The protective ways of the body from cell damage at the diabetes mellitus

2016 ◽  
Vol 10 (1) ◽  
pp. 0-0
Author(s):  
Макишева ◽  
R. Makisheva
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Insulin Action ◽  
Cell Damage ◽  
Glycogen Synthesis ◽  
The Body ◽  
Diabetic Patients ◽  
Β Cell ◽  
Extracellular Medium ◽  
Compensation Mechanisms

Recognition hyperinsulinemia as the root cause of type 2 diabetes mellitus is becoming more supporters. The overload nutrition cell and insulin resistance is developing as a result of hyperinsulinemia. Insulin resistance is not the only one protection mechanism. Functional system to limited excessive insulin action includes other mechanisms. This review describes the reactions that develop in the tissues in diabetic patients and their relationship with excessive exposure to insulin. Negative feedback mechanism under excessive stimulation of insulin action includes action contrainsular hormones, no β-cell response on increasing the glucose in the extracellular medium, reduction of C-peptide, induction of β-cell apoptosis. The compensation mechanisms includes the restriction of consumption of substances and flow of information, the redirecting excess in the adi-pose tissue, the glycogen synthesis and the activation of kinase-3 synthase glycogen. The conditions GI insulin is able to bind and activate receptors IGF-type 1 to a greater extent than insulin receptors. At diabetes the repro-duction, the growth and the differentiation of cells are accelerated, leading to tumor growth, the accumulation of senescent cells. The depletion and reduction of telomerase activity in diabetes mellitus also have an adaptive value. Contact with receptors undifferentiated cells caused by their high sensitivity and low capacity for insulin resistance, operates referral mechanism power is the same as for obesity. Young cells of functionally active or-gans die, some cells accelerate differentiation and less active peripheral located in hypoxic conditions, may be-come cancerous. The author believes that the growth of tumors after intensive treatment of diabetes is associated with excess insulin action.

scholarly journals DEMONSTRATION OF PRECISE RELATIONSHIPS AND LINKS BETWEEN TYPE 2 DIABETES MELLITUS, INSULIN RESISTANCE AND PARKINSON’S DISEASE

2020 ◽  
Vol 7 (12) ◽  
pp. 259-270
Author(s):  
Habib ur Rehman ◽  
Kaleemullah ◽  
Abdul Malik Tareen
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Type 2 Diabetes Mellitus ◽  
The Body ◽  
Diabetic Patients ◽  
The Brain

Diabetes is a metabolic disorder that intessssrferes with the body's ability to consume food and convert it into energy. The most common mode of diabetes in type 2 diabetes mellitus (T2DM) is that the body cannot effectively use insulin produced by the pancreas. This is called insulin resistance. Parkinson's Disease (PD) is a chronic neurodegenerative motor defect whose properties work is hindrance with locomotion. This is due to the loss of neurons in the substantia nigra area under the brain that produces dopamine, a chemical messenger that transmits signals that produce smooth, meaningful movement. Dopamine loss caused by neuronal damage and death causes impaired movement. Cells rely on glucose for energy, and insulin helps to convert glucose into energy. In both Parkinson's disease and type 2 diabetes, changes in the brain can result in signaling interruptions that affect normal functioning. Insulin resistance also reaches the brain and produces severe changes in the nerve cells, increasing the risk of Parkinson's disease and abnormally promoting high blood sugar leads to high-rise the inflammation, associated with the development of Parkinson's disease. Diabetes suffering peoples are more likely to have Parkinson's disease. Parkinson's disease is 32% higher in people with type 2 diabetes than in non-diabetic patients. Patients with type 2 diabetes along with its complication have a 49% higher risk of Parkinson’s disease, while those having only type 2 diabetes without complications have a 30% risk of parkinson’s disease. In particular, younger patients with diabetes (25 to 44 years of age) have an approximately fourfold increased risk of developing Parkinson's compared with adults of similar age without diabetes. Researchers has estimated the high risk of developing PD based on longitudinal data methodology for people with type 2 diabetes. Initial studies have reported more than 400 genes linked in both conditions. The potential link between type 2 diabetes and Parkinson's disease has been the topic of medical dialogue and scientific research for years. Recently, animal and in vitro studies have shown that the pathophysiology and clinical symptoms of Parkinson's disease are concerned more with insulin dysregulation and changes in insulin action.

