DIABETIC ENCEPHALOPATHY IN TYPE 2 DIABETES

2017 ◽  
pp. 52-58
Author(s):  
Van Vy Hau Nguyen ◽  
Hai Thuy Nguyen ◽  
Dinh Toan Nguyen

Type 2 diabetes is a common metabolic disease with a rising global prevalence. It is associated with slowly progressive end-organ damage in the eyes and kidneys, but also in the brain. The latter complication is often referred to as "diabetic encephalopathy" and is characterized by mild to moderate impairments in cognitive functioning. It is also associated with an increased risk of dementia. Diabetic encephalopathies are now accepted complications of diabetes. To date, its pathogenetic mechanisms are largely unclear. They appear to differ in type 1 and type 2 diabetes as to underlying mechanisms and the nature of resulting cognitive deficits. The increased incidence of Alzheimer’s disease in type 2 diabetes is associated with insulin resistance, hyperinsulinemia and hyperglycemia, and commonly accompanying attributes such as hypercholesterolemia, hypertension and obesity. However, cognitive impairement in type 1 diabetes have other differences with type 2 diabetes. The major underlying component here appears to be insulin deficiency with downstream effects on the expression of neurotrophic factors, neurotransmitters, oxidative and apoptotic stressors resulting in defects in neuronal integrity, connectivity and loss commonly occurring in the still developing brain.

2010 ◽  
Vol 06 (01) ◽  
pp. 28 ◽  
Author(s):  
Amir A Moheet ◽  
Elizabeth R Seaquist ◽  
◽  

Diabetes affects many organ systems including the brain. Both type 1 and type 2 diabetes have been associated with reduced performance on multiple domains of cognitive function, including memory, psychomotor efficiency and executive function. In addition, structural abnormalities in the brain have been noted in subjects with both type 1 and type 2 diabetes using a variety of imaging techniques. The underlying pathophysiological mechanisms causing these changes in cognition and structure are not well understood but hyperglycemia, insulin resistance and vascular disease are likely to have key roles. Future research is needed to better understand of the natural history of the cerebral complications of diabetes and to identify the underlying mechanisms that lead to changes in brain function and structure.


2020 ◽  
Vol 105 (3) ◽  
pp. e245-e254 ◽  
Author(s):  
Thomas Jacobi ◽  
Lucas Massier ◽  
Nora Klöting ◽  
Katrin Horn ◽  
Alexander Schuch ◽  
...  

Abstract Context Common genetic susceptibility may underlie the frequently observed co-occurrence of type 1 and type 2 diabetes in families. Given the role of HLA class II genes in the pathophysiology of type 1 diabetes, the aim of the present study was to test the association of high density imputed human leukocyte antigen (HLA) genotypes with type 2 diabetes. Objectives and Design Three cohorts (Ntotal = 10 413) from Leipzig, Germany were included in this study: LIFE-Adult (N = 4649), LIFE-Heart (N = 4815) and the Sorbs (N = 949) cohort. Detailed metabolic phenotyping and genome-wide single nucleotide polymorphism (SNP) data were available for all subjects. Using 1000 Genome imputation data, HLA genotypes were imputed on 4-digit level and association tests for type 2 diabetes, and related metabolic traits were conducted. Results In a meta-analysis including all 3 cohorts, the absence of HLA-DRB5 was associated with increased risk of type 2 diabetes (P = 0.001). In contrast, HLA-DQB*06:02 and HLA-DQA*01:02 had a protective effect on type 2 diabetes (P = 0.005 and 0.003, respectively). Both alleles are part of the well-established type 1 diabetes protective haplotype DRB1*15:01~DQA1*01:02~DQB1*06:02, which was also associated with reduced risk of type 2 diabetes (OR 0.84; P = 0.005). On the contrary, the DRB1*07:01~DQA1*02:01~DQB1*03:03 was identified as a risk haplotype in non–insulin-treated diabetes (OR 1.37; P = 0.002). Conclusions Genetic variation in the HLA class II locus exerts risk and protective effects on non–insulin-treated type 2 diabetes. Our data suggest that the genetic architecture of type 1 diabetes and type 2 diabetes might share common components on the HLA class II locus.


