Two Forms of Diabetes Mellitus

Diabetes mellitus is a metabolic disorder, which occurs due to the inability of the body to regulate the level of blood sugar. According to the literature review,4 the insufficient amount of insulin in the body causes type I diabetes, while insensitivity of cells and tissues to the normal level of insulin in the body causes type II diabetes. When the pancreas is unable to produce sufficient amount of insulin due to destruction of beta cells, cells and tissues in the body fails to utilize blood sugar, and thus, individuals develop type I diabetes. Comparatively, when cells and tissues develop resistance to insulin, individuals are unable to utilize blood sugar and start developing type II diabetes.

“Aging, obesity, insufficient energy consumption, alcohol drinking, and smoking are independent risk factors of pathogenesis of type II diabetes mellitus.”4 In some instances, both conditions of diabetes, type I and type II, occur among individuals. The epidemiological studies reveal that the prevalence of diabetes increases exponentially due to change of lifestyles. Projections hold that by 2030, the diabetic populations would reach 370 million, a figure that doubles the current prevalence of diabetes.4

The increasing prevalence of diabetes shows that it is becoming a serious challenge in the healthcare system. Evidently, type II diabetes is the most common form of diabetes because it comprises 90% of all cases.4 Since the incidences of two forms of diabetes mellitus are increasing across the world, it is important to unravel their pathogenesis and pathophysiology.

Type I diabetes has numerous pathophysiological effects, which influence metabolism of glucose, lipids, and proteins. The inability of cells and tissues to utilize blood sugar causes hyperglycemia. Since type I diabetes occurs due to the insufficient amount of insulin in the body, cells and tissues experience physiological hunger because they are unable to utilize blood glucose. As a consequent of physiological hunger, the body triggers the release of glucagon, which initiates the production of glucose from the stored glycogen. The plasma glucose levels increase and cause hyperglycemia because of reduced breakdown of glucose by cells and tissues, and enhanced hepatic production of glucose production.4

The resultant impact of hyperglycemia is the release of glucose via urine, dehydration, and increased hunger. In the metabolism of lipids, insufficient insulin triggers the breakdown of lipids as the body tries to respond to physiological hunger. The overall outcome of the breakdown of lipids is the accumulation of ketone bodies, which cause ketoacidosis.4 In the metabolism of proteins, type I diabetes stimulates breakdown of proteins in a bid to supplement the physiological deficiency of glucose in the body.

The table below presents causes of insulin resistance and clinical characteristics of type I and type II diabetes mellitus.4

Table 1.

Clinical characteristics
Causes of Insulin resistance Type I diabetes Type II diabetes
  • Overweight and obesity
  • Onset before the age of 20 years
  • Onset after the age of 30 years
  • High levels of glucorticoids
  • Body mass deteriorates
  • Body mass becomes obese
  • Polycystic ovary disease
  • Nil or low plasma insulin
  • Normal or high plasma insulin
  • High levels of growth hormone
  • High or suppressed glucagon levels in plasma
  • High or suppressed levels of glucagon in plasma
  • Gestational diabetes
  • Enhanced blood glucose
  • Enhanced blood sugar
  • Mutation of insulin receptor and other receptors
  • Sensitivity of insulin is normal
  • Sensitivity of insulin is low
  • Autoimmune disease
  • Insulin therapy is effective
  • Effective therapies are the use of insulin, metformin, sulfonylureas, thiazolidinediones, and weight loss
  • Hemachromatosis
  • Body mass deteriorates
  • Body mass becomes obese
  • Lipodystrophy

Type II diabetes is more complex than type I diabetes because of the pathogenesis. Pathogenesis of type II diabetes mellitus emanates from the dysfunctional secretion of insulin by the beta cells of the pancreas and its physiological impairment owing to the resistance of the peripheral cells and tissues.4 Due to the complexity of type II diabetes, the genetic factors appear to be the most predisposing factors. The concordance rate of 40% of type II diabetes among twins and high prevalence rates among ethnicities such as Pima Indians and Arabs supports the assertion that genetic factors are more predisposing than environmental factors.4

Mutations in the genes responsible for the production of insulin or peripheral receptors cause type II diabetes. Mutations in the genes for the synthesis of insulin hamper effective conversion of proinsulin to insulin. Evidently, genetic studies have identified 10 mutations that affect amino acid synthesis, 3 mutations that affect protein structure, and 3 mutations that affect the transcription of RNA.4. Therefore, these types of mutations cause type II diabetes among individuals.

The above depicts pathogenesis of type II diabetes.
Figure 1: The above depicts pathogenesis of type II diabetes.4

Environmental factors also play a central role in the pathogenesis of type II diabetes. National Institute of Health cites obesity, overeating, lack of exercise, aging, smoking, and drinking alcohol as some of the environmental factors that contribute to the occurrence of diabetes.4 Obesity causes type II diabetes because of the accumulation of fats in the adipose tissues forming visceral fats, which reduce mass of muscles and induce resistance of cells and tissues to insulin. Overeating of food rich in carbohydrates such as fats and sugars contributes to obesity, which induces insulin resistance in the body.

