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      The total alkaloids from Coptis chinensis Franch improve cognitive deficits in type 2 diabetic rats

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          Abstract

          Background

          Coptis chinensis Franch is extensively used in traditional Chinese medicine to treat diabetes and dementia. Alkaloids are the main active ingredients of C. chinensis.

          Purpose

          This study was designed to probe the effects and possible mechanisms of the total alkaloids from C. chinensis (TAC) on cognitive deficits in type 2 diabetic rats.

          Methods

          Cognitive deficits were induced in rats by streptozotocin and high glucose/high fat diet. After treatment with TAC (80, 120, and 180 mg/kg) for 24 weeks, the behavioral parameters of each rat were assessed by Morris water maze and Y-maze tests. The indexes of glucose and lipid metabolism, pathological changes of brain tissue, and the phosphorylation levels of insulin signaling related proteins were also evaluated.

          Results

          The type 2 diabetic rats showed significantly elevated levels of fasting blood glucose, glycosylated hemoglobin and glycosylated serum protein, as well as apolipoprotein B, free fatty acid, triglyceride and total cholesterol but decreased the content of apolipoprotein A1, and TAC treatment dose-dependently reversed these abnormal changes. Furthermore, the behavioral results showed that TAC alleviated the cognitive deficits in type 2 diabetic rats. Moreover, immunohistochemical and histopathologic examinations indicated that the diabetic rats showed significant Aβ deposition, and neuronal damage and loss, which can be reversed by TAC treatment. The western blot results showed that TAC treatment markedly increased the phosphorylation of IRS, PI3K, and Akt, and inhibited the overactivation of GSK3β in the brain of type 2 diabetic rats.

          Conclusion

          These findings conclude that TAC prevents diabetic cognitive deficits, most likely by ameliorating the disorder of glucose and lipid metabolism, attenuating Aβ deposition, and enhancing insulin signaling.

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          Most cited references 27

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          Efficacy of berberine in patients with type 2 diabetes mellitus.

          Berberine has been shown to regulate glucose and lipid metabolism in vitro and in vivo. This pilot study was to determine the efficacy and safety of berberine in the treatment of type 2 diabetes mellitus patients. In study A, 36 adults with newly diagnosed type 2 diabetes mellitus were randomly assigned to treatment with berberine or metformin (0.5 g 3 times a day) in a 3-month trial. The hypoglycemic effect of berberine was similar to that of metformin. Significant decreases in hemoglobin A1c (from 9.5%+/-0.5% to 7.5%+/-0.4%, P<.01), fasting blood glucose (from 10.6+/-0.9 mmol/L to 6.9+/-0.5 mmol/L, P<.01), postprandial blood glucose (from 19.8+/-1.7 to 11.1+/-0.9 mmol/L, P<.01), and plasma triglycerides (from 1.13+/-0.13 to 0.89+/-0.03 mmol/L, P<.05) were observed in the berberine group. In study B, 48 adults with poorly controlled type 2 diabetes mellitus were treated supplemented with berberine in a 3-month trial. Berberine acted by lowering fasting blood glucose and postprandial blood glucose from 1 week to the end of the trial. Hemoglobin A1c decreased from 8.1%+/-0.2% to 7.3%+/-0.3% (P<.001). Fasting plasma insulin and homeostasis model assessment of insulin resistance index were reduced by 28.1% and 44.7% (P<.001), respectively. Total cholesterol and low-density lipoprotein cholesterol were decreased significantly as well. During the trial, 20 (34.5%) patients experienced transient gastrointestinal adverse effects. Functional liver or kidney damages were not observed for all patients. In conclusion, this pilot study indicates that berberine is a potent oral hypoglycemic agent with beneficial effects on lipid metabolism.
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            Cognition and diabetes: a lifespan perspective.

            Diabetes mellitus is associated with cognitive dysfunction and abnormalities that can be seen with brain imaging. Recent studies provide important new insights into the nature and severity of these cerebral complications that help to explain why some patients with diabetes have clinically relevant neurocognitive morbidity, whereas most are apparently unaffected. This Personal View investigates the hypothesis that clinically relevant diabetes-related cognitive decrements mainly occur at two crucial periods in life: when the brain is developing in childhood, and when the brain undergoes neurodegenerative changes associated with ageing. Outside of these periods cognitive decrements mainly occur in patients with notable diabetes-related comorbidities, in particular microvascular or macrovascular complications. The identification of crucial periods and conditions for the development of diabetes-related cognitive decrements helps to draw the attention of physicians to individuals at risk and can direct future studies into the mechanisms that underlie these conditions.
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              Vascular factors and metabolic interactions in the pathogenesis of diabetic neuropathy.

              Diabetes mellitus is a major cause of peripheral neuropathy, commonly manifested as distal symmetrical polyneuropathy. This review examines evidence for the importance of vascular factors and their metabolic substrate from human and animal studies. Diabetic neuropathy is associated with risk factors for macrovascular disease and with other microvascular complications such as poor metabolic control, dyslipidaemia, body mass index, smoking, microalbuminuria and retinopathy. Studies in human and animal models have shown reduced nerve perfusion and endoneurial hypoxia. Investigations on biopsy material from patients with mild to severe neuropathy show graded structural changes in nerve microvasculature including basement membrane thickening, pericyte degeneration and endothelial cell hyperplasia. Arterio-venous shunting also contributes to reduced endoneurial perfusion. These vascular changes strongly correlate with clinical defects and nerve pathology. Vasodilator treatment in patients and animals improves nerve function. Early vasa nervorum functional changes are caused by the metabolic insults of diabetes, the balance between vasodilation and vasoconstriction is altered. Vascular endothelium is particularly vulnerable, with deficits in the major endothelial vasodilators, nitric oxide, endothelium-derived hyperpolarising factor and prostacyclin. Hyperglycaemia and dyslipidaemia driven oxidative stress is a major contributor, enhanced by advanced glycation end product formation and polyol pathway activation. These are coupled to protein kinase C activation and omega-6 essential fatty acid dysmetabolism. Together, this complex of interacting metabolic factors accounts for endothelial dysfunction, reduced nerve perfusion and function. Thus, the evidence emphasises the importance of vascular dysfunction, driven by metabolic change, as a cause of diabetic neuropathy, and highlights potential therapeutic approaches.
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                Author and article information

                Journal
                Drug Des Devel Ther
                Drug Des Devel Ther
                Drug Design, Development and Therapy
                Drug Design, Development and Therapy
                Dove Medical Press
                1177-8881
                2018
                31 August 2018
                : 12
                : 2695-2706
                Affiliations
                [1 ]Department of Pathophysiology, West China College of Basic and Forensic Medicine, Sichuan University, Chengdu, China, huangpanxiao@ 123456sina.com ; azure521@ 123456gmail.com
                [2 ]Department of Traditional Chinese Medicine, College of Pharmacy, Southwest Minzu University, Chengdu, China
                [3 ]Key Laboratory of Birth Defects and Related Diseases of Women and Children (Ministry of Education), West China Second University Hospital, Sichuan University, Chengdu, China
                Author notes
                Correspondence: Ning Huang; Jingyu Li, Department of Pathophysiology, West China College of Basic and Forensic Medicine, Sichuan University, No 17, Third Section, South Ren-min Road, Chengdu 610041, China, Email huangpanxiao@ 123456sina.com ; azure521@ 123456gmail.com
                Article
                dddt-12-2695
                10.2147/DDDT.S171025
                6124445
                © 2018 Li et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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