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Diabetology
Special Issues
Brain and Diabetes
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Brain and Diabetes

A special issue of Diabetology (ISSN 2673-4540).

Deadline for manuscript submissions: closed (15 June 2023) | Viewed by 7629

Special Issue Editors

Dr. Rashmi Kumari

E-Mail Website
Guest Editor
Department of Neural & Behavioral Sciences, College of Medicine, Pennsylvania State University, Hershey, PA, USA
Interests: type-2 diabetes; metabolic disorders; insulin resistance; dyslipidemia; hypercorticism; immune-suppression; stroke; vascular permeability; diagnosis; prevention; development and validation of tests and prospective treatment
Dr. Gayatri Devraj

E-Mail Website
Guest Editor
Institut für Medizinische Mikrobiologie und Krankenhaushygiene, Goethe-Universität Frankfurt am Main, Frankfurt am Main, Germany
Interests: brain infection; hypoxia; signaling pathway; blood–brain barrier

Special Issue Information

Dear Colleagues,

Diabetes is an epidemic, and it contributed to social, financial, and healthcare burdens across the world. Keeping blood sugar under control through diet, physical activity and medicine is a lifelong challenge for people with diabetes and the persistent high glucose level causes generalized vascular damage to the heart, eyes, kidneys, brain, and nerves, resulting in various complications. Along with hyperglycemia, dyslipidemia, hyperinsulinemia, hypercorticism and insulin resistance are the common characteristics of diabetes and how these chronic metabolic disorders affect brain health is a critical issue, especially in the growing aging population. Therefore, the content of this Special Issue will focus on the effects of diabetes on the brain in the context of vascular permeability and vascular remodeling in the brain upon stroke and with aging. We will assemble the clinical and basic science knowledge related to diabetes complications such as mediated dementia, depression and psychotic behavior and their impacts on cognitive decline, early diagnosis, prevention, and potential treatment.

Dr. Rashmi Kumari
Dr. Gayatri Devraj
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Diabetology is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • diabetes
  • metabolic disorder
  • vascular permeability
  • stroke
  • brain
  • cognitive impairment
  • dementia

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Published Papers (3 papers)

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Research

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10 pages, 1111 KiB  
Article
Glucocorticoid Receptor Blockers Pretreatment Did Not Improve Infarct Volume in Type-2 Diabetic Mouse Model of Stroke
by Rashmi Kumari and Lisa Willing
Diabetology 2022, 3(4), 539-548; https://doi.org/10.3390/diabetology3040041 - 21 Oct 2022
Cited by 2 | Viewed by 1861
Abstract
Impaired glucocorticoid signaling in diabetes mellitus and its relation to suppressed immune function and hyperglycemia during acute stroke has been shown to be detrimental. Therefore, the aim of this study was to examine the effect of glucocorticoid receptor (GCR) blockers in a type-2 [...] Read more.
Impaired glucocorticoid signaling in diabetes mellitus and its relation to suppressed immune function and hyperglycemia during acute stroke has been shown to be detrimental. Therefore, the aim of this study was to examine the effect of glucocorticoid receptor (GCR) blockers in a type-2 diabetic mouse model following hypoxia–ischemia (HI). We induced stroke in diabetic db/db and non-diabetic db/+ mice by unilateral common carotid artery ligation followed by 20 min of HI. Mice were pretreated with RU-486, GCRII blocker (40 mg/kg), intraperitoneally, the day before, during stroke and post-HI. Blood and brain samples were collected at 24 h post-HI to measure blood glucose, corticosterone and infarct size. Similarly, another set of mice was pretreated with RU-486 + spironolactone, GCR1 blocker (25 mg/kg) subcutaneously for a week before inducing stroke and during recovery. Samples were collected at 48 h post-HI for various analyses. RU-486 treatment did not lower the blood glucose significantly, but RU-486 + spironolactone decreased the blood glucose in db/db mice post-HI. However, none of the treatment groups decreased the ischemia-induced serum corticosterone level or infarct size. This study suggests that even though GCR blockers improve hyperglycemia, they did not improve the infarct volume. Full article
(This article belongs to the Special Issue Brain and Diabetes)
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7 pages, 807 KiB  
Article
Hypothetical Reason for the Restoration of HbA1c Level for Pre-Diabetic Patients through the Recovery of Arterial Blood Flow Access to Rhomboid Fossa
by Alexandre A. Vetcher, Kirill V. Zhukov, Bagrat A. Gasparyan and Alexander Y. Shishonin
Diabetology 2022, 3(3), 470-476; https://doi.org/10.3390/diabetology3030035 - 16 Aug 2022
Cited by 7 | Viewed by 1998
Abstract
We demonstrate that the recovery of cervical vertebral arterial blood flow access to the rhomboid fossa causes the restoration of HbA1c level for the patients with pre-diabetic (pre-DM) condition. This observation is in good agreement with the consideration of the human body as [...] Read more.
We demonstrate that the recovery of cervical vertebral arterial blood flow access to the rhomboid fossa causes the restoration of HbA1c level for the patients with pre-diabetic (pre-DM) condition. This observation is in good agreement with the consideration of the human body as a dissipative structure. Such consideration is the focus of the recently announced centralized aerobic-anaerobic energy balance compensation (CAAEBC) theory. According to the theory, observed connections between high blood pressure (HBP) and the lifted level of HbA1c can be hypothetically linked through the restrictions of blood flow access to rhomboid fossa, causing the delivery of incorrect information of blood oxygen availability. Below we provide detailed information of how in this case CAAEBC theory explains the very initiation of multiple chronic diseases, starting with type 2 Diabetes Mellitus (DM). Full article
(This article belongs to the Special Issue Brain and Diabetes)
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Review

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9 pages, 269 KiB  
Review
Is Non-Alcoholic Fatty Liver Disease Connected with Cognition? The Complex Interplay between Liver and Brain
by Matina Kouvari, Domenico Sergi, Nathan M. D’Cunha, Amanda Bulman, Demosthenes B. Panagiotakos and Nenad Naumovski
Diabetology 2022, 3(2), 355-363; https://doi.org/10.3390/diabetology3020026 - 14 Jun 2022
Cited by 3 | Viewed by 3051
Abstract
The prevalence of non-alcoholic fatty liver disease (NAFLD) and its progressive form, non-alcoholic steatohepatitis (NASH), is increasing in parallel with the rising rates of obesity and type 2 diabetes. Approximately one in four adults are diagnosed with liver steatosis globally. NAFLD is associated [...] Read more.
The prevalence of non-alcoholic fatty liver disease (NAFLD) and its progressive form, non-alcoholic steatohepatitis (NASH), is increasing in parallel with the rising rates of obesity and type 2 diabetes. Approximately one in four adults are diagnosed with liver steatosis globally. NAFLD is associated with insulin resistance, hypertension, obesity, visceral adiposity, and dyslipidaemia. These risk factors are often accompanied by inflammation and oxidative stress, which also play a role in extrahepatic diseases, including conditions related to the central nervous system, such as mild cognitive impairment and Alzheimer’s disease. The number of people living with dementia is approximately 55 million and is estimated to increase to approximately 2 billion people by 2050. Recent studies have found that NAFLD is associated with poorer cognition. The aim of this review was to summarise the findings of hitherto studies that have linked NAFLD with cognition and dementia, as well as to discuss the potential liver–brain pathways. Full article
(This article belongs to the Special Issue Brain and Diabetes)
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