scholarly journals Clinical, metabolic and hormonal features of the formation of impaired hypoglycemia awareness

Author(s):  
I.А. Reva ◽  
◽  
I.А. Bondar ◽  

The review presents the prevalence, pathogenetic aspects of the development of impaired hypoglycemia awareness in diabetes mellitus and its effect on the course of the disease. A key aspect in the pathogenesis of atypical hypoglycemias is the brain adaptation to a low glucose concentration in blood, which entails a disorder of hormonal response to hypoglycemia. This process is an autonomous dysfunction associated with hypoglycemia. It is noted the role of atypical hypoglycemia in the development of cardiovascular complications, cognitive impairments and pregnancy failure in patients with diabetes mellitus.

Biology ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 621
Author(s):  
Ernest Adeghate ◽  
Crystal M. D’Souza ◽  
Zulqarnain Saeed ◽  
Saeeda Al Jaberi ◽  
Saeed Tariq ◽  
...  

Nociceptin (NC) consists of 17 amino acids (aa) and takes part in the processing of learning and memory. The role of NC in the induction of endogenous antioxidants in still unclear. We examined the effect of NC on the expression of endogenous antioxidants in kidney, liver, cerebral cortex (CC), and hippocampus after the onset of diabetes mellitus, using enzyme-linked immunosorbent assay and immunohistochemistry. Exogenous NC (aa chain 1–17; 10 µg/kg body weight) was given intraperitoneally to normal and diabetic rats for 5 days. Our results showed that catalase (CAT) is present in the proximal (PCT) and distal (DCT) convoluted tubules of kidney, hepatocytes, and neurons of CC and hippocampus. The expression of CAT was significantly (p < 0.05) reduced in the kidney of normal and diabetic rats after treatment with NC. However, NC markedly (p < 0.001) increased the expression CAT in the liver and neurons of CC of diabetic rats. Superoxide dismutase (SOD) is widely distributed in the PCT and DCT of kidney, hepatocytes, and neurons of CC and hippocampus. NC significantly (p < 0.001) increased the expression of SOD in hepatocytes and neurons of CC and the hippocampus but not in the kidney. Glutathione reductase (GRED) was observed in kidney tubules, hepatocytes and neurons of the brain. NC markedly increased (p < 0.001) the expression of GRED in PCT and DCT cells of the kidney and hepatocytes of liver and neurons of CC. In conclusion, NC is a strong inducer of CAT, SOD, and GRED expression in the kidney, liver and brain of diabetic rats.


2013 ◽  
Vol 126 (7) ◽  
pp. 471-482 ◽  
Author(s):  
Vaibhav B. Patel ◽  
Nirmal Parajuli ◽  
Gavin Y. Oudit

Diabetes mellitus results in severe cardiovascular complications, and heart disease and failure remain the major causes of death in patients with diabetes. Given the increasing global tide of obesity and diabetes, the clinical burden of diabetes-induced cardiovascular disease is reaching epidemic proportions. Therefore urgent actions are needed to stem the tide of diabetes which entails new prevention and treatment tools. Clinical and pharmacological studies have demonstrated that AngII (angiotensin II), the major effector peptide of the RAS (renin–angiotensin system), is a critical promoter of insulin resistance and diabetes mellitus. The role of RAS and AngII has been implicated in the progression of diabetic cardiovascular complications and AT1R (AngII type 1 receptor) blockers and ACE (angiotensin-converting enzyme) inhibitors have shown clinical benefits. ACE2, the recently discovered homologue of ACE, is a monocarboxypeptidase which converts AngII into Ang-(1–7) [angiotensin-(1–7)] which, by virtue of its actions on the MasR (Mas receptor), opposes the effects of AngII. In animal models of diabetes, an early increase in ACE2 expression and activity occurs, whereas ACE2 mRNA and protein levels have been found to decrease in older STZ (streptozotocin)-induced diabetic rats. Using the Akita mouse model of Type 1 diabetes, we have recently shown that loss of ACE2 disrupts the balance of the RAS in a diabetic state and leads to AngII/AT1R-dependent systolic dysfunction and impaired vascular function. In the present review, we will discuss the role of the RAS in the pathophysiology and treatment of diabetes and its complications with particular emphasis on potential benefits of the ACE2/Ang-(1–7)/MasR axis activation.


2021 ◽  
Vol 22 ◽  
Author(s):  
Raghuvir Keni ◽  
Abinitha Sekhar ◽  
Karthik Gourishetti ◽  
Pawan Ganesh Nayak ◽  
Manas Kinra ◽  
...  

Statins have transformed the treatment of cardiovascular diseases through primary and secondary prevention of events. Despite the success of statin's inefficient management of cardiovascular conditions, certain clinical trials, reviews, and meta-analysis point out that statins have the propensity to induce diabetes. The risk further increases with intensive statin therapy or in with patients with diabetes. A proper mechanism for the induction of the diabetic condition has not yet been determined. The involvement of statin with beta cells in insulin secretion and peripheral cells in insulin resistance has been widely studied and established. The present review provides an update on recent understanding of statin-induced diabetes. This covers the origin of statins, their development, possible mechanisms that explain the adverse effects in glucose homeostasis, and probable targets to remedy the condition.


