Influence of insulin resistance on the course of ischemic stroke in the acute period

2020 ◽  
Vol 18 (5) ◽  
pp. 93-98
Author(s):  
L. B. NOVIKOVA ◽  
◽  
G. I. IZHBULDINA ◽  
Keyword(s):  
Insulin Resistance ◽  
Ischemic Stroke ◽  
Clinical Outcome ◽  
Carbohydrate Metabolism ◽  
Neurological Deficit ◽  
Glucose Metabolism Disorders ◽  
C Peptide ◽  
Acute Period

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.

scholarly journals METABOLIC ASPECTS OF ACUTE stage ISCHEMIC STROKE

2018 ◽  
Vol 35 (1) ◽  
pp. 5-11
Author(s):  
G I Izhbuldina ◽  
L B Novikova ◽  
D A Timerbayeva ◽  
E V Sharipova ◽  
R V Murzabayeva
Keyword(s):  
Diabetes Mellitus ◽  
Ischemic Stroke ◽  
Blood Glucose ◽  
Clinical Outcome ◽  
Arterial Hypertension ◽  
Fasting Blood Glucose ◽  
Acute Stage ◽  
Immunoreactive Insulin ◽  
C Peptide ◽  
Acute Period

Aim. To study the influence of hyperglycemia on the course of ischemic stroke in its acute period. Materials and methods. 116 patients with primary ischemic stroke, associated with arterial hypertension, and with no diabetes mellitus in anamnesis were examined. Fasting blood glucose, glycolyzed hemoglobin, immunoreactive insulin and C-peptide levels were determined. Results. Raised levels of glycemia to 5.31 ± 0.68 mmol/l, C-peptide to 0.90 ± 0.31 nmol/l and decreased level of insulin to 9.38 ± 4.34 mcIU/ml were detected. C-peptide to insulin ratio values were reliably higher in patients with severe course of stroke (by 35.6 %, p < 0.05) and unfavorable outcome of disease (by 39.6 %, p < 0.05). Conclusions. Development of ischemic stroke is accompanied by high blood C-peptide levels against the background of normo-and-hypoinsulinemia, hyperglycemia. Manifestation of disorders is connected with severity and clinical outcome of this disease.

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

2020 ◽  
pp. 3-14
Author(s):  
Viktoria N. Shadenko
Keyword(s):  
Insulin Resistance ◽  
Glucose Metabolism ◽  
Insulin Receptors ◽  
Glucose Metabolism Disorders ◽  
Review Of Literature ◽  
Brain Functions ◽  
Age Dependent ◽  
Relationship Of

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.

scholarly journals Insulin resistance in pathogenesis of type 2 diabetes mellitus

2011 ◽  
Vol 14 (1) ◽  
pp. 35-45 ◽  
Author(s):  
Alexander Yur'evich Mayorov
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Carbohydrate Metabolism ◽  
Glucose Utilization ◽  
Normal Subjects ◽  
Fasting Glycemia ◽  
Hypoglycemic Therapy

This review focuses on the mechanisms of impaired sensitivity to insulin associated withevolution of carbohydrate metabolism disorders from enhanced fasting glycemia (EFG) to impaired glucose tolerance (IGT) and type 2 diabetes.Disturbances of glucose utilization at the receptor and post-receptor levels are considered along with the role of glucose and lipotoxicity. Original dataon insulin resistance (IR) in patients with disorders of carbohydrate metabolism are presented. Insulin sensitivity in DM2, EFG and IGT is shownto be 50, 25 and 15% lower respectively than in normal subjects. M-index positively correlates with BMI and quality of metabolic control (HbA1cand triglyceride levels). The differences in clinical and biochemical characteristics of DM2 patients are analysed depending on the degree of IR.Adiponectin and resistin levels in DM2 are shown to be lower than in healthy subjects while TNF-a and proinsulin levels increase. Therapy withmetformin, pyoglitazone, and insulin improves insulin sensitivity even in patients with early disturbances of carbohydrate metabolism. It is concludedthat intensive hypoglycemic therapy should be initiated before marked deterioration of insulin sensitivity developed.

1758-P: Type 2 Diabetes–Associated Mood Disorders: Role of Insulin Resistance in Serotonergic Neurons

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 1758-P
Author(s):  
HUGO MARTIN ◽  
SÉBASTIEN BULLICH ◽  
FABIEN DUCROCQ ◽  
MARION GRALAND ◽  
CLARA OLIVRY ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Mood Disorders ◽  
Serotonergic Neurons ◽  
P Type

scholarly journals Magnesium, Little Known But Possibly Relevant: A Link between NASH and Related Comorbidities

Biomedicines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 125
Author(s):  
Jorge Simón ◽  
Teresa Cardoso Delgado ◽  
Luis Alfonso Martinez-Cruz ◽  
Maria Luz Martínez-Chantar
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Inflammatory Process ◽  
Fibrotic Response ◽  
Hepatic Lipid Accumulation ◽  
Root Cause ◽  
Worldwide Population ◽  
Global Health Problem

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.

scholarly journals Isoform- and Paralog-Switching in IR-Signaling: When Diabetes Opens the Gates to Cancer

Biomolecules ◽  
2020 ◽  
Vol 10 (12) ◽  
pp. 1617
Author(s):  
Pierluigi Scalia ◽  
Antonio Giordano ◽  
Caroline Martini ◽  
Stephen J. Williams
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Growth Factor ◽  
Solid Tumors ◽  
Common Finding ◽  
Absolute Increase ◽  
Preferential Expression ◽  
Exon 11

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.

scholarly journals Adipose tissue inflammation and metabolic dysfunction: a clinical perspective

2013 ◽  
Vol 15 (1) ◽  
Author(s):  
Charmaine S. Tam ◽  
Leanne M. Redman
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Low Grade ◽  
Metabolic Dysfunction ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
Proinflammatory Mediators ◽  
Low Grade Inflammation

AbstractObesity is characterized by a state of chronic low-grade inflammation due to increased immune cells, specifically infiltrated macrophages into adipose tissue, which in turn secrete a range of proinflammatory mediators. This nonselective low-grade inflammation of adipose tissue is systemic in nature and can impair insulin signaling pathways, thus, increasing the risk of developing insulin resistance and type 2 diabetes. The aim of this review is to provide an update on clinical studies examining the role of adipose tissue in the development of obesity-associated complications in humans. We will discuss adipose tissue inflammation during different scenarios of energy imbalance and metabolic dysfunction including obesity and overfeeding, weight loss by calorie restriction or bariatric surgery, and conditions of insulin resistance (diabetes, polycystic ovarian syndrome).

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