Treadmill exercise increases cell proliferation in dentate gyrus of rats with streptozotocin-induced diabetes

Kim, Hyun Bae; Jang, Mi Hyeon; Shin, Min Chul; Lim, Baek Vin; Kim, Young Pyo; Kim, Kyung Ji; Kim, Ee Hwa; Kim, Sang Hoon

doi:10.1016/s1056-8727(02)00186-1

Cited by 54 publications

(33 citation statements)

References 22 publications

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“…Type 2 diabetes results in decreased responsiveness of the pancreas to GIP, because of decreased expression of Gipr mRNA and GIPR protein in pancreatic islets (Lynn et al, 2001). Deficits in spatial learning (Biessels et al, 1996) as well as lower cell-proliferation rates in the DG (Jackson-Guilford et al, 2000) that can be improved by treadmill exercise (Kim et al, 2003) have been demonstrated in streptozotocin-induced diabetic rats, suggesting a link between adult neurogenesis and diabetes. Gipr Ϫ/Ϫ mice also exhibit glucose intolerance and impaired insulin secretion after orally administered glucose (Miyawaki et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

Glucose-Dependent Insulinotropic Polypeptide Is Expressed in Adult Hippocampus and Induces Progenitor Cell Proliferation

Nyberg

Anderson²,

Meister³

et al. 2005

J. Neurosci.

155

116

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The hippocampal dentate gyrus (DG) is an area of active proliferation and neurogenesis within the adult brain. The molecular events controlling adult cell genesis in the hippocampus essentially remain unknown. It has been reported previously that adult male and female rats from the strains Sprague Dawley (SD) and spontaneously hypertensive (SHR) have a marked difference in proliferation rates of cells in the hippocampal DG. To exploit this natural variability and identify potential regulators of cell genesis in the hippocampus, hippocampal gene expression from male SHR as well as male and female SD rats was analyzed using a cDNA array strategy. Hippocampal expression of the gene-encoding glucose-dependent insulinotropic polypeptide (GIP) varied strongly in parallel with cell-proliferation rates in the adult rat DG. Moreover, robust GIP immunoreactivity could be detected in the DG. The GIP receptor is expressed by cultured adult hippocampal progenitors and throughout the granule cell layer of the DG, including progenitor cells. Thus, these cells have the ability to respond to GIP. Indeed, exogenously delivered GIP induced proliferation of adult-derived hippocampal progenitors in vivo as well as in vitro, and adult GIP receptor knock-out mice exhibit a significantly lower number of newborn cells in the hippocampal DG compared with wild-type mice. This investigation demonstrates the presence of GIP in the brain for the first time and provides evidence for a regulatory function for GIP in progenitor cell proliferation.

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Section: Discussionmentioning

confidence: 99%

Glucose-Dependent Insulinotropic Polypeptide Is Expressed in Adult Hippocampus and Induces Progenitor Cell Proliferation

Nyberg

Anderson²,

Meister³

et al. 2005

J. Neurosci.

155

116

View full text Add to dashboard Cite

show abstract

“…An important consideration, especially in relation to hippocampal function, is whether these neuroanatomical changes represent the initiation of irreversible neuronal damage in diabetic subjects. Neuronal apoptosis and suppression of cell proliferation/neurogenesis are observed in the hippocampus of diabetic rodents [5][6][7][8], albeit under conditions of uncontrolled hyperglycemia. As such, the relationship of these findings to the clinical situation in which patients attempt to maintain tight glycmeic control remains to be determined.…”

