Cerebral ischemic damage in diabetes: an inflammatory perspective.

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diabetes mellitus 1 endocrinologydiseases
hyperglycemia 7 endocrinologydiseases
hypoglycemia 77 endocrinologydiseases
obesity 2 endocrinologydiseases

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diabetes mellitus 49665 and T2D [[275], [276]]. TLR ligands activate B cell cytokine production, most significantly IL-8, in diabetes mellitus vs. non-diabetic donors [[277]]. The circulating levels of danger molecules including the high-mobility
hyperglycemia 2697 use of insulin or other drugs, which stimulates insulin secretion, as the main treatment to prevent hyperglycemia and its long-term complications has resulted in an increase in the incidence of hypoglycemia in diabetic
hyperglycemia 8017 either by ischemic stroke or cardiovascular diseases (CVD) [[36], [37]]. In most animal studies, acute hyperglycemia immediately before or during ischemia exacerbates the ischemic brain injury [[38]–[41]]. Meta-analysis
hyperglycemia 46904 number of hypoglycemia episodes and the risk for developing dementia.Inflammatory response in diabetes/ hyperglycemia Increased systemic and cerebrovascular inflammation is one of the key pathophysiological features in
hyperglycemia 47229 multifactorial, chronic inflammation is thought to play a critical role [[255], [256]]. Key mechanisms of hyperglycemia -induced inflammation include NFkB-dependent production of proinflammatory cytokines, TLR expression,
hyperglycemia 48118 well as with TNF-α or IL-1 [[264]]. NFκB controls the induction of many inflammatory genes. During hyperglycemia , NFκB is rapidly and dramatically activated in vascular cells resulting in a subsequent increase in
hyperglycemia 48612 pathways, was reported in cultured astrocytes treated with high glucose [[265]]. Under diabetic conditions, hyperglycemia also causes inflammatory reactions in other organs and tissues in vivo [[266], [267]]. It has been reported
hyperglycemia 56843 higher following hyperglycemic ischemia than hyperglycemic shams [[321]]. Lin et al. demonstrated that hyperglycemia triggered early, massive deposition of neutrophils in the post-ischemic brain, which exacerbated injury
hypoglycemia 1333 neuroinflammation to increased cerebral ischemic damage in diabetics. We also describe the role of hypoglycemia in neuroinflammation and cerebral ischemic damage in diabetics. Understanding the role of neuroinflammatory
hypoglycemia 2546 stages is accompanied by failure of pancreatic β cells [[3], [4]].Glucose-lowering drugs and risk of hypoglycemia During the last decades, the intensive use of insulin or other drugs, which stimulates insulin secretion,
hypoglycemia 2791 prevent hyperglycemia and its long-term complications has resulted in an increase in the incidence of hypoglycemia in diabetic patients [[5]]. An intensively treated individual with T1D can experience up to 10 episodes
hypoglycemia 2923 patients [[5]]. An intensively treated individual with T1D can experience up to 10 episodes of symptomatic hypoglycemia per week and severe temporarily disabling hypoglycemia at least once a year (reviewed in [[6]]). In
hypoglycemia 2978 experience up to 10 episodes of symptomatic hypoglycemia per week and severe temporarily disabling hypoglycemia at least once a year (reviewed in [[6]]). In addition, an impaired counter-regulatory response results
hypoglycemia 3118 (reviewed in [[6]]). In addition, an impaired counter-regulatory response results in frequent episodes of hypoglycemia in diabetic patients [[7], [8]]. However, hypoglycemia becomes progressively more frequent, depending
hypoglycemia 3173 counter-regulatory response results in frequent episodes of hypoglycemia in diabetic patients [[7], [8]]. However, hypoglycemia becomes progressively more frequent, depending upon the history of hypoglycemia and the duration of
hypoglycemia 3253 [[7], [8]]. However, hypoglycemia becomes progressively more frequent, depending upon the history of hypoglycemia and the duration of insulin treatment [[9], [10]]. Hypoglycemia is estimated to account for about 2–4%
