Type 2 diabetes is one of the most common metabolic disorders in primary care, and a leading cause of microvascular and macrovascular diseases in the United States. It is a progressive disorder characterized by relative insulin deficiency resulting from pancreatic beta-cell dysfunction and insulin resistance in target organs (Chatterjee, Khunti, & Davies, 2017). Diabetes can begin at any age. There has been a recent rise in type 2 diabetes during childhood and adolescence due to obesity, sedentary lifestyle, and genetic predisposition to the disease. If left untreated or inadequately managed, type 2 diabetes can lead to a profound psychological and physical distress to both patients and caregivers, leaving a massive burden on the health care system. Currently, type 2 diabetes has no cure.
Early detection, lifestyle modification, and intensive patient centered management of the disease remains the cornerstone of quality patient outcome and decrease in morbidity and mortality associated with the disease process. Despite research and increasing knowledge of the risk factors for type 2 diabetes, and evidence for successful prevention and management programs available, the incidence and prevalence of the disease continues to rise (Chatterjee et al., 2017). Like many other progressive chronic diseases, managing type 2 diabetes can be very challenging.
It requires time, effort, support, and an individualized treatment plan to adequately manage. As the disease progresses, management typically requires a multidisciplinary approach to managing other body systems affected by the disease. Unlike type 1 diabetes that always requires insulin to manage, type 2 diabetes is not dependent on insulin therapy only. It can be successfully managed by lifestyle modification such as healthy diet, exercise, weight loss, oral hypoglycemic agents, insulin, or other subcutaneous hypoglycemic injections. Insulin generally indicated as a second step when lifestyle modifications and oral or subcutaneous agents fails control hyperglycemia. EpidemiologyType 2 diabetes accounts for more than 90% to 95% of all diabetes cases in the United States.
According to the Centers for Disease Control and Prevention (2018), the incidence and prevalence of type 2 diabetes have been rising steadily due to obesity and overweight in the population. An estimated 84.1 million adults have prediabetes and 9 out of 10 people with prediabetes do not know they have prediabetes. The lifetime risk of developing type 2 diabetes mellitus is now equal for both men and women at 40% and 50% for African Americans in the United States. Type 2 diabetes most often develops in people over age 45, but more children, teens, and young adults are developing the disease due to predisposition to the risk factors such as obesity, genetics, ethnicity, and environmental risk factors. The mean age of onset is 12 to 16 years coinciding with puberty, a period when physiologic state of insulin resistance develops. Type 2 diabetes develops at puberty stage in males because of inadequate beta cell function associated with obesity, genetic, or environmental factors (Baynes, 2015).
Overall, patients with type 2 diabetes have a 15% increased risk of all-cause mortality, which is twice as high in young people, and in those who are younger than 55 years of age (Chatterjee et al., 2017). PathophysiologyType 2 diabetes is a non-communicable disease characterized by insulin insensitivity resulting from decline in insulin production, insulin resistance, and failure of the pancreatic beta cell leading to decrease in the glucose transport to the liver, muscle cells, and fat cells. (Olokoba, Obateru, & Olokoba, 2012). The presence of insulin resistance is the primary factor in type 2 diabetes. Insulin resistance can be present in a personal for several years before diagnosis and remain present as the diabetes progresses. Buttaro, Trybulski, Polgar-Bailey, & Sanberg-Cook (2017) and Trasher (2017), noted a new model of type 2 diabetes pathophysiology described by DeFronzo as the ominous octet in recognition that there are eight mechanisms that contribute to the development type 2 diabetes. These additional mechanisms include increased mechanism glucagon secretion, increase glucose reabsorption by the kidney, increased lipolysis, decreased incretin effect, and neurotransmitter dysfunction in the brain.
Increased hepatic glucose production in the impaired first phase of insulin secretion leads to fasting hyperglycemia. Decreased uptake of glucose by the skeletal muscles is caused by post prandial hyperglycemia. In response to elevated blood glucose levels, the insulin pathways become resistant to hormonal impulses resulting in hyperinsulinemia. It is important to note that hyperinsulinemia increases as insulin resistance increases and as the degree of glucose intolerance increases, hyperglycemia results from the inadequate insulin production by beta cells (Buttaro et al., 2017). Up to 50% of the pancreatic beta cells are destroyed in most cases before diagnosis is made.