Section: Is Accelerated Brain Aging a Consequence Of Diabetes?mentioning

confidence: 99%

Insulin signaling effects on memory and mood

Reagan¹

2007

Current Opinion in Pharmacology

109

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The escalating obesity/diabetes epidemic is an important health care issue that has critical socioeconomic ramifications. The complications of diabetes/obesity phenotypes extend to the central nervous system, including the hippocampus, a brain region that is particularly vulnerable to hyperglycemia and insulin resistance. Deficits in hippocampal synaptic plasticity observed in diabetes ultimately have deleterious consequences upon cognitive function. For example, recent studies using brain imaging technologies have identified cerebral atrophy in diabetic patients, suggesting that the neuroanatomical changes observed in experimental models of diabetes may accurately reflect what is occurring in the clinical setting. Deficits in insulin receptor signaling and impairments in hypothalamic-pituitary-adrenal (HPA) axis function also contribute to the neurological complications of diabetes phenotypes. The pathophysiological similarities between diabetes and stress-related mood disorders suggest that common mechanistic mediators may be involved in the etiology and progression of the neurological complications of these disorders. When combined with the accumulating evidence from pre-clinical models, these data support the hypothesis that a long-term consequence of diabetes/obesity phenotypes is accelerated brain aging that results in neuropsychological deficits and increased vulnerability to co-morbidities such as depressive illness.

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“…28 Exogenous erythropoietin infusion has been found to improve ischaemic damage of hippocampal CA1 neurons and ischaemia induced learning deficits. Similarly, reduction of brain temperature may provide robust neuroprotection for hypoxia-ischaemia in the brain of laboratory animals.…”

Section: Insulin Dysregulationmentioning

confidence: 99%

“…Physical exercises like aerobics apart from improving glycemic control are also beneficial in reducing cognitive decline 28 . On the other hand, stressful events in life should be minimized and for this yoga and meditation may be helpful.…”

Section: Conclusion:-mentioning

confidence: 99%

Cognitive Function-a Comparison Between Elderly Non Diabetic and Diabetic Subjects.

Mohan¹,

Kannan²

2016

IJAR

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Introduction:-Increase in life expectancy and fall in death rate has led to rise in the proportion of the elderly in the community all over the world. The ageing population is facing a double epidemic of dementia including Alzheimer"s disease and diabetes mellitus. The increase in diabetes among elderly is concerning because, in addition to the traditional diabetes complications like acute hyperglycemic and hypoglycemic events and vascular complications, diabetes also affects the central nervous system, a complication referred to as "diabetic encephalopathy", which presents as impaired cognitive functioning and is also associated with an increased risk of dementia. Hence this study was under taken to draw attention to the occurrence of cognitive impairment in type 2 diabetes mellitus, in our community, and thereby pave the way for future initiatives to reduce its incidence.Aim and objectives:-To compare the cognitive functions of elderly nondiabetic subjects with that of elderly type 2 diabetes mellitus subjects using standard neuropsychological tests and to correlate with their blood sugar and lipid levels. Materials and methods:-The study was conducted in 60 participants in the age group of 58-65 years. Of these the case group comprised of 30 individuals with type 2 diabetes mellitus and the control group was formed by age, gender and education matched non-diabetic individuals. Blood samples were collected from all participants. After a brief screening test the participants were asked to take the neuropsychological test battery for evaluating their cognitive status. Comparison of the raw test scores of the cases and controls was done using the student"t" test.Results and conclusion:-The diabetes group showed poorer performance in all the cognitive function tests than the non-diabetes group with no correlation between blood glucose and cholesterol levels and the neuropsychological test scores of the patients. Hence, it can be concluded that periodical assessment of cognitive functions in diabetes clinics would be helpful in early identification and management of cases with cognitive impairment, which in turn can reverse the cognitive decline and prevent the development of dementias in these patients.

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Treadmill exercise increases cell proliferation in dentate gyrus of rats with streptozotocin-induced diabetes

Cited by 54 publications

References 22 publications

Glucose-Dependent Insulinotropic Polypeptide Is Expressed in Adult Hippocampus and Induces Progenitor Cell Proliferation

Glucose-Dependent Insulinotropic Polypeptide Is Expressed in Adult Hippocampus and Induces Progenitor Cell Proliferation

Insulin signaling effects on memory and mood

Cognitive Function-a Comparison Between Elderly Non Diabetic and Diabetic Subjects.

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