hypoglycemia 3553 continuous glucose monitoring (CGM) has revealed frequent and prolonged asymptomatic (glucose <65 mg/dl) hypoglycemia in almost 70% of patients [[12]]. A similar study in relatively older T1D patients observed that these
hypoglycemia 3689 patients [[12]]. A similar study in relatively older T1D patients observed that these patients experience hypoglycemia (glucose ≤70 mg/dl) for an average of 60–89 min/day, or 4–6% of the time [[13]].The increased
hypoglycemia 3818 ≤70 mg/dl) for an average of 60–89 min/day, or 4–6% of the time [[13]].The increased prevalence of hypoglycemia has also been noticed in a more recent study on T2D using the CGM system [[14]]. In this study on 108
hypoglycemia 4208 experienced at least one asymptomatic hypoglycemic episode during observation period. High prevalence of hypoglycemia (82% had at least one hypoglycemic event) has been noticed by another study that monitored T2D patients
hypoglycemia 4445 using the CGM system [[15]]. T2D patients are known to suffer from several episodes of asymptomatic hypoglycemia every week, symptomatic hypoglycemia as frequently as twice per week, and experience one episode of
hypoglycemia 4482 patients are known to suffer from several episodes of asymptomatic hypoglycemia every week, symptomatic hypoglycemia as frequently as twice per week, and experience one episode of severe (episodes that require assistance
hypoglycemia 4622 week, and experience one episode of severe (episodes that require assistance of another individual) hypoglycemia per year [[16]].Hypoglycemia is a threatening condition, as normal brain functioning is highly dependent
hypoglycemia 4809 functioning is highly dependent on a continuous supply of glucose from the blood [[17]]. Episodes of hypoglycemia can include symptoms such as warmth, weakness and fatigue, difficulty in thinking, confusion, behavioral
hypoglycemia 5022 behavioral changes, and emotional lability. Seizures and loss of consciousness are observed during severe hypoglycemia . In more severe cases, brain damage and even death are possible [[17]].The most common cause of hypoglycemia
hypoglycemia 5131 hypoglycemia. In more severe cases, brain damage and even death are possible [[17]].The most common cause of hypoglycemia is intensive glycemic control, the involuntary intake of excessive doses of insulin or other glucose-decreasing
hypoglycemia 5266 control, the involuntary intake of excessive doses of insulin or other glucose-decreasing drugs, or hypoglycemia unawareness [[16]]. Skipping meals, eating smaller meals, and having an irregular eating pattern are
hypoglycemia 5408 meals, eating smaller meals, and having an irregular eating pattern are also known risk factors for hypoglycemia . Children with T1D are at higher risk of hypoglycemia due to difficulty in insulin dosing, unpredictable
hypoglycemia 5462 eating pattern are also known risk factors for hypoglycemia. Children with T1D are at higher risk of hypoglycemia due to difficulty in insulin dosing, unpredictable activity and  eating patterns, and limitations
hypoglycemia 5590 difficulty in insulin dosing, unpredictable activity and  eating patterns, and limitations in detecting hypoglycemia in this population [[18]]. Variety of other factors such as aging, patients with vascular disease or
hypoglycemia 5795 disease or renal failure, pregnant women, and young T1D patients also contributes to the high risk of hypoglycemia [[5], [18]]. In T2D individuals, the risk of hypoglycemia gradually increases due to progressive insulin
hypoglycemia 5853 patients also contributes to the high risk of hypoglycemia [[5], [18]]. In T2D individuals, the risk of hypoglycemia gradually increases due to progressive insulin deficiency, longer duration of diabetes, and tight glycemic
hypoglycemia 6355 extracellular overflow of excitatory amino acids produced by the brain itself [[20], [21]]. Severe hypoglycemia can lead to brain damage when accompanied by the silencing of the brain activity (electroencephalographic
hypoglycemia 6816 also been reported in diabetic children and adults with poor glycemic control after experiencing acute hypoglycemia [[25]–[28]]. Although moderate hypoglycemia is not life-threatening, if recurrent, it may have serious
