Physical activity (PA) is now recognized as neuroprotective in models of neuronal injury and degeneration. Objectives: To examine whether PA will ameliorate IH-induced deficits. Methods: Young adult Sprague-Dawley rats were randomly assigned to one of four treatment groups including normal activity (NA) or PA for 3 months and then subjected to either normoxia (RA) or exposure to IH during the light phase during the last 14 days. Measurements and Main Results: Significant impairments in IHexposed rats emerged on both latency and pathlength to locate the hidden platform in a water maze and decreased spatial bias during the probe trials. These impairments were not observed in PA-IH rats. In addition, the PA-IH group, relative to NA-IH, conferred greater resistance to both lipid peroxidation and 8-hydroxy-29-deoxyguanosine (DNA damage) in both the cortex and hippocampus. In support of a neuroprotective effect from PA, PA-IH versus NA-IH rats showed greater AKT activation and neuronal insulin growth factor-1 in these regions. Conclusions: Behavioral modifications such as increased physical activity are associated with decreased susceptibility to IH-induced spatial task deficits and lead to reduced oxidative stress, possibly through improved preservation of insulin growth factor-1-Akt neuronal signaling. Considering the many advantages of PA, interventional strategies targeting behavioral modifications leading to increased PA should be pursued in patients with sleep-disordered breathing.

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Section: Discussionsupporting

confidence: 53%

Section: Resultsmentioning

confidence: 99%

Physical Activity Attenuates Intermittent Hypoxia-induced Spatial Learning Deficits and Oxidative Stress

Gozal

Nair²,

Goldbart³

2010

Am J Respir Crit Care Med

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“…By reducing the ability of insulin to propagate its intracellular signal, the continuous activation of GSK3-β promotes hyperphosphorylation of tau protein 9 and the subsequent formation of neurofibrillary tangles. All this mechanism results deleterious effects on synaptic dysfunction and cognitive impairment 1 . The accumulation of β-amyloid oligomers is another pathogenic aspect of AD.…”

Section: Hippocampal Insulin Signalingmentioning

confidence: 99%

“…Alzheimer's disease (AD) is the most common form of dementia manifestation 1 and its prevalence increases with aging population 2 . Alzheimer's Disease International 3 estimates that dementias reach around 46.8 million people in the world in 2015.…”

Section: Introductionmentioning

confidence: 99%

“…Changes in insulin and growth factors signaling disrupts neuronal survival contributing to AD pathogenesis. The neuropathology hallmark of AD is characterized by accumulation of β-amyloid, synaptic dysfunction, neuronal inflammation, phosphorylation of tau protein and neurofibrillary tangle formation 1,6 . Exercise has been shown to attenuate inflammation in the hippocampus 7 .…”

Section: Introductionmentioning

confidence: 99%

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Hippocampal insulin signaling and neuroprotection mediated by physical exercise in Alzheimer´s Disease

Kuga

Botezelli

Gaspar

et al. 2017

Motriz: rev. educ. fis.

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-Epidemiological studies indicate continuous increases in the prevalence of Alzheimer's Disease (AD) in the next few decades. The key feature of this disease is hippocampal neurodegeneration. This structure has an important role in learning and memory. Intense research efforts have sought to elucidate neuroprotective mechanisms responsible for hippocampal integrity. Insulin signaling seems to be a very promising pathway for the prevention and treatment of AD. This hormone has been described as a powerful activator of neuronal survival. Recent research showed that reduced insulin sensitivity leads to low-grade inflammation, and both phenomena are closely related to AD genesis. Concomitantly, exercise has been shown to exert anti-inflammatory effects and to promote improvement in insulin signaling in the hippocampus, which supports neuronal survival and constitutes an interesting non-pharmacological alternative for the prevention and treatment of AD. This review examines recent advances in understanding the molecular mechanisms involved in hippocampal neuroprotection mediated by exercise.

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Spatial memory in sedentary and trained diabetic rats: Molecular mechanisms

et al. 2014

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Diabetes mellitus is a chronic disease that has been associated with memory loss, neurological disorders, and Alzheimer's disease. Some studies show the importance of physical exercise to prevent and minimize various neurological disorders. It is believed that the positive effects of exercise on brain functions are mediated by brain insulin and insulin-like growth factor-1 (IGF-1) signaling. In this study, we investigate the role of swimming exercise training on hippocampus proteins related to insulin/IGF-1 signaling pathway in Type 1 diabetic rats and its effects on spatial memory. Wistar rats were divided into four groups namely sedentary control, trained control, sedentary diabetic (SD), and trained diabetic (TD). Diabetes was induced by Alloxan (ALX) (32 mg/kg b.w.). The training program consisted in swimming 5 days/week, 1 h/day, per 6 weeks, supporting an overload corresponding to 90% of the anaerobic threshold. We employed ALX-induced diabetic rats to explore learning and memory abilities using Morris water maze test. At the end of the training period, the rats were sacrificed 48 h after their last exercise bout when blood samples were collected for serum glucose, insulin, and IGF-1 determinations. Hippocampus was extracted to determinate protein expression (IR, IGF-1R, and APP) and phosphorylation (AKT-1, AKT-2, Tau, and β-amyloide proteins) by Western Blot analysis. All dependent variables were analyzed by two-way analysis of variance with significance level of 5%. Diabetes resulted in hyperglycemia and hypoinsulinemia in both SD and TD groups (P < 0.05); however, in the training-induced group, there was a reduction in blood glucose in TD. The average frequency in finding the platform decreased in SD rats; however, exercise training improved this parameter in TD rats. Aerobic exercise decreased Tau phosphorylation and APP expression, and increased some proteins related to insulin/IGF-1 pathway in hippocampus of diabetic rats. Thus, these molecular adaptations from exercise training might contribute to improved spatial learning and memory in diabetic organisms.

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Effects of exercise training on hippocampus concentrations of insulin and IGF‐1 in diabetic rats

Cited by 28 publications

References 47 publications

Physical Activity Attenuates Intermittent Hypoxia-induced Spatial Learning Deficits and Oxidative Stress

Physical Activity Attenuates Intermittent Hypoxia-induced Spatial Learning Deficits and Oxidative Stress

Hippocampal insulin signaling and neuroprotection mediated by physical exercise in Alzheimer´s Disease

Spatial memory in sedentary and trained diabetic rats: Molecular mechanisms

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