Insulin action and resistance in obesity and noninsulin-dependent type II diabetes mellitus

1982 ◽  
Vol 243 (1) ◽  
pp. E15-E30 ◽  
Author(s):  
J. M. Olefsky ◽  
O. G. Kolterman ◽  
J. A. Scarlett
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Insulin Receptor ◽  
Insulin Action ◽  
Insulin Receptors ◽  
Tissue Level ◽  
Dependent Diabetes Mellitus ◽  
Target Tissue ◽  
Severe Insulin Resistance ◽  
Glucose Clamp Technique

Resistance to the action of insulin can result from a variety of causes, including the formation of abnormal insulin or proinsulin molecules, the presence of circulating antagonists to insulin or the insulin receptor, or defects in insulin action at the target tissue level. Defects of the latter type are characteristic of obesity and of noninsulin-dependent diabetes mellitus. Analysis of the nature of the insulin resistance in those disorders has been investigated in intact subjects with the use of the euglycemic glucose clamp technique, and both insulin receptors and insulin-mediated glucose metabolism have been studied in adipocytes and monocytes from affected individuals. In both conditions, the cause of insulin resistance is heterogeneous. In some, insulin resistance appears to be due to a defect in the insulin receptor, whereas others have a defect both in the receptor and at the postreceptor level. In both groups, more severe insulin resistance is due to the postreceptor lesion and is correctable with appropriate therapy.

scholarly journals The effect of obesity and Insulin Resistance on Liver Enzymes in Type2 Diabetes Mellitus

2015 ◽  
Vol 12 (3) ◽  
pp. 536-545
Author(s):  
Baghdad Science Journal
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Alkaline Phosphatase ◽  
Negative Correlation ◽  
Liver Enzymes ◽  
Alanine Transaminase ◽  
Obese Group ◽  
Control Group ◽  
Diabetic Patients ◽  
And Control

Diabetes mellitus (DM) has been defined as a clinical syndrome that is characterized by abnormal carbohydrate metabolism. The chronic hyperglycemia of diabetes is associated with long term damage, dysfunction, and failure of different organs, especially the liver .This study was conducted to assess the effect obesity and insulin resistance on liver enzymes in diabetic Iraqi patients.A comparative study of (90) Iraqi adults divided to three subgroup(30) obese ,(30) nonobese diabetic patients and(30)person had used as control. The analysis included Liver enzyme ALP,ALT,AST,GGT ,Fasting Plasma Glucose (FBG) , Lipid Profile , Hemoglobin A1C , insulin and homeostasis model assessment of insulin resistance (HOMA IR) were measured. Subjects were excluded from this study if they had liver disease, alcohol intake, medications for lowering lipid, insulin treatment, pregnant women and women taking contraceptive pills . The study shows significantly higher of liver enzymes level ( gamma glutamyl transpeptidase (GGT), alkaline phosphatase, Aspartate Amino Transferase , Alanine Transaminase) in obese diabetic patients compared with non-obese diabetic patients and control subject and HOMA IR showed significantly higher in obese diabetic patients compared with non-obese with diabetic patients and control (P < 0.05). The lipids level showed significantly higher in obese diabetic patients compared with non-obese diabetic patients and control.The HbA1c level showed higher significantly in obese diabetic patients compared with control and ther is a posative correlation between insulin and HOMA IR , ALP in obeses diabetic patients while there was negative correlation between ALT and cholesterol in obese group and with HbA1c in control group. The liver enzymes level of(alkaline phosphatase, alanine transaminase, aspartate transaminase gama glutaminase transferase ) is significantly higher in obese diabetic patients than non –obese diabetic patients and control group , also There was posative correlation between ALP and HOMA IR while there was negative correlation between ALT and cholesterol in obese group and with HbA1c in control group .

scholarly journals Common Risk Factors in Relatives and Spouses of Patients with Type 2 Diabetes in Developing Prediabetes

Healthcare ◽  
2021 ◽  
Vol 9 (8) ◽  
pp. 1010
Author(s):  
Wei-Hao Hsu ◽  
Chin-Wei Tseng ◽  
Yu-Ting Huang ◽  
Ching-Chao Liang ◽  
Mei-Yueh Lee ◽  
...  
Keyword(s):  
Risk Factors ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
Cell Function ◽  
Diabetic Patients ◽  
Β Cell ◽  
Tyg Index ◽  
Β Cell Function

Prediabetes should be viewed as an increased risk for diabetes and cardiovascular disease. In this study, we investigated its prevalence among the relatives and spouses of patients with type 2 diabetes or risk factors for prediabetes, insulin resistance, and β-cell function. A total of 175 individuals were included and stratified into three groups: controls, and relatives and spouses of type 2 diabetic patients. We compared clinical characteristics consisting of a homeostatic model assessment for insulin resistance (HOMA-IR) and beta cell function (HOMA-β), a quantitative insulin sensitivity check index (QUICKI), and triglyceride glucose (TyG) index. After a multivariable linear regression analysis, the relative group was independently correlated with high fasting glucose, a high TyG index, and low β-cell function; the relatives and spouses were independently associated with a low QUICKI. The relatives and spouses equally had a higher prevalence of prediabetes. These study also indicated that the relatives had multiple factors predicting the development of diabetes mellitus, and that the spouses may share a number of common environmental factors associated with low insulin sensitivity.