2021 ◽  
pp. 8-9
Author(s):  
Murugesan Thinakaran ◽  
Thangadurai Chitra

Background and objects: Patients with diabetes mellitus are at high risk of cardiovascular events because of abnormal lipid status. Dyslipidemia is common in diabetes mellitus and is associated with cardiovascular complications. Early diagnosis and treatment is the main cornerstone in the prevention of its multiple complications. The aim of the study was to determine the prevalence of abnormal lipid prole levels. Materials and Method: The study population was made up of Eighty-ve (85) already diagnosed type 2 diabetic patients and Ninety-two (92) with an age range of 28 to 70 years, who come from routine health, follow up at various tertiary hospitals in Erode. The samples were analyzed using the chemical analyzer COBAS INTEGRA 400. Results and Conclusion: Dyslipidemia was found in 63.52% in type2 diabetes patients and 43.47% in non-diabetic patients. High TG, high LDL-C, high TC and low HDL-C exhibited an increasing trend in the proportion of patients with dyslipidemia. The following risk factors namely female sex, age above 50- years, BMI (overweight and obese), poor glycemic control, central obesity and physical inactivity were associated with diabetic dyslipidemia. This study presents some interesting and novel ndings which may be very important in the care and management of patients with type-2 diabetes.


1979 ◽  
Vol 17 (22) ◽  
pp. 85-87

Dietary control is a central part of management of diabetes mellitus. Traditional advice is primarily concerned with carbohydrate restriction, calorie control and the timing of meals. The importance of the fat and fibre content is largely ignored although fats might influence the development of cardiovascular complications and fibre the blood glucose concentration and the response to hypoglycaemic agents. The composition of the diabetic diet needs reappraisal.


Author(s):  
Pratik Choudhary ◽  
Stephanie A. Amiel

Hypoglycaemia (low blood glucose concentration) is the most important acute complication of the pharmacological treatment of diabetes mellitus. Low blood glucose impairs brain (and, potentially, cardiac) function. The brain has minimal endogenous stores of energy, with small amounts of glycogen in astroglial cells. The brain is therefore largely dependent on circulating glucose as the substrate to fuel cerebral metabolism and support cognitive performance. If blood glucose levels fall sufficiently, cognitive dysfunction is inevitable. In health, efficient glucose sensing and counterregulatory mechanisms exist to prevent clinically significant hypoglycaemia. These are impaired by diabetes and by its therapies. Patients with diabetes rank fear of hypoglycaemia as highly as fear of chronic complications such as nephropathy or retinopathy (1). Fear of hypoglycaemia, hypoglycaemia itself and attempts to avoid hypoglycaemia limit the degree to which glycaemic control can be intensified to reduce the risk of chronic complications of diabetes both for type 1 and type 2 diabetes.


2019 ◽  
Vol 4 (2) ◽  
pp. 90-92 ◽  
Author(s):  
Li Zhang ◽  
Michael Chopp ◽  
Quan Jiang ◽  
Zhenggang Zhang

Diabetes mellitus (DM) is a common metabolic disease in the middle-aged and older population, and is associated with cognitive impairment and an increased risk of developing dementia. The glymphatic system is a recently characterised brain-wide cerebrospinal fluid and interstitial fluid drainage pathway that enables the clearance of interstitial metabolic waste from the brain parenchyma. Emerging data suggest that DM and ageing impair the glymphatic system, leading to accumulation of metabolic wastes including amyloid-β within the brain parenchyma, and consequently provoking cognitive dysfunction. In this review, we concisely discuss recent findings regarding the role of the glymphatic system in DM and ageing associated cognitive impairment.


2019 ◽  
Vol 30 (8) ◽  
pp. 869-879 ◽  
Author(s):  
Tao Li ◽  
Zeyi Huang ◽  
Xianwen Wang ◽  
Ju Zou ◽  
Sijie Tan

Abstract Sevoflurane is a widely used inhalational anesthetic in pediatric surgeries, which is considered reasonably safe and reversible upon withdrawal. However, recent preclinical studies suggested that peri-neonatal sevoflurane exposure may cause developmental abnormalities in the brain. The present review aimed to present and discuss the accumulating experimental data regarding the undesirable effects of sevoflurane on brain development as revealed by the laboratory studies. First, we summarized the long-lasting side effects of neonatal sevoflurane exposure on cognitive functions. Subsequently, we presented the structural changes, namely, neuroapoptosis, neurogenesis and synaptogenesis, following sevoflurane exposure in the immature brain. Finally, we also discussed the potential mechanisms underlying subsequent cognitive impairments later in life, which are induced by neonatal sevoflurane exposure and pointed out potential strategies for mitigating sevoflurane-induced long-term cognitive impairments. The type A gamma-amino butyric acid (GABAA) receptor, the main targets of sevoflurane, is excitatory rather than inhibitory in the immature neurons. The excitatory effects of the GABAA receptors have been linked to increased neuroapoptosis, elevated serum corticosterone levels and epigenetic modifications following neonatal sevoflurane exposure in rodents, which might contribute to sevoflurane-induced long-term cognitive abnormalities. We proposed that the excitatory GABAA receptor-mediated HPA axis activity might be a novel mechanism underlying sevoflurane-induced long-term cognitive impairments. More studies are needed to investigate the effectiveness and mechanisms by targeting the excitatory GABAA receptor as a prevention strategy to alleviate cognitive deficits induced by neonatal sevoflurane exposure in future.


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