Diabetes mellitus is a disorder that affects the body’s ability to make or use insulin.
Insulin is a hormone produced in the pancreas that helps transport glucose (blood sugar) from the bloodstream into the cells so they can break it down and use it for fuel. People cannot live without insulin. Diabetes results in abnormal levels of glucose in the bloodstream.
This can cause severe short-term and long-term consequences ranging from brain damage to amputations and heart disease.
Diabetes mellitus is sometimes referred to as sugar diabetes but usually is simply called diabetes, there is also a rare disease called diabetes insipidus (water diabetes) in which the kidney releases too much water. Like diabetes mellitus, it has excessive urination as a symptom, but these two endocrine disorders are otherwise unrelated.
The term diabetes mellitus describes a metabolic disorder of multiple etiology characterized by high blood glucose level with disturbance of carbohydrate, fat and protein metabolism resulting from defects in insulin secretion, insulin action, or both.
The effect of diabetes mellitus includes long-term damage, dysfunction, and failure of various organs. It is the most common none communicable disease worldwide and the fourth to the fifth leading cause of death in developed countries.
The traditional treatment of diabetes may include a low sugar and carbohydrate diet accompanied with exercise for mild cases. For severe and harder to control glucose levels, diabetes can be treated by the administration of insulin and/or by sulfonylurea antidiabetics drugs that stimulate the production of insulin and therefore lower the blood glucose levels.
The reference drug that will be used in this experiment is tolbutamide, which starts to work within one hour and is effective for 6-12 hours.
For sulfonylurea antidiabetic drugs to work there has to be some cells of the pancreas that are working and therefore are able to be stimulated to produce an appropriate amount of insulin. Tolbutamide, along with all other sulfonylureas’ drugs, increases the output of insulin by binding to the receptors of the beta cells of the islet of Langerhans located in the pancreas.
Once they bind to the sulfonylurea’s receptors, the K+ -ATP channels are closed and therefore the membrane is depolarized and insulin production is stimulated.
Though the pancreatic β-cell and its secretory product insulin are central in the pathophysiology of diabetes exist which are caused by a complex interaction of genetics, environmental factors, and lifestyle choices. Some forms are characterized by absolute insulin resistance as their underlying aetiology.
The World Health Organization has recommended that much research should be done on hypoglycemic plants. More than 400 species of plants have been reported to display the hypoglycemic effect, but only a few of them have been investigated.
CLASSIFICATION OF DIABETES MELLITUS AND OTHER CATEGORIES OF GLUCOSE REGULATION.
TYPE 1 diabetes (β-cell destruction, usually leading to absolute insulin deficiency)
This form of diabetes, which accounts for only 5-10% of those with diabetes, previously encompassed by the term insulin-dependent diabetes mellitus (IDDM), type 1 diabetes, or juvenile-onset diabetes, results from cellular-mediated autoimmune destruction of the β -cell of the pancreas. Markers of the immune destruction of the β -cell includes islet cell autoantibodies, autoantibodies to insulin, autoantibodies to glutamic acid decarboxylase (GAD65), and autoantibodies to the tyrosine phosphatases 1A-2 and.
One and usually more of these autoantibodies are present in 85-90% of individuals when fasting hyperglycemia is initially detected. In this form of diabetes, the rate of β -cell destruction is quite variable, being rapid in some individuals (mainly infants and children) and slow in others (mainly adults). some patients, particularly children, and adolescents may present with ketoacidosis as the first manifestation of the disease.
Others have modest fasting hyperglycemia that can rapidly change to severe hyperglycemia and/or ketoacidosis in the presence of infection or other stress. still others, particularly adults, may retain residual β-cell function sufficient to prevent ketoacidosis for many years; such individuals eventually become dependent on insulin for survival and are at risk for ketoacidosis.
At this latter stage of the disease, there is little or no insulin secretion, as manifested by low or undetectable levels of plasma c-peptide. Immune-mediated diabetes commonly occurs in childhood and adolescence, but it can occur at any age, even in the 8th and 9th decades of life.
Autoimmune destruction of β-cell has multiple genetic predispositions and is also related to environmental factors that are still poorly defined.
Some forms of type 1 diabetes have no known etiologies. Some of these patients have permanent insulinogenic and are prone to ketoacidosis, but have no evidence of autoimmunity.
Although only a minority of patients with type 1 diabetes fall into this category, of those who do, most are of African or Asian ancestry. An individual with this form of diabetes suffers from episodes of ketoacidosis and exhibits varying degrees of insulin deficiency between episodes.
This form of diabetes is strongly inherited, lacks immunological evidence β-cell autoimmunity, and is no HLA association. An absolute requirement for insulin replacement therapy in affected patients may come and go.
Although patients are rarely obese when they present with this type of diabetes, the presence of obesity is not incompatible with the diagnosis.
These patients are also prone to other autoimmune disorders such as graves’ disease, Hashimoto’s thyroiditis, Addison’s disease, vitiligo, celiac sprue, autoimmune hepatitis, myasthenia gravis, and pernicious anemia.
Type 2 diabetes (ranging from predominantly insulin resistance with relative insulin deficiency to predominantly an insulin secretory defect with insulin resistance)
This form of diabetes, which accounts for 90-95% of those with diabetes, previously referred to as non-insulin dependent Diabetes Mellitus (NIDDM), type 11 diabetes, or adult-onset diabetes, encompasses individuals who have insulin resistance and usually have relative (rather than absolute) insulin deficiency.
At least initially, and often throughout their lifetime, these individuals do not need insulin treatment to survive. There are probably many different causes of this form of diabetes. Although the specific etiologies are not known, autoimmune destruction of β-cell does not occur, and patients do not have any of the other causes of diabetes.
Most patients with this form of diabetes are obese, and obesity itself causes some degree of insulin resistance. Patients who are not obese by traditional weight criteria may have an increased percentage of body fat distributed predominantly in the abdominal region.
Ketoacidosis seldom occurs spontaneously in this type of diabetes; when seen, it usually arises in association with the stress of another illness such as infection. This form of diabetes frequently goes undiagnosed for many years because the hyperglycemia develops gradually and at earlier stages is often not severe enough for the patient to notice any of the classic symptoms of diabetes.
Nevertheless, such patients are at increased risk of developing macrovascular and microvascular complications. Whereas patients with this form of diabetes may have insulin levels that appear normal or elevated, the higher blood glucose levels in these diabetic patients would be expected to result in even higher insulin values had their β-cell function been normal.
Thus, insulin secretion is defective in these patients and insufficient to compensate for insulin resistance.
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Other specific types of diabetes
Genetic defects of the β-cell, genetic defects in insulin action, diseases of the exocrine pancreas, endocrinopathies, drug or chemical-induced diabetes.
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