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brain insulin resistance

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https://www.readbyqxmd.com/read/28105773/exosomal-biomarkers-of-brain-insulin-resistance-associated-with-regional-atrophy-in-alzheimer-s-disease
#1
Roger J Mullins, Maja Mustapic, Edward J Goetzl, Dimitrios Kapogiannis
: Brain insulin resistance (IR), which depends on insulin-receptor-substrate-1 (IRS-1) phosphorylation, is characteristic of Alzheimer's disease (AD). Previously, we demonstrated higher pSer312-IRS-1 (ineffective insulin signaling) and lower p-panTyr-IRS-1 (effective insulin signaling) in neural origin-enriched plasma exosomes of AD patients vs. CONTROLS: Here, we hypothesized that these exosomal biomarkers associate with brain atrophy in AD. We studied 24 subjects with biomarker-supported probable AD (low CSF Aβ42 )...
January 20, 2017: Human Brain Mapping
https://www.readbyqxmd.com/read/28102395/sesamol-ameliorates-high-fat-and-high-fructose-induced-cognitive-defects-via-improving-insulin-signaling-disruption-in-the-central-nervous-system
#2
Zhigang Liu, Yali Sun, Qinglian Qiao, Tong Zhao, Wentong Zhang, Bo Ren, Qian Liu, Xuebo Liu
Sesamol, a nutritional component from sesame, possesses antioxidant, lipid lowering and antidepressant activities. Nonetheless, few studies report its effects on high-energy-dense diet-induced cognitive loss. The present research aimed to elucidate the action of sesamol on high-fat and high-fructose (HFFD) "western"-diet-induced central nervous system insulin resistance and learning and memory impairment, and further determined the possible underlying mechanism. 3 month-old C57BL/6J mice were divided into 3 groups with/without sesamol in the drinking water (0...
January 19, 2017: Food & Function
https://www.readbyqxmd.com/read/28094952/effect-of-an-enhanced-nose-to-brain-delivery-of-insulin-on-mild-and-progressive-memory-loss-in-the-senescence-accelerated-mouse
#3
Noriyasu Kamei, Misa Tanaka, Hayoung Choi, Nobuyuki Okada, Takamasa Ikeda, Rei Itokazu, Mariko Takeda-Morishita
Insulin is now considered to be a new drug candidate for treating dementias, such as Alzheimer's disease, whose pathologies are linked to insulin resistance in the brain. Our recent work has clarified that a noncovalent strategy involving cell-penetrating peptides (CPPs) can increase the direct transport of insulin from the nasal cavity into the brain parenchyma. The present study aimed to determine whether the brain insulin level increased by intranasal coadministration of insulin with the CPP penetratin has potential for treating dementia...
January 17, 2017: Molecular Pharmaceutics
https://www.readbyqxmd.com/read/28093305/role-of-leptin-in-conditioned-place-preference-to-high-fat-diet-in-leptin-deficient-ob-ob-mice
#4
Yoshiyuki Shimizu, Cheol Son, Daisuke Aotani, Hidenari Nomura, Takatoshi Hikida, Kiminori Hosoda, Kazuwa Nakao
Leptin is an adipocyte-derived anorexic hormone that exerts its effects via the hypothalamus and other brain regions, including the reward system. Leptin-deficient ob/ob mice that present morbid obesity, hyperphagia, insulin resistance, and infertility are one of the most investigated mouse models of obesity. Conditioned place preference (CPP) paradigm is a standard behavioral model to evaluate the rewarding value of substrates. While leptin is reported to decrease the CPP of lean mice for high fat diet (HFD), it is unknown how CPP toward HFD is affected by leptin replacement in the pathophysiological condition of ob/ob mice...
January 13, 2017: Neuroscience Letters
https://www.readbyqxmd.com/read/28093279/obesity-and-insulin-resistance-are-associated-with-reduced-activity-in-core-memory-regions-of-the-brain
#5
Lucy G Cheke, Heidi M Bonnici, Nicola S Clayton, Jon S Simons
Increasing research in animals and humans suggests that obesity may be associated with learning and memory deficits, and in particular with reductions in episodic memory. Rodent models have implicated the hippocampus in obesity-related memory impairments, but the neural mechanisms underlying episodic memory deficits in obese humans remain undetermined. In the present study, lean and obese human participants were scanned using fMRI while completing a What-Where-When episodic memory test (the "Treasure-Hunt Task") that assessed the ability to remember integrated item, spatial, and temporal details of previously encoded complex events...