hypoglycemia 6862 adults with poor glycemic control after experiencing acute hypoglycemia [[25]–[28]]. Although moderate hypoglycemia is not life-threatening, if recurrent, it may have serious clinical implications. The presence of oxidative
hypoglycemia 7016 may have serious clinical implications. The presence of oxidative stress and neuronal death during hypoglycemia has been documented previously by several investigators [[29]–[31]]. Hypoglycemia can also activate
hypoglycemia 7448 diabetes. Many health issues stem from this disease including heart disease, increased risk of stroke, hypoglycemia , vision loss, kidney failure, amputations, and complications within the central nervous system (CNS)
hypoglycemia 9157 accounting for about 87% of all strokes [[47]]. Ischemia leads to irreversible brain damage. In addition, hypoglycemia and diabetes have been reported to aggravate damage following cerebrovascular disorder owing to the
hypoglycemia 10274 hypoglycemic conditions)Thus, it is important to understand how neuroinflammatory mediators following hypoglycemia and diabetes-associated cerebral ischemia produce irreversible CNS injury. This will provide a basis
hypoglycemia 41144 studies. These could be potential targets for future studies focusing on therapeutic approach.Diabetes and hypoglycemia Severe hypoglycemia is considered a medical emergency as it causes organ and brain damage. The types
hypoglycemia 41163 potential targets for future studies focusing on therapeutic approach.Diabetes and hypoglycemiaSevere hypoglycemia is considered a medical emergency as it causes organ and brain damage. The types of symptoms that depend
hypoglycemia 41309 as it causes organ and brain damage. The types of symptoms that depend on duration and severity of hypoglycemia includes autonomic symptoms (sweating, irritability, and tremulousness), cognitive impairment, seizures,
hypoglycemia 41533 coma. Brain damage, trauma, cardiovascular complications, and death are major complications of severe hypoglycemia [[223]]. The incidence of hypoglycemia depends on the degree of glycemic control. Threefold increase
hypoglycemia 41572 cardiovascular complications, and death are major complications of severe hypoglycemia [[223]]. The incidence of hypoglycemia depends on the degree of glycemic control. Threefold increase in incidences of severe hypoglycemia and
hypoglycemia 41671 hypoglycemia depends on the degree of glycemic control. Threefold increase in incidences of severe hypoglycemia and coma in intensively treated group was observed when compared to conventionally treated group in
hypoglycemia 41873 treated group in the Action to Control Cardiovascular Risk in Diabetes (ACCORD) study [[224]].The risk of hypoglycemia in randomized controlled trials of glucose regulation in stroke settings has been reported ranging from
hypoglycemia 42066 been reported ranging from 7 to 76% [[225]–[230]]. The ischemic brain is particularly susceptible to hypoglycemia [[231]]. In the presence of stroke, it is possible that incidents of hypoglycemia may be mistaken for
hypoglycemia 42148 particularly susceptible to hypoglycemia [[231]]. In the presence of stroke, it is possible that incidents of hypoglycemia may be mistaken for progressing severity of stroke, given that symptoms of hypoglycemia include impaired
hypoglycemia 42236 incidents of hypoglycemia may be mistaken for progressing severity of stroke, given that symptoms of hypoglycemia include impaired cognitive functioning, hemiparesis, seizures, and coma.Hypoglycemia is proposed to
hypoglycemia 42728 damage [[237]], presenting several potential mechanisms through which acute and chronic episodes of hypoglycemia may increase CVD risk.Increased levels of C-reactive protein (CRP), IL-6, IL-8, TNF-α, and endothelin-1
hypoglycemia 42869 risk.Increased levels of C-reactive protein (CRP), IL-6, IL-8, TNF-α, and endothelin-1 have been shown during hypoglycemia [[238], [239]]. Wright et al. [[240]] and Gogitidze Joy et al. [[32]] confirmed that hypoglycemia induced
hypoglycemia 42967 during hypoglycemia [[238], [239]]. Wright et al. [[240]] and Gogitidze Joy et al. [[32]] confirmed that hypoglycemia induced an increase in proinflammatory mediators and platelet activation, and has an inhibitory effect