As lack of exercise slows down the metabolic activities in the body and reduces mass of muscles, it encourages accumulation of visceral fats, which have an overall impact of inducing insulin resistance in the body. Aging is also a significant risk factor that contributes to the insulin resistance because of the accumulation of visceral fats and reduced physiological functions of cells and tissues. Lifestyles such as smoking and drinking of alcohol contribute to the obesity because they interfere with metabolism and cause accumulation of visceral fats. Consequently, increased visceral fats reduce mass of muscles and cause underutilization of blood sugar resulting in type II diabetes.

Table 2.

Factors Outcomes
  1. Factors associated with stress
  1. Overeating and craving for sugars
  1. Excessive intake of alcohol
  1. Smoking
  1. Abnormalities in central nervous system and endocrine system (excessive cortisol and unbalanced sex hormones)
  1. Lower consumption of energy
  1. Inactivity of muscles, cells, and tissues
  1. Underutilization of blood sugar
  1. Genetic factors
  1. Mutations of insulin genes
  1. Mutation of insulin receptors
  1. Aging
  1. Aging of cells and tissues
  1. Reduced metabolic activities of cells and tissues
  1. Muscle wasting

Factors that contribute to the accumulation of visceral fats.4

The pathophysiology of type II diabetes is a combination of impaired secretion of insulin by beta cells of the pancreas and resistance to insulin by peripheral cells and tissues. People with impaired regulation of blood glucose usually have normal levels of insulin in the body, which implies that the resistance of the cells and tissues to insulin is the issue.4 Normal levels of insulin in the body are not enough to stimulate insulin receptors and tissues in the body to increase utilization of blood glucose. Owing to the underutilization of blood glucose, diabetic patients experience hyperglycemia.

When there is a physiological deficiency of insulin, the body experiences physiological hunger, which triggers production of glucose in the liver via the process of gluconeogenesis. The impaired glucose tolerance, which ensues due to the decreased levels of insulin, contributes the type II diabetes mellitus.4 Hence, decreased level of insulin primarily contributes to the pathophysiology of type II diabetes. Overall, diminished insulin level in the body contributes to the occurrence of impaired glucose tolerance, which leads to hyperglycemia and causes type II diabetes.

Although the insulin level may be normal among diabetic patients, pathophysiology emanates from the resistance of peripheral cells and tissues to insulin. Since the utilization of glucose in the body is dependent on the action of insulin receptors, impaired functioning of insulin receptors in peripheral cells and tissues creates a physiological deficiency of insulin, which triggers gluconeogenesis in the liver.

Receptor and post-receptor defects contributes to the resistance of cells and tissues to the normal levels of insulin in the body.4 Defects in insulin receptors owing to mutation or mechanism of action makes cells and tissues to be insensitive to the presence of insulin in the body. Consequently, the body experiences physiological hunger and trigger the breakdown of lipids, proteins, and glycogen as a way of overcoming physiological deficiency of glucose.

Glycohemoglobin (HbA1c) test, fasting plasma glucose test, and oral glucose tolerance test are three methods that are applicable in the diagnosis of diabetes and prediabetes among individuals. Glycohemoglobin test is a method that is applicable in detecting average level of blood glucose over a long period like three months. This method of diagnosis does not assess daily fluctuation of blood glucose and does not require fasting. The results of glycohemoglobin test exist in the form of percentages in which the percentages below 5.7 indicates lower risks of diabetes, the percentages between 5.7 and 6.4 shows prediabetes, and the percentages above 6.5 indicates diabetes.5 Comparatively, fasting plasma glucose test is applicable in testing diabetes and prediabetes after 8 hours of fasting to enhance accuracy of results.

Fasting glucose concentration of above 126mg/dL is diabetes, while fasting glucose concentration of 100 to 125mg/dL indicates prediabetes.5 The most sensitive and accurate method of detecting diabetes, prediabetes, and gestational diabetes is oral glucose tolerance test. The 2-hour concentration of blood glucose of between 140mg/dL and 199mg/dL shows prediabetes, while concentration of blood glucose of above 200mg/dL indicates diabetes.5 Diagnosis of diabetes and prediabetes using these methods of diagnosis is very accurate, sensitive, and reliable.

Type II diabetes causes microvascular and macrovascular complications among diabetic patients. Microvascular complications comprise retinopathy, nephropathy, and neuropathy.6 Diabetic retinopathy is the dominant complication of type II diabetes, which contributes to the occurrence of blindness among diabetic patients. When the glucose concentration increases in the blood, aldose reductase converts the excess glucose through the polyol pathway to glucose alcohol, which is responsible for the diabetic retinopathy. Nephropathy is also a common complication of microvascular that contributes to the occurrence of renal failure.