January 16, 2017: Neuropsychologia
https://www.readbyqxmd.com/read/28093241/new-isatin-derivative-inhibits-neurodegeneration-by-restoring-insulin-signaling-in-brain
#6
Meha Fatima Aftab, Shabbir Khan Afridi, Uzma Rasool Mughal, Aneela Karim, Darakhshan Jabeen Haleem, Nurul Kabir, Khalid M Khan, Rahman M Hafizur, Rizwana S Waraich
Diabetes is associated with neurodegeneration. Glycation ensues in diabetes and glycated proteins cause insulin resistance in brain resulting in amyloid plaques and NFTs. Also glycation enhances gliosis by promoting neuroinflammation. Currently there is no therapy available to target neurodegenration in brain therefore, development of new therapy that offers neuroprotection is critical. The objective of this study was to evaluate mechanistic effect of isatin derivative URM-II-81, an anti-glycation agent for improvement of insulin action in brain and inhibition of neurodegenration...
January 13, 2017: Journal of Chemical Neuroanatomy
https://www.readbyqxmd.com/read/28092161/estimation-of-ellagic-acid-and-or-repaglinide-effects-on-insulin-signaling-oxidative-stress-and-inflammatory-mediators-of-liver-pancreas-adipose-tissue-and-brain-in-insulin-resistant-type-2-diabetic-rats
#7
Mohamed M Amin, Mahmoud S Arbid
Even though ellagic acid has previously been valued in many models of cancer, so far its full mechanistic effect as a natural antiapoptotic agent in the prevention of type 2 diabetes complications has not been completely elucidated, which was the goal of this study. We fed albino rats a high-fat fructose diet (HFFD) for 2 months to induce insulin resistance/type 2 diabetes and then treated the rats with ellagic acid (10 mg/kg body weight, orally) and/or repaglinide (0.5 mg/kg body weight, orally) for 2 weeks...
October 21, 2016: Applied Physiology, Nutrition, and Metabolism, Physiologie Appliquée, Nutrition et Métabolisme
https://www.readbyqxmd.com/read/28050343/brain-insulin-resistance-deteriorates-cognition-by-altering-the-topological-features-of-brain-networks
#8
Fan Su, Hao Shu, Qing Ye, Zan Wang, Chunming Xie, Baoyu Yuan, Zhijun Zhang, Feng Bai
Insulin resistance represents one of the mechanisms underlying the link between type 2 diabetes (T2D) and Alzheimer's disease (AD), and we explored its in vivo neurobiology related to cognition based on a pathway-based genetic association analyses. Eighty-seven mild cognitive impairment (MCIs) subjects and 135 matched controls (HCs) were employed at baseline, and they underwent functional MRI scans, clinical evaluations and exon sequencings of 20 genes related to brain insulin resistance. A longitudinal study for an average of 35 months was performed to assess their cognitive decline over time...
2017: NeuroImage: Clinical
https://www.readbyqxmd.com/read/28049397/insulin-resistance-in-alzheimer-disease-p53-and-micrornas-as-important-players
#9
Kazimierz Gąsiorowski, Barbara Brokos, Jerzy Leszek, Ghulam Md Ashraf, Gjumrakch Aliev
Glucose homeostasis is crucial for neuronal survival, synaptic plasticity, and is indispensable for learning and memory. Reduced sensitivity of cells to insulin and impaired insulin signaling in brain neurons participate in the pathogenesis of Alzheimer disease (AD). The tumor suppressor protein p53 coordinates with multiple cellular pathways in response to DNA damage and cellular stresses. However, prolonged stress conditions unveil deleterious effects of p53-evoked insulin resistance in neurons; enhancement of transcription of pro-oxidant factors, accumulation of toxic metabolites (e...
January 3, 2017: Current Topics in Medicinal Chemistry
https://www.readbyqxmd.com/read/28049395/type-3-diabetes-mellitus-a-novel-implication-of-alzheimer-disease
#10
Jerzy Leszek, Elżbieta Trypka, Vadim V Tarasov, Ghulam Md Ashraf, Gjumrakch Aliev
The brain of patients with Alzheimer disease (AD) showed the evidence of reduced expression of insulin and neuronal insulin receptors, as compared with those of age-matched controls. This event gradually and certainly leads to a breakdown of the entire insulin-signaling pathway, which manifests insulin resistance. This in turn affects brain metabolism and cognitive functions, which are the best-documented abnormalities in AD. These observations led Dr. de la Monte and her colleagues to suggest that AD is actually a neuroendocrine disorder that resembles type 2 diabetes mellitus...