hypoglycemia 43418 increased risk for CVD events [[241]]. Furthermore, IL-1 has been shown to increase the severity of hypoglycemia [[242]]. Moderate hypoglycemia acutely increases circulating levels of plasminogen activator inhibitor-1
hypoglycemia 43449 [[241]]. Furthermore, IL-1 has been shown to increase the severity of hypoglycemia [[242]]. Moderate hypoglycemia acutely increases circulating levels of plasminogen activator inhibitor-1 (PAI-1), VEGF, vascular adhesion
hypoglycemia 43713 and markers of platelet activation (P-selectin) in T1D patients and healthy individuals [[32]]. Thus, hypoglycemia can result in complex vascular effects including activation of prothrombotic, proinflammatory, and proatherogenic
hypoglycemia 44080 death in T1D patients without CVD, also known as “dead in bed” syndrome [[243]].Recurrent severe hypoglycemia results in brain damage [[244]], with preferential vulnerability in the cerebral cortex and hippocampus
hypoglycemia 44268 cerebral cortex and hippocampus [[244]–[246]]. Evidence suggests that neuronal damage resulting from hypoglycemia is enhanced in diabetic compared to non-diabetic brains [[245]]. Hypoglycemia causes a loss of ionic
hypoglycemia 44488 homeostasis or increase in ROS that can further lead to neuronal inflammation and death [[246]].Impact of hypoglycemia in the diabetic brainHypoglycemia is of major concern in diabetes as it leads to severe impairment of
hypoglycemia 44645 major concern in diabetes as it leads to severe impairment of CNS function. Severe and/or long duration hypoglycemia may result in severe morbidity and even death. Repeated episodes of hypoglycemia are suggested to increase
hypoglycemia 44726 and/or long duration hypoglycemia may result in severe morbidity and even death. Repeated episodes of hypoglycemia are suggested to increase the risk of atherosclerosis [[247]]. Acute hypoglycemia results in endothelial
hypoglycemia 44808 Repeated episodes of hypoglycemia are suggested to increase the risk of atherosclerosis [[247]]. Acute hypoglycemia results in endothelial dysfunction, vasoconstriction, white blood cell activation, and release of inflammatory
hypoglycemia 45144 All these changes increase the risk of myocardial and cerebral ischemia [[240]].Recurrent/moderate hypoglycemia also aggravates post-ischemic brain damage in diabetic rats [[53]]. In this study, rats treated with
hypoglycemia 45427 44% increase in neuronal death compared with rats similarly treated with insulin but not exposed to hypoglycemia , demonstrating that prior exposure to recurrent hypoglycemia can lead to more extensive cerebral ischemic
hypoglycemia 45488 treated with insulin but not exposed to hypoglycemia, demonstrating that prior exposure to recurrent hypoglycemia can lead to more extensive cerebral ischemic damage. Relatively severe recurrent hypoglycemia itself
hypoglycemia 45582 recurrent hypoglycemia can lead to more extensive cerebral ischemic damage. Relatively severe recurrent hypoglycemia itself induces neuronal death in the CA1 hippocampus and cortex of streptozotocin-induced diabetic rats
hypoglycemia 45780 streptozotocin-induced diabetic rats [[248], [249]].Bree and collaborators [[245]] showed that insulin-induced severe hypoglycemia in normal animals elicits brain damage in the cortex, cornus ammonis (CA)1, and CA3 hippocampal regions,
hypoglycemia 46099 areas. These results suggest that diabetes can be a critical factor aggravating neuronal damage in hypoglycemia .Decreased cognitive function can also lead to an increased risk of hypoglycemia and CVD events, and
hypoglycemia 46179 neuronal damage in hypoglycemia.Decreased cognitive function can also lead to an increased risk of hypoglycemia and CVD events, and thus mortality [[250]]. In a study examining magnetic resonance imaging of the brain
hypoglycemia 46540 hypoglycemic episodes [[251]]. In some of the strongest evidence to date of the detrimental effects of hypoglycemia on cognitive function, Whitmer et al. [[252]] investigated the association of hospitalization or emergency