2012 ◽  
Vol 19 (6) ◽  
pp. 793-803 ◽  
Author(s):  
Prue J Hardefeldt ◽  
Senarath Edirimanne ◽  
Guy D Eslick

The aim of this meta-analysis was to collate and analyse all primary observational studies investigating the risk of breast cancer (BC) associated with diabetes. In addition, we aimed to complete subgroup analyses by both type of diabetes and gender of study participants to further clarify the origin of any such association between the two. Studies were obtained from a database search of MEDLINE, EMBASE, PubMed, Current Contents Connect and Google Scholar with additional cross-checking of reference lists. Collated data were assessed for heterogeneity and a pooled odds ratio (OR) calculated. Forty-three studies were included in the meta-analysis with 40 studies investigating BC in women and six studies investigating BC in men. Overall, we found a significantly increased risk of BC associated with diabetes in women (OR 1.20, 95% confidence interval (CI) 1.13–1.29). After subgroup analysis by type of diabetes, the association was unchanged with type 2 diabetes (OR 1.22, 95% CI 1.07–1.40) and nullified with gestational diabetes (OR 1.06, 95% CI 0.79–1.40). There were insufficient studies to calculate a pooled OR of the risk of BC associated with type 1 diabetes. There was an increased risk of BC in males with diabetes mellitus; however, the results did not reach statistical significance (OR 1.29, 95% CI 0.99–1.67). In conclusion, diabetes increases the risk of BC in women. This association is confirmed in women with type 2 diabetes and supports the hypothesis that diabetes is an independent risk factor for BC.


Author(s):  
Sarah Wild ◽  
Jackie Price

Diabetes mellitus represents a group of metabolic disorders characterized by hyperglycaemia, which may or may not be associated with symptoms. The chronic hyperglycaemia of diabetes results from defects in insulin secretion, insulin action, or both, and is associated with long-term organ damage, particularly in the eyes, kidneys, nerves, heart, and blood vessels. Patients with type 2 diabetes have a higher prevalence of obesity (particularly abdominal obesity), hypertension, and lipid disorders, as well as an increased risk of macrovascular disease in coronary, peripheral, and cerebral arterial circulations, than people without diabetes. Microvascular complications of diabetes include retinopathy, which can lead to loss of vision, nephropathy (leading to renal failure), neuropathy (with an increased risk of foot ulcers, amputations, and foot deformations), and autonomic neuropathy, causing cardiovascular, gastrointestinal, genitourinary, and sexual dysfunction. Diabetes may have a serious emotional and social impact on affected individuals and their families, and has major economic implications for society as a whole in both developed and developing countries.


2019 ◽  
Vol 20 (24) ◽  
pp. 6345 ◽  
Author(s):  
Amélie I. S. Sobczak ◽  
Alan J. Stewart

Diabetes (both type-1 and type-2) affects millions of individuals worldwide. A major cause of death for individuals with diabetes is cardiovascular diseases, in part since both types of diabetes lead to physiological changes that affect haemostasis. Those changes include altered concentrations of coagulatory proteins, hyper-activation of platelets, changes in metal ion homeostasis, alterations in lipid metabolism (leading to lipotoxicity in the heart and atherosclerosis), the presence of pro-coagulatory microparticles and endothelial dysfunction. In this review, we explore the different mechanisms by which diabetes leads to an increased risk of developing coagulatory disorders and how this differs between type-1 and type-2 diabetes.


Endocrinology ◽  
2009 ◽  
Vol 150 (12) ◽  
pp. 5294-5301 ◽  
Author(s):  
Bhumsoo Kim ◽  
Carey Backus ◽  
SangSu Oh ◽  
John M. Hayes ◽  
Eva L. Feldman

Abstract As the population of the United States ages, the incidence of age-related neurodegenerative and systemic diseases including Alzheimer’s disease (AD) and diabetes is increasing rapidly. Multiple studies report that patients with diabetes have a 50–75% increased risk of developing AD compared with age- and gender-matched patients without diabetes. Abnormally phosphorylated tau is a major building block of neurofibrillary tangles, a classic neuropathological characteristic of AD. In addition, proteolytic tau cleavage promotes AD progression due to cleaved tau serving as a nucleation center for the pathological assembly of tau filaments. The current study examines tau modification in type 1 (streptozotocin-injected) and type 2 (db/db) mouse models of diabetes. Tau phosphorylation is increased in the cortex and hippocampus of db/db mice compared with db+ control mouse brain. Interestingly, there is an age-dependent increase in tau cleavage that is not observed in age-matched control db+ animals. Streptozotocin injection also increased tau phosphorylation; however, the increase was less significant compared with the type 2 mouse model, and more importantly, no tau cleavage was detected. Our results suggest tau modification caused by insulin dysfunction and hyperglycemia may contribute to the increased incidence of AD in diabetes. We hypothesize that type 1 and type 2 diabetes may contribute to AD through different mechanisms; in type 2 diabetes, hyperglycemia-mediated tau cleavage may be the key feature, whereas insulin deficiency may be the major contributing factor in type 1 diabetes.


