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What is Type 2 Diabetes?

Through the history of the evolution of the descriptions and definitions of type 2 diabetes, one can begin to understand the disease. First described in the Ebbers papyrus, diabetes is a disease that has affected mankind for more than three millennia. During the renaissance, the term diabetes was coined as a disease. This Word came from a Greek word that meant siphon or to pass through. Later, physicians would attribute this name to the manifestation of excessive urine. Years later, diabetes would be classified into two major groups, diabetes mellitus, and diabetes insipidus.

What is Type 2 Diabetes?

Diabetes insipidus is characterized by dilute urine without sugar. Contrasting with diabetes mellitus which did have sugar. This is reflected in the etymological descriptors of each disease, insipidus meaning insipid or tasteless and mellitus meaning sweet. It is odd to think of professionals, like a physician, would taste the urine of men, however, it has been said that before the advances in biochemistry, a urine-ant test would be performed.  Urine would be left out on the outside for a certain time if it attracted ants this meant that sugar was present in the patient’s urine.

The difference between the two types was the origin of each.  Diabetes insipidus is related to abnormal urine concentration abnormalities. While diabetes mellitus is directly associated with abnormalities in sugar blood levels.  Afterward, it was observed that diabetes mellitus had several subtypes associated with its etiology, the most important subtypes being type 1 diabetes mellitus and type 2 diabetes mellitus. The initial difference was defined by the patient’s response to insulin. If the patient responded to insulin and this resulted in a decrease in glucose levels, the patient would be identified as insulin sensitive or type 1 diabetes. In contrast, type 2 diabetes patients would not respond to the administration of insulin.

A complete definition of type 2 diabetes is far from complete if only the historical context, previously mentioned, is described. In order to completely describe type 2 diabetes mellitus, it is essential to provide a definition associating the current research and current context of the disease. A conceptual definition of type 2 diabetes mellitus could be the following.

Type 2 diabetes is a disease resulting from the endocrine dysfunction of both the endocrine organ and the target organs which result in a chronic condition of hyperglycemia that is currently associated with this global chronic disease epidemic. Additionally, it is a disease with severe repercussions that can cause dysfunction in the diverse organ system leading to a decrease the quality of life or even death in some patients.

The essential process ongoing in type 2 diabetes mellitus is the dysfunction of the endocrine regulation of the patient’s glycemia. Two essential processes of glycemic regulation are disrupted in type 2 diabetes, a patient’s sensibility to insulin effects in diverse organs and the pancreatic beta-cell secretion of insulin.

In regular patients without type 2 diabetes, the variations in their glycemia are regulated through the following physiological process. First, after a meal two signals trigger the beta-cells to secrete insulin. The first signals originate from cells in the gastrointestinal tract which detect the contents of the meal and later relay messages to the pancreas that stimulate insulin secretion in the pancreatic beta-cells. These messages from the gastrointestinal tract are called the incretin hormones and include the glucagon-like peptide-1 and the gastrointestinal peptide. These chemical messages cause an increase in insulin secretion before the post-prandial glucose spike in blood levels. The second signal begins after food is absorbed through the gastrointestinal tract and increases glucose blood levels. Later pancreatic beta-cells sense the increase in the patient’s glycemia and secrete insulin. Finally, as a result of insulin secretion, several organs are induced into decreasing blood sugar levels.

In a diabetic patient, as a result of genetic predisposition and numerous environmental factors, it is theorized there is an initial state of hyperglycemia, which triggers the secretion of insulin. Initially, the body is able to decrease the blood sugar levels but as time passes, with constant hyperglycemic conditions, the desensitization of insulin’s target organ can result. This desensitization is defined by the organ’s lack of responses towards insulin. Therefore, organs such as the muscles and the liver stop processing the signal and this results in further hyperglycemia which will, in turn, lead to more insulin secretion. This worsens the condition as hyperglycemia is further extended for longer periods Because of this type 2 diabetes can be described as a vicious cycle that perpetuates itself without clinical treatment.

Recently, a second aspect has been observed in patients diagnosed with type 2 diabetes. In some patients, there is an impaired insulin secretion in addition to insulin sensitivity. This is believed to be the result of the inflammatory state of diabetic patients. It is thought that the constant levels of increased blood sugar provoke this state of inflammation in the body. Additionally, beta-cells are particularly sensitive to the harmful effects of this inflammation and this induces a cellular death process. This results in the decrease in pancreatic beta-cell mass and consequently beta-cell functions.

It is vital to point out that this is not the same situation with the pathogenesis of type one diabetes in which there is a destruction of beta-cells as a result of autoimmune abnormalities. The initial decrease in pancreatic beta-cell mass is the origin of the disease in type 1 diabetes.  In contrast, in type two diabetes the decrease of beta-cell mass is believed to be a result of the initial process that caused the disease. This later will add on to the vicious cycle found in type 2 diabetes. However, it undeniable that there is some overlap in the pathogenic mechanism in which each disease is produced, each differing in their causes and epidemiology.