Pathological effects such as thickness of glomerular basement membrane, mesangial nodule formation, and mecroneurysm cause protenuria and microalbuminuria.6 Type II diabetes also cause neuropathy because it interferes with the functions of the central nervous system. Accumulation of glucose alcohol and enhanced oxidative stress due to increased levels of glucose in blood cause neuropathy.

Macrovascular complications such as atherosclerosis, stroke, coronary artery disease, and peripheral arterial disease occur due to type II diabetes. Atherosclerosis emanates from the oxidative stress from lipids and glucose molecules, which have accumulated in the body. Moreover, differentiation of monocytes into macrophages causes accumulation of oxidized lipids, and thus, stimulates proliferation of the smooth muscles of the blood vessels.6

Type II diabetes cause cardiovascular diseases such as coronary artery disease and peripheral arterial disease owing to the impaired metabolic mechanisms. Since hypertension, obesity, hyperlipidemia, and hyperglycemia occur due to the diabetes, they increase the risk of cardiovascular diseases by 150-400% among diabetic patients.6 Regarding the pathophysiology of type II diabetes, the deadly complications are the macrovascular ones.

Effective management of diabetes requires regular medical assessment to ascertain progress and prevent occurrence of complications. Diabetic patients should undergo screening tests for serum creatinine and proteins for early detection of nephropathy. If a diabetic patient has micro- and macro-albuminuria, physician must administer angiotensin-converting enzyme inhibitors to prevent the occurrence of albuminuria.6 Moreover, diabetic patients should undergo a comprehensive examination of eyes to monitor the occurrence of retinopathy. As diabetic patients are prone to neuropathy, regular assessment is essential to prevent the occurrence of diabetic foot. Owing to high risks of cardiovascular disorders, regular assessment of blood pressure is essential.

Lifestyle interventions such as eating a healthy diet and performing physical activities are very important in the prevention and management of type II diabetes among individuals. Taking diet that is low in calorie and fat content reduces the chances of obesity, which is a major risk factor for type II diabetes.7 Excess energy and fats in the body cause accumulation of fats in the adipose tissues, reduce mass of muscles, and make cells and tissues to be resistant to insulin.

Physical activity is also a lifestyle intervention that is effective in the prevention and management of type II diabetes. The Diabetes Prevention Program Outcomes Study found out that physical activity causes weight loss, improves metabolic functions, delays the occurrence of diabetes by 4 years, and prevents the occurrence of type II diabetes.5 Therefore, it is recommendable that people should eat healthy diets and exercise well to prevent and manage type II diabetes effectively.

The table 3 shows uses, advantages, disadvantages, and side effects of each of the medications applicable in treatment of type II diabetes.7

Table 3.

Medication Uses Advantage Disadvantages/side effects
Metformin Lowers A1C by 1-2%
Decreases hepatic production of glucose
Maintain weight Side effects are glucose intolerance and renal failure
Insulin Lowers A1C by 1.5-3.5%
Lowers blood sugar and increases peripheral utilization
Immediate effect and improve lipid profile Painful injections, weight gain, hypoglycemia, and expensive
Sulfonylureas Lowers A1C by 1-2%
Stimulates secretion of insulin
Immediate effect Causes weight gain and hypoglycemia
Thiazolidinediones Lowers A1C by 0.5-1.4%
Insulin sensitizers
Enhance lipid profile Weight gain, fluid retention, expensive, and can cause fracture of bones
GLP-1 Agonist Lowers A1C by 0.5-1%
Stimulates secretion of insulin
Weight loss Painful injections, expensive medicine, and low safety margin
Glucosidase inhibitor Lowers A1C by 0.5-0.8%
Reduces digestion of polysaccharides
Maintains weights
Does not cause hypoglycemia
Glucose intolerance, effects and expensive drug
Glinide Lowers A1C by 0.5-1.5%
Stimulates secretion of insulin
Immediate effect Weight gain, expensive, and hypoglycemia
Pramlintide Lowers A1C by 0.5-1%
Inhibits glucagon production
Loss of weight Frequent painful injections, glucose intolerance, and low safety margin
DPP-4 Inhibitor Lowers A1C by 0.5-0.8%
Increases insulin and suppresses glucagon
Maintain weight Expensive and long-term safety unknown

References

Ozougwu, JC, Obimba, KC, Belonwu, CD, & Unakalamba, CB. The pathogenesis and pathophysiology of type 1 and type 2 diabetes mellitus. Journal of Physiology and Pathophysiology. 2013;4(4):46-57.

National Institute of Health and National Diabetes Clearinghouse. Diagnosis of diabetes and prediabetes. Web.

Fowler, M. Microvascular and macrovascular complications of diabetes. Journal of Clinical Diabetes. 2008;26(2):77-82.

Nathan, D, Buse, D, Davidson, M. A consensus statement of the American diabetes association and the European association for the study of diabetes. Journal of Diabetes Care. 2009;32(1):193-203.

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