Insulin Neuroprotection and the Mechanisms

Yu, Liyun; Pei, Yu

doi:10.4103/0366-6999.154323

Cited by 24 publications

(16 citation statements)

References 67 publications

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“…Insulin modulates neurotransmitter release [ 60 ], neuronal cell survival [ 61 ], and synaptic plasticity [ 62 ] and it improves cognition and memory function in the brain[ 63 64 ]. Insulin resistance in the brain is defined as decreased uptake of insulin into the brain, leading to the dysregulation of amyloid beta level and inflammation [ 65 ].…”

Section: Pgc-1α Insulin Resistance and Cognitive Dysfunction In Admentioning

confidence: 99%

The association between PGC-1α and Alzheimer's disease

Sweeney

Song

2016

Anat Cell Biol

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Alzheimer's disease (AD) is a neurodegenerative disorder and its reported pathophysiological features in the brain include the deposition of amyloid beta peptide, chronic inflammation, and cognitive impairment. The incidence of AD is increasing worldwide and researchers have studied various aspects of AD pathophysiology in order to improve our understanding of the disease. Thus far, the onset mechanisms and means of preventing AD are completely unknown. Peroxisome proliferator-activated receptor-γ coactivator (PGC-1α) is a protein related to various cellular mechanisms that lead to the alteration of downstream gene regulation. It has been reported that PGC-1α could protect cells against oxidative stress and reduce mitochondrial dysfunction. Moreover, it has been demonstrated to have a regulatory role in inflammatory signaling and insulin sensitivity related to cognitive function. Here, we present further evidence of the involvement of PGC-1α in AD pathogenesis. Clarifying the relationship between PGC-1α and AD pathology might highlight PGC-1α as a possible target for therapeutic intervention in AD.

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Section: Pgc-1α Insulin Resistance and Cognitive Dysfunction In Admentioning

confidence: 99%

The association between PGC-1α and Alzheimer's disease

Sweeney

Song

2016

Anat Cell Biol

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“…Neuroprotective roles of insulin have been outlined in previous reviews. 78 According to the results summarized in Table 5 , the DC brains had lower insulin levels. Similar findings have been obtained in other rat models of diabetes.…”

Section: Discussionmentioning

confidence: 99%

Improvement of spatial learning and memory, cortical gyrification patterns and brain oxidative stress markers in diabetic rats treated with Ficus deltoidea leaf extract and vitexin

Nurdiana

Goh

Ahmad

et al. 2018

Journal of Traditional and Complementary Medicine

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Despite the fact that Ficus deltoidea and vitexin played important roles in controlling hyperglycemia, an effective mitigation strategy dealing with cognitive deficit observed in diabetes, little is known about its neuroprotective effects. The study is aimed to determine changes in behavioral, gyrification patterns and brain oxidative stress markers in streptozotocin (STZ)-induced diabetic rats following F. deltoidea and vitexin treatments. Diabetic rats were treated orally with metformin, methanolic extract of F. deltoidea leaves and vitexin for eight weeks. Morris water maze (MWM) test was performed to evaluate learning and memory functions. The patterns of cortical gyrification were subsequently visualized using micro-computed tomography (micro-CT). Quantification of brain oxidative stress biomarkers, insulin, amylin as well as serum testosterone were measured using a spectrophotometer. The brain fatty acid composition was determined using gas chromatography (GC). Biochemical variation in brain was estimated using Fourier transform infrared (FT-IR) spectroscopy. Results showed that oral administration of F. deltoidea extract and vitexin to diabetic rats attenuated learning and memory impairment, along with several clusters of improved gyrification. Both treatments also caused a significant increase in the superoxide dismutase (SOD) and glutathione peroxidase (GPx) values, as well as a significant reduction of TBARS. Strikingly, improvement of cortical gyrification, spatial learning and memory are supported by serum testosterone levels, fatty acid composition of brain and FT-IR spectra.

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“…The results of this correlation reinforce the assumption that the smaller the GCS value or the worse the awareness of the acute traumatic SDH patient, the higher the blood lactate level and the blood glucose level of the acute traumatic SDH patient, so that the GCS of the acute traumatic SDH patient can reflect an increase in blood lactate levels and blood glucose levels; due to hyperglycolysis and glucose metabolic disorders that occur. 5,7,8,17,18 The next correlation analysis was the operation time interval with preoperative blood lactate levels which showed a very weak positive correlation. Meanwhile, the correlation analysis of the operation time interval with the preoperative blood glucose level also showed a weak positive correlation.…”

Section: Discussionmentioning

confidence: 99%

“…that occurs and the duration of glucose metabolic disorders and hyperglycolysis that occurs so as to produce large amounts of lactate. [6][7][8]17 The correlation of SDH hematoma thickness and preoperative blood lactate levels showed a strong positive correlation. Meanwhile, the correlation between SDH thickness and preoperative blood glucose levels showed a moderate (moderate) positive correlation.…”

Section: Discussionmentioning

confidence: 99%

Correlation between Head Computed Tomography Scan, Pre-operative Blood Lactate, and Pre-operative Glucose Level in Acute Traumatic Subdural Hematoma

Henky

Faried

2021

mkb

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Acute traumatic subdural hematoma (SDH) is a focal brain injury resulting in alteration of cerebral perfusion and glucose metabolism, which would also results in hyperglicemia-induced-hyperlactatemia. A cross-sectional study was performed to analyze acute traumatic SDH patients by head CT scan and observe the effect on pre-operative blood lactate and blood glucose levels in 40 acute traumatic SDH patients at Dr. Hasan Sadikin Hospital, Bandung, Indonesia during the period of July-September 2013. Somers' D correlation were used in the analysis with a p-value of ≤0.05 considered as significant with 95% confidence interval. The mean values of pre-operative blood lactate and blood glucose levels were 3.16±1.49 mmol/L and 155.85±32.95 mg/dl, respectively with a strong positive correlation between the hematoma thickness and the increase in blood lactate (r= 0.656; p= 0.021) and a moderate positive correlation with increased blood glucose (r= 0.556; p= 0.025). In addition, the compressed cistern also had a very weak positive correlation with increase in blood lactate (r =0.156; p=0.043) and very weak positive correlation with increase in blood glucose (r= 0.139; p=0.056) while the midline shift had a weak positive correlation with increased blood lactate (r=0.353; p= 0.041) and a weak positive correlation with increased blood glucose (r = 0.333; p= 0.046). In conclusion, increased hematoma thickness, compressed cistern, and midline shift seen on head CT scan correlate with increasing blood lactate and glucose levels in acute traumatic SDH. Head CT scan, blood lactate level, and blood glucose level can be considered as one of the routine examinations to determine acute traumatic SDH severity at the macroscopic and cellular level.

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Insulin Neuroprotection and the Mechanisms

Cited by 24 publications

References 67 publications

The association between PGC-1α and Alzheimer's disease

The association between PGC-1α and Alzheimer's disease

Improvement of spatial learning and memory, cortical gyrification patterns and brain oxidative stress markers in diabetic rats treated with Ficus deltoidea leaf extract and vitexin

Correlation between Head Computed Tomography Scan, Pre-operative Blood Lactate, and Pre-operative Glucose Level in Acute Traumatic Subdural Hematoma

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