Current studies are trying to portray the dysfunction of incretins in models of type 2 diabetes.  There are not many studies addressing this issue but some have pointed out lower secretion levels of incretin.  Nevertheless, due to the limited amount of research, the incretins are just beginning to be appreciated as essential agents in the pathogenesis of type 2 diabetes.

Type 2 diabetes is also part of obesity, metabolic syndrome, and related chronic disease epidemics.  Obesity is a strongly associated risk factor of insulin, and many hypotheses have been proposed to explain these associations. One of these is associated with the inflammatory basis of pancreatic beta-cell loss. The enlarged mass of fat cells in obese patients can also produce inflammatory messengers, provoking even greater loss of beta-cell mass. Additionally, several risk factors such as sedentary lifestyles along with inadequate nutrition (consumption of food with high caloric value but low nutritional value) are associated with both. Foods with excess sugars or fats can either cause or worsen the condition of diabetic and obese patients.  Additional to obesity, dyslipidemias, and chronic arterial hypertension also are associated with risk factors associated with diabetes. When several of these chronic diseases manifest themselves, it is described as metabolic syndrome. It is of particular interest because all of these diseases can contribute to lesions in diverse organ systems.

However, it is important to recognize that obesity and other diseases are not always present in patients with type 2 diabetes. And that regardless of the strong association, diabetes can manifest itself in patients who sometimes seem to be healthy on the outside. In order to identify patients suffering from type 2 diabetes, doctors do different types of blood tests to demonstrate hyperglycemia and study the patient to determine the origin of the abnormal concentrations of glucose.

Currently, physicians perform several tests to evaluate a patient’s glucose concentration along with their ability to regulate their level. The tests along with the results which indicate diabetes are the following.

  • Glycosylated hemoglobin test equal to or greater than 6.5%
  • Fasting plasma glucose equal to or greater than 126 mg per deciliter
  • 2-hour plasma glucose after an oral glucose test equal to or greater than 200 mg per deciliter

Even if patients seem healthy, it is essential that the patient is evaluated of any signs or symptoms of diabetes that might be present. This is in order to decrease the glycemia to prevent target organs’ damage. The organs principally affected by the chronic hyperglycemia in patients are divided into two groups, those affected by microvasculature damage or those affected by macrovasculature damage. This classification identifies the mechanism by which diabetes affects these organs.

In the group composed of those affected by microvasculature, lesions are found in the eye, kidneys, and nerves. It has been observed that these lesions are closely related to the appropriate management of type 2 diabetes.  Common lesions in the eye affect the retina, which if left untreated can result in blindness. Diabetes is also a common cause of renal dysfunction, a common cause of death in patients. Finally, damage to nerves can result in numerous lesions such as neuropathic pain, loss of sensibility, autonomic dysfunction, and many others.

Macrovasculature lesions, on the other hand, harm the heart, the brain, and other arterial mediated lesions. Diabetic heart lesions are commonly associated with coronary heart disease which can result in many different lesions of the heart. Diabetes is also associated with numerous diseases in the brain reneging from neurodegenerative processes to cerebrovascular disease. These differ that the management of type 2 diabetes doesn’t have a strong association. Nevertheless, the proper management of the disease does lower risk, just to a lesser extent than the other group of illness.

In other to prevent the previously mentioned complications treating the disease promptly is essential. Treating type 2 diabetes requires collaboration from the healthcare personnel, the patient, and his or her family. As seen through numerous studies, the disease originates from the interaction of genetics and environmental factors. A patient might not be able to change their genetics, but they can change the environmental factors. Among these are correcting their dietary habits and incorporating physical exercise into their daily lives. These aspects are essential because, without them, medication will not be able to control the disease and ultimately end in severe life impairments or even death.

Type 2 diabetes, was usually described as a disease found in older patients. However, patients can be diagnosed with type 2 diabetes mellitus from an early age. As sedentary lifestyles and improper nutrition become part of the general culture, the younger ones follow and engage in these risk factors. As a consequence, patients are being diagnosed with type 2 diabetes mellitus from an early age. Additionally, early diagnosis of diseases that revolve around the metabolic syndrome is being performed increasingly at an early age.

Therefore, the previous label of adult-type diabetes does not apply when describing type 2 diabetes. Only after reviewing the components of the disease one can add labels to describe this disease. Type 2 diabetes, first of all, is a disease whose pathogenesis is characterized by the progressive loss of the body’s ability to regulate glucose levels. Secondly, it is a disease of multifactorial etiology whose causes are beginning to be understood. Thirdly, it is an illness that is part of the current chronic disease epidemic associated with sedentary lifestyles. Finally, it is a disease with numerous harmful effects on other organ systems with possibly fatal consequences.

So, to conclude, Type 2 diabetes is a chronic disease whose multifactorial causes lead to the progressive inability to regulate glucose level which results in hyperglycemia which in turn will lead to numerous lesions in other organ systems also targeted by the other disease that accompanies type 2 diabetes in the current epidemic associated with sedentary lifestyles. The understanding of this definition that describes most of the components of the disease will allow the physician to establish an adequate treatment plan. A treatment plan which will benefit the patient’s health and quality of life, for this is the main objective of a physician.