scholarly journals Age-dependent changes of neural functions under glucose metabolism disorders

Author(s):  
Viktoria N. Shadenko

There is a brief review of literature data about relationship of violations glucose homeostasis and cognitive brain functions. A relationship was found between impaired glucose metabolism during the formation of insulin resistance (type 2 diabetes mellitus) with the changes observed in development of a number of neurodegenerative diseases (Alzheimer’s disease). It is provides information on the role of insulin and insulin receptors in metabolic processes, development of hyperglycemia and insulin resistance during ageing. The contribution of free radical mechanisms in development of cognitive impairment caused by metabolic glucose changes is also discussed.

2020 ◽  
Vol 18 (5) ◽  
pp. 93-98
Author(s):  
L. B. NOVIKOVA ◽  
◽  
G. I. IZHBULDINA ◽  

Among the reasons that increase the risk of stroke, its severity and outcome, a special place is given to disorders of carbohydrate metabolism. However, to date, there is no consensus on the role of hyperglycemia in stroke, whether it is physiological or pathological. The purpose to study the effect of insulin resistance on the course and clinical outcome of ischemic stroke (IS) in the acute period. Material and methods. A total of 862 patients with IS (370 men, 492 women), mean age was 66,1 ± 10,8 years. The degree of neurological deficit (NIHSS scale) and clinical outcome were assessed. When admitted to hospital, the level of glycemia, insulin, and C-peptide in the fasting blood were found. Results. In 186 (21,6%) patients type 2 diabetes mellitus (DM) was diagnosed. In 27,8% of patients without DM and 76,3% of patients with DM hyperglycemia was detected. In patients without DM with hyperglycemia, compared with patients with normoglycemia, a higher representation of severe neurological deficit (by 14,7%), a lower frequency of noticeable positive dynamics (by 14,8%), and a higher mortality rate (by 11,5%) were found. In patients with DM, hyperglycemia was associated with a lower incidence of noticeable positive dynamics (by 27,7%). The development of IS is accompanied by an increase in the blood level of C-peptide more than twice. High values of the C-peptide/insulin ratio are associated with a higher frequency of severe neurological deficit in patients with DM (by 32,4%) and without DM (by 23,8%), and a decrease in the incidence of noticeable positive dynamics (by 23,5% and 20,9%, respectively). Conclusion. Development of IS is characterized by high representation of disorders of carbohydrate metabolism. The severity of glucose metabolism disorders is interrelated with the severity and clinical outcome of the disease.


2020 ◽  
Vol 27 (39) ◽  
pp. 6643-6657 ◽  
Author(s):  
Geir Bjørklund ◽  
Maryam Dadar ◽  
Lyudmila Pivina ◽  
Monica Daniela Doşa ◽  
Yuliya Semenova ◽  
...  

The prevalence of Type 2 Diabetes Mellitus (T2DM) is internationally ever-growing. Therefore, prevention, diagnostics, and control of insulin resistance and T2DM are of increasing importance. It has been suggested that mechanisms leading to insulin resistance and diabetes and its complications include high intake of refined and energy-rich food, which is presumed to be accompanied by suboptimal intake of trace elements, such as Zinc (Zn), Selenium (Se), Chromium (Cr), and Copper (Cu), which are essential and crucial for various biological processes. The purpose of this review is to highlight the role of Zn, Se, and Cu in T2DM. Diabetes seems prevalent when Zn, Se, and Cu are deficient, which may result from excessive intake of refined food. The literature search was conducted in PubMed and Scopus, supplemented with the reference lists of relevant articles and a Google Scholar search. We critically assessed all relevant citations, both review and research papers in English. The search terms that were used included Zn, Cu, diabetes, and diabetes mellitus. Research has shown that Zn, Se and Cu are involved in the pathogenesis of diabetes, but these trace elements can in excessive amounts be toxic. Zinc appears to activate key molecules that are involved in cell signaling, which maintain the homeostasis of glucose. Zinc also regulates insulin receptors, prolong the action of insulin, and promote healthy lipid profiles. Copper in excess can create oxidative stress, which is a factor in the onset and the progression of T2DM. Abnormal Zn and Cu metabolism appears to accompany and may also cause diabetes complications.


Author(s):  
Dorota Łojko ◽  
Maciej Owecki ◽  
Aleksandra Suwalska

Bipolar patients have a higher risk of type 2 diabetes and obesity, which are associated with cardiovascular diseases as the leading cause of death in this group. Additionally, there is growing evidence that impaired glucose metabolism in bipolar patients is associated with rapid cycling, poor response to mood stabilizers and chronic course of illness. The aim of the study was to assess the prevalence of type 2 diabetes and other types of impaired glucose metabolism in bipolar patients along with an evaluation of the Fasting Triglycerides and Glucose Index (TyG) as a method of the insulin sensitivity assessment. The analysis of fasting glycemia, insulinemia and lipid profile in euthymic bipolar patients was performed, and the Homeostasis model assessment for insulin resistance (HOMA-IR) and TyG were computed. Type 2 diabetes was observed in 9% and insulin resistance with HOMA-IR in 48% of patients. The TyG and HOMA-IR indices were correlated (p < 0.0001), the TyG index value of 4.7 had the highest sensitivity and specificity for insulin resistance detection. The usefulness of TyG in the recognition of insulin resistance in bipolar patients was suggested. The significant role of psychiatrists in the detection and management of impaired glucose metabolism in bipolar patients was presented.


2013 ◽  
Vol 20 (2) ◽  
pp. 177-181
Author(s):  
Adina Mitrea ◽  
Simona Georgiana Popa ◽  
Cristina Muntean ◽  
Andreea Soare ◽  
Laura Trotta ◽  
...  