Su1480 CONTROLLING GLYCEMIC HOMEOSTASIS ALLEVIATES ISLET β CELL DAMAGE AND REDUCES THE RISK OF DIABETES MELLITUS FOLLOWING ACUTE PANCREATITIS

2020 ◽  
Vol 158 (6) ◽  
pp. S-596-S-597
Author(s):  
Qiao Shi ◽  
Xiaoyi Zhang ◽  
Hanjun Li ◽  
Xingcheng Xiong ◽  
Weixing Wang ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Acute Pancreatitis ◽  
Cell Damage ◽  
Β Cell

scholarly journals ALTERATIONS OF LIPID LEVELS MAY INDUCE THE INSULIN RESISTANCE IN TYPE TWO DIABETES MELLITUS: A SYSTEMIC REVIEW

2020 ◽  
pp. 9-20
Author(s):  
DIVYA JYOTHI P ◽  
DOONDI PHANI KUMAR N ◽  
VINAY MOHAN A ◽  
RAMYA A
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Microvascular Complications ◽  
Hormone Secretion ◽  
International Diabetes Federation ◽  
The Body ◽  
Systemic Review ◽  
Cardiac Complications ◽  
Sequence Of Events ◽  
Chronic Hyperglycemia

Diabetes mellitus (DM) is not one disorder; it represents a series of metabolic conditions related to hyperglycemia and caused by defects in hormone secretion and hormone action. Exposure to chronic hyperglycemia may result in microvascular complications in the retina (diabetic retinopathy), kidney (diabetic nephropathy), neuron (diabetic-neuropathy), skin, foot, and cardiac complications (stroke, hypertension…etc.). International Diabetes Federation estimates that 1.1 million children and adolescents aged 14–19 years have type one DM. Without interventions to halt the increase in diabetes, there will be at least 629 million people living with diabetes by 2045. In the body, white adipose tissue is the leading site for the storage of excess energy produced from the food intake in large quantities, of the development of insulin resistance (IR) and type 2 DM by the over intake of fatty acid in the body. It results in the accumulation of fatty acyl co-A (FA-CoA) within the myocytes. It leads to improper signaling of the insulin and reduces the level in the myocytes and pancreases beta cells. It combines with genetically reduces the expression of peroxisome proliferator-activated receptor-gamma (PPAR-γ) coactivator-1, initiates the inflammation process by the activation of the tumor necrotic factor alpha and protein kinase C. These alterations lead to further increase the intramyocellular FA-CoA and triglycerides. The sequence of events may develop mitochondrial dysfunction in the sarcolemma outer layers. Finally improves IR also with increasing intramyocellular lipids. This concept might be helpful to those who are pursuing endocrinology specialization, nursing staff, pharmacists, and other medical departments.

scholarly journals Associations between Fatty Acid-Binding Protein 4–A Proinflammatory Adipokine and Insulin Resistance, Gestational and Type 2 Diabetes Mellitus

Cells ◽  
2019 ◽  
Vol 8 (3) ◽  
pp. 227 ◽  
Author(s):  
Marcin Trojnar ◽  
Jolanta Patro-Małysza ◽  
Żaneta Kimber-Trojnar ◽  
Bożena Leszczyńska-Gorzelak ◽  
Jerzy Mosiewicz
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Fatty Acid ◽  
Fatty Acid Binding Protein ◽  
Binding Protein ◽  
Clinical Aspects ◽  
Diabetic Patients ◽  
Fatty Acid Binding ◽  
Acid Binding Protein

There is ample scientific evidence to suggest a link between the fatty acid-binding protein 4 (FABP4) and insulin resistance, gestational (GDM), and type 2 (T2DM) diabetes mellitus. This novel proinflammatory adipokine is engaged in the regulation of lipid metabolism at the cellular level. The molecule takes part in lipid oxidation, the regulation of transcription as well as the synthesis of membranes. An involvement of FABP4 in the pathogenesis of obesity and insulin resistance seems to be mediated via FABP4-dependent peroxisome proliferator-activated receptor γ (PPARγ) inhibition. A considerable number of studies have shown that plasma concentrations of FABP4 is increased in obesity and T2DM, and that circulating FABP4 levels are correlated with certain clinical parameters, such as body mass index, insulin resistance, and dyslipidemia. Since plasma-circulating FABP4 has the potential to modulate the function of several types of cells, it appears to be of extreme interest to try to develop potential therapeutic strategies targeting the pathogenesis of metabolic diseases in this respect. In this manuscript, representing a detailed review of the literature on FABP4 and the abovementioned metabolic disorders, various mechanisms of the interaction of FABP4 with insulin signaling pathways are thoroughly discussed. Clinical aspects of insulin resistance in diabetic patients, including women diagnosed with GDM, are analyzed as well.

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