scholarly journals Risk of dementia and cognitive dysfunction in individuals with diabetes or elevated blood glucose

2019 ◽  
Vol 29 ◽  
Author(s):  
I K Wium-Andersen ◽  
J Rungby ◽  
M B Jørgensen ◽  
A Sandbæk ◽  
M Osler ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Cognitive Performance ◽  
Reference Population ◽  
Diabetes Registry ◽  
Increased Risk ◽  
Haemoglobin Type ◽  
High Hba1c ◽  
National Patient

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.

scholarly journals A description of clinician reported diagnosis of type 2 diabetes and other non-type 1 diabetes included in a large international multicentered pediatric diabetes registry (SWEET)

2016 ◽  
Vol 17 ◽  
pp. 24-31 ◽  
Author(s):  
Danièle Pacaud ◽  
Anke Schwandt ◽  
Carine de Beaufort ◽  
Kristina Casteels ◽  
Jacques Beltrand ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Type 1 Diabetes ◽  
Diabetes Registry ◽  
Pediatric Diabetes

HLA Class II Allele Analyses Implicate Common Genetic Components in Type 1 and Non–Insulin-Treated Type 2 Diabetes

2020 ◽  
Vol 105 (3) ◽  
pp. e245-e254 ◽  
Author(s):  
Thomas Jacobi ◽  
Lucas Massier ◽  
Nora Klöting ◽  
Katrin Horn ◽  
Alexander Schuch ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Type 1 Diabetes ◽  
Class Ii ◽  
Hla Class Ii ◽  
Risk Haplotype ◽  
Genetic Components ◽  
Hla Genotypes ◽  
Increased Risk

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.

scholarly journals Diabetes increases the risk of breast cancer: a meta-analysis

2012 ◽  
Vol 19 (6) ◽  
pp. 793-803 ◽  
Author(s):  
Prue J Hardefeldt ◽  
Senarath Edirimanne ◽  
Guy D Eslick
Keyword(s):  
Breast Cancer ◽  
Type 2 Diabetes ◽  
Reference Lists ◽  
Meta Analysis ◽  
Statistical Significance ◽  
Increased Risk ◽  
And Gender ◽  
Study Participants

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.

scholarly journals Effects of linagliptin vs glimepiride on cognitive performance in type 2 diabetes: results of the randomised double-blind, active-controlled CAROLINA-COGNITION study

Diabetologia ◽  
2021 ◽  
Author(s):  
Geert Jan Biessels ◽  
Chloë Verhagen ◽  
Jolien Janssen ◽  
Esther van den Berg ◽  
Gudrun Wallenstein ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Cardiovascular Risk ◽  
Cognitive Performance ◽  
Mmse Score ◽  
Cognitive Outcome ◽  
Cognitive Changes ◽  
Double Blind ◽  
Treatment Assignment ◽  
Increased Risk

Abstract Aims/hypothesis Type 2 diabetes, particularly with concomitant CVD, is associated with an increased risk of cognitive impairment. We assessed the effect on accelerated cognitive decline (ACD) of the DPP-4 inhibitor linagliptin vs the sulfonylurea glimepiride in individuals with type 2 diabetes. Methods The CAROLINA-COGNITION study was part of the randomised, double-blind, active-controlled CAROLINA trial that evaluated the cardiovascular safety of linagliptin vs glimepiride in individuals with age ≥40 and ≤85 years and HbA1c 48–69 mmol/mol (6.5–8.5%) receiving standard care, excluding insulin therapy. Participants were randomised 1:1 using an interactive telephone- and web-based system and treatment assignment was determined by a computer-generated random sequence with stratification by center. The primary cognitive outcome was occurrence of ACD at end of follow-up, defined as a regression-based index score ≤16th percentile on either the Mini-Mental State Examination (MMSE) or a composite measure of attention and executive functioning, in participants with a baseline MMSE score ≥24. Prespecified additional analyses included effects on ACD at week 160, in subgroups (sex, age, race, ethnicity, depressive symptoms, cardiovascular risk, duration of type 2 diabetes, albuminuria), and absolute changes in cognitive performance. Participants, caregivers, and people involved in measurements, examinations or adjudication, were all masked to treatment assignment. Results Of 6033 participants recruited from hospital and primary care sites, 3163 (38.0% female, mean age/diabetes duration 64/7.6 years, MMSE score 28.5, HbA1c 54 mmol/mol [7.1%]) represent the CAROLINA-COGNITION cohort. Over median 6.1 years, ACD occurred in 27.8% (449/1618, linagliptin) vs 27.6% (426/1545, glimepiride), OR 1.01 (95% CI 0.86, 1.18). Also, no differences in ACD were observed at week 160 (OR 1.07 [0.91, 1.25]), between treatments across subgroups, or for absolute cognitive changes. Conclusions/interpretation In a large, international outcome trial in people with relatively early type 2 diabetes at elevated cardiovascular risk, no difference in risk for ACD was observed between linagliptin and glimepiride over 6.1 years. Funding This study was sponsored by Boehringer Ingelheim. Trial registration ClinicalTrials.gov NCT01243424. Graphical abstract

DIABETIC ENCEPHALOPATHY IN TYPE 2 DIABETES

2017 ◽  
pp. 52-58
Author(s):  
Van Vy Hau Nguyen ◽  
Hai Thuy Nguyen ◽  
Dinh Toan Nguyen
Keyword(s):  
Type 2 Diabetes ◽  
Cognitive Deficits ◽  
Organ Damage ◽  
Diabetic Encephalopathy ◽  
Downstream Effects ◽  
Increased Risk ◽  
Underlying Mechanisms ◽  
The Brain

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.

scholarly journals Relationships Between Hyperglycemia and Cognitive Performance Among Adults With Type 1 and Type 2 Diabetes

Diabetes Care ◽  
2004 ◽  
Vol 28 (1) ◽  
pp. 71-77 ◽  
Author(s):  
D. J. Cox ◽  
B. P. Kovatchev ◽  
L. A. Gonder-Frederick ◽  
K. H. Summers ◽  
A. McCall ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Cognitive Performance

scholarly journals Coagulatory Defects in Type-1 and Type-2 Diabetes

2019 ◽  
Vol 20 (24) ◽  
pp. 6345 ◽  
Author(s):  
Amélie I. S. Sobczak ◽  
Alan J. Stewart
Keyword(s):  
Type 2 Diabetes ◽  
Lipid Metabolism ◽  
Cardiovascular Diseases ◽  
Metal Ion ◽  
Ion Homeostasis ◽  
Physiological Changes ◽  
Metal Ion Homeostasis ◽  
Increased Risk

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.

scholarly journals Increased Tau Phosphorylation and Cleavage in Mouse Models of 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
Keyword(s):  
Type 2 Diabetes ◽  
Mouse Models ◽  
The United States ◽  
Tau Phosphorylation ◽  
Age Related ◽  
Increased Risk ◽  
And Gender ◽  
Tau Cleavage

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.

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