Insulin, C-peptide, hyperglycemia, and central nervous system complications in diabetes

Sima, Anders A. F.; Kamiya, Hideke; Li, Zhen Guo

doi:10.1016/j.ejphar.2004.02.056

Cited by 164 publications

(138 citation statements)

References 138 publications

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“…Diabetic encephalopathy is a recognised consequence of diabetes and is associated with neuronal damage in the central nervous system, as well as cognitive deficits [5]. The mechanism of neuronal damage is thought to be related to the effects of hyperglycaemia, namely oxidative stress and the accumulation of advanced glycation endproducts (AGE).…”

Section: Discussionmentioning

confidence: 99%

“…A recent review indicates that individuals with diabetes have a greater risk of cognitive decline and a greater risk of developing dementia than do non-diabetic individuals [3]. Among others, possible mechanisms for this association include oxidative stress, accelerated ischaemic brain damage [5] and impaired use of glucose during cognitive tasks [6].…”

Section: Introductionmentioning

confidence: 99%

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Presence of the APOE ε4 allele modifies the relationship between type 2 diabetes and cognitive performance: the Maine–Syracuse Study

et al. 2009

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Aims/hypothesis The primary aim of this study was to determine whether the presence of one or more APOE ε4 alleles modifies the association between diabetes (defined by glucose ≥7 mmol/l or treatment) and cognitive function. Methods Diabetic status and APOE genotype interactions were assessed cross-sectionally for 826 communitydwelling, stroke-free, non-demented individuals (526 nondiabetic non-APOE ε4 carriers, 174 non-diabetic APOE ε4 carriers, 87 diabetic APOE ε4 non-carriers, 39 diabetic APOE ε4 carriers) ranging in age from 50 to 98 years. Cognitive function was assessed using the Mini-Mental State Examination (MMSE), the similarities subtest from the Wechsler Adult Intelligence Scale, and four composite scores derived from 17 additional neuropsychological tests. Multiple linear regression analyses were employed to relate diabetes and APOE genotype to cognitive performance and to examine the interaction between these two risk factors as they relate to cognitive performance. Multiple cardiovascular disease risk factors were statistically controlled. Results With adjustment for age, education, sex, race/ ethnicity and APOE genotype, performance level was lower for the diabetic than for the non-diabetic group for the MMSE, the similarities subtest and each of the cognitive composites with the exception of the verbal memory composite. Interactions (p<0.05) between diabetes and APOE genotype were found for all but the visual-spatial memory/organisation composite. The negative association between diabetes and cognitive performance was of a higher magnitude for individuals who carry one or more APOE ε4 alleles. Results were similar with additional adjustment for cardiovascular disease and associated risk factors. Conclusions/interpretation The presence of one or more APOE ε4 alleles modifies the association between diabetes and cognitive function.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Presence of the APOE ε4 allele modifies the relationship between type 2 diabetes and cognitive performance: the Maine–Syracuse Study

et al. 2009

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“…The results of animal and human case studies suggest that hypoglycemia may induce cell death in the brain, possibly through excitotoxic or apoptotic processes (18,19). However, although both chronic hyperglycemia and recurrent episodes of hypoglycemia may lead to central nervous system damage, the long-term effects of DM on the central nervous system are still controversial (20,21). To the best of our knowledge, no study has attempted to explore the association between ADHD and DM.…”

mentioning

confidence: 97%

Association of attention-deficit/hyperactivity disorder with diabetes: a population-based study

et al. 2013

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Background: cognitive impairment has been documented in adult diabetes but is unclear in pediatric diabetes. No study had been conducted to explore the relationship between attention-deficit/hyperactivity disorder (aDhD) and diabetes. Using a population-based data set, we aimed to examine the association between aDhD and a prior diagnosis of diabetes mellitus (DM) in Taiwan. Methods: a total of 4,302 patients with aDhD were selected as cases and 21,510 randomly selected subjects as controls. We used conditional logistic regression to calculate the odds ratio (OR) for having previously received a diagnosis of DM between subjects with and without aDhD. results: In this study, 116 of the 25,812 sampled subjects (0.5%) had received a diagnosis of DM prior to their index date. subjects with aDhD had a higher proportion of prior DM diagnoses than controls (0.9% vs. 0.4%, P < 0.001). after adjusting for age, sex, index year, geographic location, and obesity, aDhD was significantly associated with a prior diagnosis of type 2 DM (OR = 2.75, 95% confidence interval (cI) = 1.82-4.16). however, no significant association was observed between aDhD and type 1 DM. conclusion: The findings suggest that aDhD was associated with a previous diagnosis of type 2 DM.

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“…Plasma C-peptide levels are often used as a marker of actual insulin secretion, and inversely related to the development of diabetic complications including neuropathy [22,28,29]. For a long time, C-peptide had been considered to be biological inert.…”

Section: Introductionmentioning

confidence: 99%

“…For a long time, C-peptide had been considered to be biological inert. However, recent studies have shown that C-peptide is an active peptide hormone with potentially important physiological effects against diabetic complications in patients with type 1 diabetes and experimental models [2,4,8,10,11,22,28,29]. For example, short-term infusion of C-peptide improves impaired cardiac autonomic nerve functions, mainly parasympathetic components, in patients with polyneuropathy and type 1 diabetes [10].…”

Section: Introductionmentioning

confidence: 99%

Proinsulin C-peptide activates vagus efferent output in rats

et al. 2005

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The aim of this study was to examine the effect of proinsulin C-peptide on the autonomic nervous systems in rats. Intravenous administration of C-peptide gradually increased electrophysiological activity of the vagus nerves into the stomach and pancreas for at least 90 min. It also slightly increased gastric acid secretion that was suppressed by the treatment with atropine. Intraperitoneal injection of C-peptide did not affect the basal and stress-induced norepinephrine turnover rate, a biochemical index of sympathetic nerve activity. These results indicate that C-peptide increases parasympathetic nerve activity without affecting sympathetic nerve activity. This could explain, at least in part, the ameliorating effects of C-peptide on impaired cardiac autonomic nerve functions in patients with type 1 diabetes.

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Insulin, C-peptide, hyperglycemia, and central nervous system complications in diabetes

Cited by 164 publications

References 138 publications

Presence of the APOE ε4 allele modifies the relationship between type 2 diabetes and cognitive performance: the Maine–Syracuse Study

Presence of the APOE ε4 allele modifies the relationship between type 2 diabetes and cognitive performance: the Maine–Syracuse Study

Association of attention-deficit/hyperactivity disorder with diabetes: a population-based study

Proinsulin C-peptide activates vagus efferent output in rats

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