Hyperglycemia is a morbid condition wherein a surfeit of glucose(blood sugar) is observed in the blood of an individual. Surplus blood sugar levels hinder the flow of blood by dwindling the resilience of blood vessels.
Comprehensive research on hyperglycemia indicates that it is a prodigious impeller of reactive oxygen species or ROS, also known as oxygen radicals. These oxygen radicals are responsible for inhibiting or activating various mechanisms and signal transduction cascades as well. Under hyperglycaemic phenomenon; xanthine oxidase, NADPH oxidase, and mitochondria are known to cause paroxysm of oxygen radicals(ROS). This immoderate production of oxygen radicals causes oxidative stress, and plays a part in the occurrence of complications pertaining to hyperglycaemia.
What is hyperglycemia?
Hyperglycemia is more prevalent in diabetic individuals. It results from the impaired secretions of insulin hormone with anomalous levels of peripheral insulin resistance syndrome.
Different levels of blood sugar(glucose)
There are many circumstances that influence hyperglycemic responses but nonketotic hyperosmolar coma, diabetic ketoacidosis or DKA(principally observed in Type I diabetic patients), and parenteral hyperalimentation are considered as the major factors.
What causes hyperglycemia?
The explicit mechanism of hyperglycaemic response is yet indistinct; and is perhaps associated with the downregulation of GLUT-1 and GLUT-3 expression, in diabetes. Attestation indicates that, in diabetes, chronic hyperglycemia can decrease the transportation of intracellular glucose; this results in a defence mechanism–where the reduced influx of glucose, subsides the cytotoxic effect of the high sugar levels. A hypothetical paradigm has been developed pertaining to this phenomenon(hyperglycemia stimulated by GLUT transporters in the brain are considered for developing a hypothetical paradigm).
This hypothetical paradigm emphasizes two outcomes.
- Hyperglycemia leveraged by pro-inflammatory cytokines might induce neuroinflammation, thus downregulating the GLUT transporter.
- Scarcity of GLUT-1 transporters might cause Hyperglycemia-induced neuronal apoptosis; as neurons are deprived of the energy source
Diabetic ketoacidosis or DKA is associated with insulin deficiency. In this insulin-deficient phenomenon, insulin is the linchpin of therapy. The truancy of insulin commutes the formation of glycogen and uptake of peripheral glucose; and expedites the phenomena of lipolysis and glycogenolysis that causes to form hyperglycemia and acidic ketone bodies.
What are the symptoms of hyperglycemia?
Hyperglycaemic responses are not observed when the levels of glucose are normal. An elevated level of blood sugar(glucose) triggers this phenomenon. Hyperglycemic symptoms may gradually develop over a period of time(several days to weeks).
Hyperglycemia can be stimulated by ill health, and stress, because during this state(ill-health and stress), the immune system of an individual produces hormones to fight the antigens and chemicals released respectively; during which the glucose levels may rise.
Individuals who are not diabetic might also develop transient hyperglycemia whereas diabetic patients require medication pertaining to diabetes so as to lessen the blood sugar when they are sick, or under stress.
- Early-onset symptoms/signs include blurred vision, fatigue, headache, excess thirst, and frequent urination.
- Untreated hyperglycemia leads to the accretion of ketones(toxic acids) in the urine, and blood; a phenomenon also called as ketoacidosis. Signs/symptoms may include abdominal pain, confusion, dry mouth, weakness, shortness of breath, coma, fruity-smelling breath, vomiting, and nausea.
What are the treatments for hyperglycemia?
Hyperglycemia alone is known to cause endothelial dysfunctions like dyslipidemia, hypertension, and also hyperglycaemia. The outcome of endothelial dysfunctions includes the upregulation of coagulation, platelet aggregation, acceleration of atherosclerosis, and downregulation of fibrinolysis. The resultant effect of these drastic changes escalates blood thrombogenicity, atherosclerosis, and subjects an individual to acute coronary syndrome.
Parasympathetic nerves activation(ACh) triggers the release of insulin hormone. Drugs like norepinephrine, epinephrine or atropine obstruct the release of insulin.
The skeletal muscles dispose of the excessive insulin-stimulated glucose with the help of antidiabetic drugs like thiazolidinedione, which majorly amends hyperglycemia; and are also known to hinder mitochondrial complex I that impedes gluconeogenesis which plays a role in triggering antidiabetic activities.
Hyperglycemia is a medical condition that is more prevalent in diabetic patients. Various factors are known to contribute to surplus blood sugar levels such as illness, stress, opting for unfavourable physical activities, non-diabetes medications, disregarding glucose-lowering medications, and unhealthy diet. When one observes an unexpected bout of increased appetite, urination, and thirst then he/she might be experiencing diabetic ketoacidosis (DKA).