2018 ◽  
Vol 142 ◽  
pp. 46-55 ◽  
Author(s):  
Chelsey George ◽  
Alan M. Ducatman ◽  
Baqiyyah N. Conway

2005 ◽  
Vol 41 (3) ◽  
pp. 281-288 ◽  
Author(s):  
L. M. A. J. Muller ◽  
K. J. Gorter ◽  
E. Hak ◽  
W. L. Goudzwaard ◽  
F. G. Schellevis ◽  
...  

2021 ◽  
Vol 11 (2) ◽  
pp. 148
Author(s):  
Julia Samoilova ◽  
Mariia Matveeva ◽  
Olga Tonkih ◽  
Dmitry Kudlau ◽  
Oxana Oleynik ◽  
...  

Diabetes mellitus type 1 and 2 is associated with cognitive impairment. Previous studies have reported a relationship between changes in cerebral metabolite levels and the variability of glycemia. However, the specific risk factors that affect the metabolic changes associated with type 1 and type 2 diabetes in cognitive dysfunction remain uncertain. The aim of the study was to evaluate the specificity of hippocampal spectroscopy in type 1 and type 2 diabetes and cognitive dysfunction. Materials and methods: 65 patients with type 1 diabetes with cognitive deficits and 20 patients without, 75 patients with type 2 diabetes with cognitive deficits and 20 patients without have participated in the study. The general clinical analysis and evaluation of risk factors of cognitive impairment were carried out. Neuropsychological testing included the Montreal Scale of Cognitive Dysfunction Assessment (MoCA test). Magnetic resonance spectroscopy (MRS) was performed in the hippocampal area, with the assessment of N-acetylaspartate (NAA), choline (Cho), creatine (Cr), and phosphocreatine (PCr) levels. Statistical processing was performed using the commercially available IBM SPSS software. Results: Changes in the content of NAA, choline Cho, phosphocreatine Cr2 and their ratios were observed in type 1 diabetes. More pronounced changes in hippocampal metabolism were observed in type 2 diabetes for all of the studied metabolites. Primary risk factors of neurometabolic changes in patients with type 1 diabetes were episodes of severe hypoglycemia in the history of the disease, diabetic ketoacidosis (DKA), chronic hyperglycemia, and increased body mass index (BMI). In type 2 diabetes, arterial hypertension (AH), BMI, and patient’s age are of greater importance, while the level of glycated hemoglobin (HbA1c), duration of the disease, level of education and insulin therapy are of lesser importance. Conclusion: Patients with diabetes have altered hippocampal metabolism, which may serve as an early predictive marker. The main modifiable factors have been identified, correction of which may slow down the progression of cognitive dysfunction.


Author(s):  
I K Wium-Andersen ◽  
J Rungby ◽  
M B Jørgensen ◽  
A Sandbæk ◽  
M Osler ◽  
...  

Abstract Aims To determine the risk of dementia in patients with type 1 or type 2 diabetes and in individuals with glycosylated haemoglobin, type A1C (HbA1c) of ⩾48 mmol/mol, which is the diagnostic limit for diabetes. Methods We included the following cohorts: all incident diabetes cases aged 15 or above registered in the National Diabetes Registry (NDR) from January 2000 through December 2012 (n = 148 036) and a reference population, adult participants from the Glostrup cohort (n = 16 801), the ADDITION Study (n = 26 586) and Copenhagen Aging and Midlife Biobank (CAMB) (n = 5408). Using these cohorts, we analysed if a diagnosis of type 1 or type 2 diabetes in the NDR or HbA1c level of ⩾ 6.5% (48 mmol/mol) in the cohorts increased risk of dementia in the Danish National Patient Registry or cognitive performance assessed by the Intelligenz-Struktur-Test 2000R (IST2000R). Results A diagnosis of type 1 or type 2 diabetes in the NDR was associated with increased risk of dementia diagnosed both before or after age 65 as well as across different subtypes of dementia. Self-reported diabetes or high HbA1c levels were associated with lower cognitive performance (p = 0.004), while high HbA1c was associated with increased risk of dementia (HR 1.94 (1.10–3.44) in the Glostrup cohort but not in the ADDITION Study (HR 0.96 (0.57–1.61)). Conclusions Both type 1 and type 2 diabetes are associated with an increased risk of dementia, while the importance of screening-detected elevated HbA1c remains less clear.


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