hypoglycemia 46682 Whitmer et al. [[252]] investigated the association of hospitalization or emergency department visits for hypoglycemia and dementia development in older adults with T2D. They reported a dose/response relationship between
hypoglycemia 46811 development in older adults with T2D. They reported a dose/response relationship between the number of hypoglycemia episodes and the risk for developing dementia.Inflammatory response in diabetes/hyperglycemiaIncreased
hypoglycemia 51237 impairment of insulin signaling and inhibition of glucose tolerance in mice [[282]].Inflammatory response in hypoglycemia Recurrent/moderate hypoglycemia induces oxidative injury in hippocampal dendrites, and microglial activation
hypoglycemia 51268 inhibition of glucose tolerance in mice [[282]].Inflammatory response in hypoglycemiaRecurrent/moderate hypoglycemia induces oxidative injury in hippocampal dendrites, and microglial activation in hippocampus and cerebral
hypoglycemia 51768 hypoglycemia-exposed diabetic rats was 194% higher than in normoglycemic rats exposed to recurrent/moderate hypoglycemia [[248]]. This study confirmed that inflammatory responses are also induced after recurrent/moderate
hypoglycemia 51881 [[248]]. This study confirmed that inflammatory responses are also induced after recurrent/moderate hypoglycemia . Microglial activation is induced in severe hypoglycemia and contributes to neuronal injury by releasing
hypoglycemia 51938 are also induced after recurrent/moderate hypoglycemia. Microglial activation is induced in severe hypoglycemia and contributes to neuronal injury by releasing neurotoxic substances, including superoxide, nitric
hypoglycemia 52298 in turn contributes to brain damage [[286], [287]]. Increased number of infiltrating neutrophils in hypoglycemia vulnerable brain regions following hypoglycemic brain injury suggests its potential role in hypoglycemic
hypoglycemia 52491 potential role in hypoglycemic brain injury [[288]].In another study by Cardoso et al. [[289]], recurrent hypoglycemia (twice daily for 2 weeks) in streptozotocin-induced diabetic rats potentiated an increase in lipid
hypoglycemia 52772 of oxidative stress, in mitochondria from diabetic animals. Previous findings showed that recurrent hypoglycemia differentially alters mitochondrial bioenergetics and the antioxidant defense response in the cortex
hypoglycemia 63163 SDF-1α/CXCR-4 is a potential target for promoting repair in wound and ischemic injury.Overall, diabetes and hypoglycemia aggravates brain damage after ischemic stroke through enhancement of the neuroinflammatory signaling
hypoglycemia 63952 patients with diabetes is two- to sixfold higher than age-matched controls. Increased incidence of hypoglycemia is the inevitable effect of treatment for aggressively tight glycemic control in diabetes, and is prevalent
hypoglycemia 64158 and is prevalent among both T1D and T2D patients. Studies have shown that diabetes and its associated hypoglycemia exacerbate cerebral ischemic damage in experimental animals. Understanding the mechanisms involved in
hypoglycemia 64365 involved in aggravating neuroinflammatory injury following cerebral ischemia in diabetes and associated hypoglycemia is important. Suppressing potential candidates involved in enhancing neuroinflammatory response may
hypoglycemia 64941 important. Better understanding of inflammatory pathways involved in diabetes, diabetes-associated hypoglycemia , and diabetic cerebral ischemia may provide unique pharmacological targets for the treatment and/or
hypoglycemia 65068 cerebral ischemia may provide unique pharmacological targets for the treatment and/or prevention of hypoglycemia and diabetes-associated stroke damage
obesity 50320 inflammasome leads to the maturation and secretion of IL-1β and is involved in the pathogenic mechanisms of obesity -induced inflammation, insulin resistance, and diabetes development [[280]]. Obesity-induced danger signals
obesity 50941 macrophage-T cell interactions that are associated with sustained levels of chronic inflammation in obesity -induced metabolic diseases [[281]]. Moreover, the saturated fatty acid palmitate induces activation

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