3, 2017: Current Topics in Medicinal Chemistry
https://www.readbyqxmd.com/read/28045402/inflammatory-mechanisms-linking-obesity-and-metabolic-disease
#11
Alan R Saltiel, Jerrold M Olefsky
There are currently over 1.9 billion people who are obese or overweight, leading to a rise in related health complications, including insulin resistance, type 2 diabetes, cardiovascular disease, liver disease, cancer, and neurodegeneration. The finding that obesity and metabolic disorder are accompanied by chronic low-grade inflammation has fundamentally changed our view of the underlying causes and progression of obesity and metabolic syndrome. We now know that an inflammatory program is activated early in adipose expansion and during chronic obesity, permanently skewing the immune system to a proinflammatory phenotype, and we are beginning to delineate the reciprocal influence of obesity and inflammation...
January 3, 2017: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/28043897/natural-products-against-alzheimer-s-disease-pharmaco-therapeutics-and-biotechnological-interventions
#12
REVIEW
Abhijit Dey, Raktim Bhattacharya, Anuradha Mukherjee, Devendra Kumar Pandey
Alzheimer's disease (AD) is a severe, chronic and progressive neurodegenerative disease associated with memory and cognition impairment ultimately leading to death. It is the commonest reason of dementia in elderly populations mostly affecting beyond the age of 65. The pathogenesis is indicated by accumulation of the amyloid-beta (Aβ) plaques and neurofibrillary tangles (NFT) in brain tissues and hyperphosphorylation of tau protein in neurons. The main cause is considered to be the formation of reactive oxygen species (ROS) due to oxidative stress...
December 30, 2016: Biotechnology Advances
https://www.readbyqxmd.com/read/28041819/circulating-tricarboxylic-acid-cycle-metabolite-levels-in-citrin-deficient-children-with-metabolic-adaptation-with-and-without-sodium-pyruvate-treatment
#13
Hironori Nagasaka, Haruki Komatsu, Ayano Inui, Mariko Nakacho, Ichiro Morioka, Hirokazu Tsukahara, Shunsaku Kaji, Satoshi Hirayama, Takashi Miida, Hiroki Kondou, Kenji Ihara, Mariko Yagi, Zenro Kizaki, Kazuhiko Bessho, Takahiro Kodama, Kazumoto Iijima, Takeyori Saheki, Tohru Yorifuji, Akira Honda
Citrin deficiency causes adult-onset type II citrullinemia (CTLN-2), which later manifests as severe liver steatosis and life-threatening encephalopathy. Long-standing energy deficit of the liver and brain may predispose ones to CTLN-2. Here, we compared the energy-driving tricarboxylic acid (TCA) cycle and fatty acid β-oxidation cycle between 22 citrin-deficient children (age, 3-13years) with normal liver functions and 37 healthy controls (age, 5-13years). TCA cycle analysis showed that basal plasma citrate and α-ketoglutarate levels were significantly higher in the affected than the control group (p<0...
December 24, 2016: Molecular Genetics and Metabolism
https://www.readbyqxmd.com/read/28039490/impaired-fasting-blood-glucose-is-associated-to-cognitive-impairment-and-cerebral-atrophy-in-middle-aged-non-human-primates
#14
Fathia Djelti, Marc Dhenain, Jérémy Terrien, Jean-Luc Picq, Isabelle Hardy, Delphine Champeval, Martine Perret, Esther Schenker, Jacques Epelbaum, Fabienne Aujard
Age-associated cognitive impairment is a major health and social issue because of increasing aged population. Cognitive decline is not homogeneous in humans and the determinants leading to differences between subjects are not fully understood. In middle-aged healthy humans, fasting blood glucose levels in the upper normal range are associated with memory impairment and cerebral atrophy. Due to a close evolutional similarity to Man, non-human primates may be useful to investigate the relationships between glucose homeostasis, cognitive deficits and structural brain alterations...
December 28, 2016: Aging
https://www.readbyqxmd.com/read/28035937/mtorc2-rictor-in-alzheimer-s-disease-and-reversal-of-amyloid-%C3%AE-expression-induced-insulin-resistance-and-toxicity-in-rat-primary-cortical-neurons
#15
Han-Kyu Lee, Bumsup Kwon, Cynthia A Lemere, Suzanne de la Monte, Kyohei Itamura, Austin Y Ha, Henry W Querfurth
Mammalian target of rapamycin complex 1 (mTORC1), a nutrient sensor and central controller of cell growth and proliferation, is altered in various models of Alzheimer's disease (AD). Even less studied or understood in AD is mammalian target of rapamycin complex 2 (mTORC2) that influences cellular metabolism, in part through the regulations of Akt/PKB and SGK. Dysregulation of insulin/PI3K/Akt signaling is another important feature of AD pathogenesis. We found that both total mTORC1 and C2 protein levels and individual C1 and C2 enzymatic activities were decreased in human AD brain samples...