Abstract Recent studies strongly suggest a significant association between diabetes mellitus and Alzheimer Disease (AD) justifying the term “type 3 diabetes”. Studies show that impairment of glucose metabolism occurs very early in the course of AD, leading to a broad range of consequences, among which the accumulation of amyloid beta (Aβ), which per se induces insulin resistance. Furthermore, adipocytokines, recognised markers of insulin resistance, seem to play a role in the development of AD. As for insulin resistance, when AD is considered, the most studied ones are leptin and adiponectin, but also a recently described adipokine - progranulin. It is our belief that both prospective and transversal studies on subjects with both AD and type 2 diabetes (T2D) may prove the role of adipokines not only in AD, but also in this most somber association.


2014 ◽  
Vol 307 (10) ◽  
pp. E859-E871 ◽  
Author(s):  
Greg M. Kowalski ◽  
Clinton R. Bruce

The incidence of insulin resistance and type 2 diabetes (T2D) is increasing at alarming rates. In the quest to understand the underlying causes of and to identify novel therapeutic targets to treat T2D, scientists have become increasingly reliant on the use of rodent models. Here, we provide a discussion on the regulation of rodent glucose metabolism, highlighting key differences and similarities that exist between rodents and humans. In addition, some of the issues and considerations associated with assessing glucose homeostasis and insulin action are outlined. We also discuss the role of the liver vs. skeletal muscle in regulating whole body glucose metabolism in rodents, emphasizing the importance of defective hepatic glucose metabolism in the development of impaired glucose tolerance, insulin resistance, and T2D.


2021 ◽  
Author(s):  
Kaibo Lyu ◽  
Wei Yue ◽  
Junhua Ran ◽  
Yunjuan Liu ◽  
Xueliang Zhu

Background: The study was aimed to investigate the potential therapeutic effect of Mori folium aqueous extracts (MFAE) on type 2 diabetes mellitus (T2DM) in vivo. Methods and Results: A rat model of T2DM was established with the combination of high sugar and high fat diet (HSFD) and streptozotocin (STZ). The T2DM rats were administrated with low (2 g kg-1) and high (5 g kg-1) dose of MFAE for 60 consecutive days. The biochemical indices of glucose metabolism disorders, insulin resistance and oxidative stress were observed. The results indicated that MFAE significantly promoted the synthesis of hepatic glycogen, reduced the levels of fasting blood glucose and fasting blood insulin, and improved the insulin sensitivity index. MFAE administration also remarkably increased the levels of superoxide dismutase (SOD) and reduced the levels of malondialdehyde (MDA). Conclusion: MFAE showed a therapeutic effect on T2DM with the bioative effect of improve glucose metabolism disorders, decrease insulin resistance, and ameliorate the anti-oxidative ability.


Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 1758-P
Author(s):  
HUGO MARTIN ◽  
SÉBASTIEN BULLICH ◽  
FABIEN DUCROCQ ◽  
MARION GRALAND ◽  
CLARA OLIVRY ◽  
...  

Biomedicines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 125
Author(s):  
Jorge Simón ◽  
Teresa Cardoso Delgado ◽  
Luis Alfonso Martinez-Cruz ◽  
Maria Luz Martínez-Chantar

Non-alcoholic steatohepatitis (NASH) is characterized by an abnormal hepatic lipid accumulation accompanied by a necro-inflammatory process and a fibrotic response. It comprises from 10% to 30% of cases of patients with non-alcoholic liver disease, which is a global health problem affecting around a quarter of the worldwide population. Nevertheless, the development of NASH is often surrounded by a pathological context with other comorbidities, such as cardiovascular diseases, obesity, insulin resistance or type 2 diabetes mellitus. Dietary imbalances are increasingly recognized as the root cause of these NASH-related comorbidities. In this context, a growing concern exists about whether magnesium consumption in the general population is sufficient. Hypomagnesemia is a hallmark of the aforementioned NASH comorbidities, and deficiencies in magnesium are also widely related to the triggering of complications that aggravate NASH or derived pathologies. Moreover, the supplementation of this cation has proved to reduce mortality from hepatic complications. In the present review, the role of magnesium in NASH and related comorbidities has been characterized, unraveling the relevance of maintaining the homeostasis of this cation for the correct functioning of the organism.


Biomolecules ◽  
2020 ◽  
Vol 10 (12) ◽  
pp. 1617
Author(s):  
Pierluigi Scalia ◽  
Antonio Giordano ◽  
Caroline Martini ◽  
Stephen J. Williams

Insulin receptor (IR) and IR-related signaling defects have been shown to trigger insulin-resistance in insulin-dependent cells and ultimately to give rise to type 2 diabetes in mammalian organisms. IR expression is ubiquitous in mammalian tissues, and its over-expression is also a common finding in cancerous cells. This latter finding has been shown to associate with both a relative and absolute increase in IR isoform-A (IR-A) expression, missing 12 aa in its EC subunit corresponding to exon 11. Since IR-A is a high-affinity transducer of Insulin-like Growth Factor-II (IGF-II) signals, a growth factor is often secreted by cancer cells; such event offers a direct molecular link between IR-A/IR-B increased ratio in insulin resistance states (obesity and type 2 diabetes) and the malignant advantage provided by IGF-II to solid tumors. Nonetheless, recent findings on the biological role of isoforms for cellular signaling components suggest that the preferential expression of IR isoform-A may be part of a wider contextual isoform-expression switch in downstream regulatory factors, potentially enhancing IR-dependent oncogenic effects. The present review focuses on the role of isoform- and paralog-dependent variability in the IR and downstream cellular components playing a potential role in the modulation of the IR-A signaling related to the changes induced by insulin-resistance-linked conditions as well as to their relationship with the benign versus malignant transition in underlying solid tumors.


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