December 30, 2016: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/28034760/insulin-resistance-in-alzheimer-s-disease
#16
REVIEW
Thomas Diehl, Roger Mullins, Dimitrios Kapogiannis
The links between systemic insulin resistance (IR), brain-specific IR, and Alzheimer's disease (AD) has been an extremely productive area of current research. This review will cover the fundamentals and pathways leading to IR, its connection to AD via cellular mechanisms, the most prominent methods and models used to examine it, an introduction to the role of extracellular vesicles (EVs) as a source of biomarkers for IR and AD, and an overview of modern clinical studies on the subject. To provide additional context, we also present a novel analysis of the spatial correlation of gene expression in the brain with the aid of Allen Human Brain Atlas data...
December 13, 2016: Translational Research: the Journal of Laboratory and Clinical Medicine
https://www.readbyqxmd.com/read/28027925/impact-of-prebiotics-on-metabolic-and-behavioral-alterations-in-a-mouse-model-of-metabolic-syndrome
#17
Lourdes Fernández de Cossío, Célia Fourrier, Julie Sauvant, Amandine Everard, Lucile Capuron, Patrice D Cani, Sophie Layé, Nathalie Castanon
Mounting evidence shows that the gut microbiota, an important player within the gut-brain communication axis, can affect metabolism, inflammation, brain function and behavior. Interestingly, gut microbiota composition is known to be altered in patients with metabolic syndrome (MetS), who also often display neuropsychiatric symptoms. The use of prebiotics, which beneficially alters the microbiota, may therefore be a promising way to potentially improve physical and mental health in MetS patients. This hypothesis was tested in a mouse model of MetS, namely the obese and type-2 diabetic db/db mice, which display emotional and cognitive alterations associated with changes in gut microbiota composition and hippocampal inflammation compared to their lean db/+ littermates...
December 24, 2016: Brain, Behavior, and Immunity
https://www.readbyqxmd.com/read/27995280/dietary-fructose-as-a-risk-factor-for-non-alcoholic-fatty-liver-disease-nafld
#18
REVIEW
Salamah Mohammad Alwahsh, Rolf Gebhardt
Glucose is a major energy source for the entire body, while fructose metabolism occurs mainly in the liver. Fructose consumption has increased over the last decade globally and is suspected to contribute to the increased incidence of non-alcoholic fatty liver disease (NAFLD). NAFLD is a manifestation of metabolic syndrome affecting about one-third of the population worldwide and has progressive pathological potential for liver cirrhosis and cancer through non-alcoholic steatohepatitis (NASH). Here we have reviewed the possible contribution of fructose to the pathophysiology of NAFLD...
December 19, 2016: Archives of Toxicology
https://www.readbyqxmd.com/read/27990361/upregulated-inflammatory-associated-factors-and-blood-retinal-barrier-changes-in-the-retina-of-type-2-diabetes-mellitus-model
#19
Rui-Jin Ran, Xiao-Ying Zheng, Li-Ping Du, Xue-Dong Zhang, Xiao-Li Chen, Shen-Yin Zhu
AIM: To examine the expression of high mobility group box-1 (HMGB-1) and intercellular adhesion molecule-1 (ICAM-1) in the retina and the hippocampal tissues; and further to evaluate the association of these two molecules with the alterations of blood-retinal barrier (BRB) and blood-brain barrier (BBB) in a rat model of type 2 diabetes. METHODS: The type-2 diabetes mellitus (DM) model was established with a high-fat and high-glucose diet combined with streptozotocin (STZ)...
2016: International Journal of Ophthalmology
https://www.readbyqxmd.com/read/27988872/insulin-resistance-and-neurodegeneration-progress-towards-the-development-of-new-therapeutics-for-alzheimer-s-disease
#20
REVIEW
Suzanne M de la Monte
Alzheimer's disease (AD) should be regarded as a degenerative metabolic disease caused by brain insulin resistance and deficiency, and overlapping with the molecular, biochemical, pathophysiological, and metabolic dysfunctions in diabetes mellitus, non-alcoholic fatty liver disease, and metabolic syndrome. Although most of the diagnostic and therapeutic approaches over the past several decades have focused on amyloid-beta (Aβ42) and aberrantly phosphorylated tau, which could be caused by consequences of brain insulin resistance, the broader array of pathologies including white matter atrophy with loss of myelinated fibrils and leukoaraiosis, non-Aβ42 microvascular disease, dysregulated lipid metabolism, mitochondrial dysfunction, astrocytic gliosis, neuro-inflammation, and loss of synapses vis-à-vis growth of dystrophic neurites, is not readily accounted for by Aβ42 accumulations, but could be explained by dysregulated insulin/IGF-1 signaling with attendant impairments in signal transduction and gene expression...
December 17, 2016: Drugs
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