Most individuals suffering from type 2 diabetes are obese, with central visceral adiposity leading to the conclusion that adipose tissue plays a crucial role in the development of type 2 diabetes of type 2 DM. Other factors responsible for the development of type 2 diabetes apart from obesity, include genetic predisposition to diabetes, sedentary lifestyles, and aging population are drug induced hyperglycemia, genetic defects, and endocrine disorders. Type 2 diabetes is a lifelong disease that has no cure but can be effectively managed by pharmacologic and non-pharmacologic interventions depending on the stage and extent of disease when diagnosed (Buttaro et al., 2017). Glucose control has always been a major focus in the management of type 2 diabetes.
However, management of type 2 diabetes should always be in the context of a comprehensive cardiovascular risk factor reduction program, including cessation of smoking and the adoption of other healthy lifestyle habits, blood pressure control, lipid management with priority to statin medications, and, in some circumstances, antiplatelet therapy (Inzucchi, Bergenstal, Buse, Diamant, Ferranninni, Nauck, … & Mathews, 2015). The key to successful management of type 2 diabetes is the promotion of self-management and compliance by supporting individuals diagnosed with the disease to make better lifestyle decisions that leads to healthier lifestyle that reduce the risk of complications associated with the disease (Malin & Kashyap, 2016). Treatment for diabetes should be individualized depending on the origin of hyperglycemia, patients’ preference, values, diabetes complications, cardiac risk factors, and activity baseline (Buttaro et al., 2017). Choice of treatment for type 2 diabetes should target the multiple patient defects, and follows a patient-centered approach that put into consideration factors beyond glycemic control, including cardiovascular risk complications associated with the disease process as mentioned above. In obese patients with type 2 diabetes, lifestyle modifications are the cornerstone of any treatment plans. It is highly effective at promoting glucose regulation and preventing microvascular and macrovascular complication associated with the disease.
However, many individuals struggle over time to maintain optimal glycemic control and body weight with lifestyle modification. When lifestyle modification fails or becomes ineffective, additional therapeutic interventions become necessary in order to manage type 2 diabetes. This involves the initiation of pharmacological interventions together with lifestyle modifications. The initiation of pharmacological interventions has been shown to offer promising results for obesity-related diabetes complications (Malin ; Kashyap, 2016).
The American Association of Clinical Endocrinologists (AACE), American College of Endocrinology (ACE) and the American Diabetes Association (ADA) recommend an initial approach consisting of lifestyle changes and monotherapy, preferably with metformin. The choice of therapy for type 2 diabetes is guided by the glycemic efficacy, safety profiles, especially their effects on weight and hypoglycemic risk, tolerability, patient comorbidities, medication administration route, patient’s preference, medication availability, and cost (Trasher, 2017). A stepwise approach consisting initial lifestyle modification and progressive approach individualizing hemoglobin A1c goals, adverse effects of therapy, and comorbidities is explained below. The stepwise and progressive approach is also supported by the AACE, ACE, and the ADA.Step 1- Type 2 diagnosis should be presented to patient as a lifelong chronic condition that can be managed and not cured. Lifestyle changes, heart healthy diet, regular exercise, and weight loss are encouraged together with diabetes self-management education.
– Metformin is initiated, and for patient with hemoglobin A1c greater than 7% provider can proceed to step 2. Step 2In addition to metformin and lifestyle interventions, one of the following can be added if hemoglobin A1c continues to be greater than 7%:- Basal Insulin (most effective) for blood glucose level greater than 300- Sulfonylurea (least expensive), care should be taken in new diagnosis and patient with risk of hypoglycemia.- Thiazolidineone (no risk of hypoglycemia)- Dipeptidyl peptidase 4 (DPP-4) inhibitor (has few contraindications)- Sodium-glucose contraspoter-2 (SGLT2) inhibitor (newest)- Glucagon-like peptide 1 (GLP-1) receptor agonist (injection)- If hemoglobin A1c is still greater than 7%, provider can proceed to step 3 below.Step 3In addition to metformin and lifestyle intervention, the following can be added or adjusted to regimen:- If basal insulin was inadequate, intensify insulin regimen- If two agents were inadequate, begin basal insulin- If hemoglobin A1c continue to be higher than 7, step 4 can be initiated or incorporated into regimen.Step 4While continuing metformin and lifestyle interventions, insulin regimen can be intensified to include mealtime rapid acting insulin.
Patient should be reassured that the need for insulin does not represent a failure on their part but rather the most appropriate treatment of the current phase of their disease (Buttaro et al, 2017, Inzucchi et al., 2015). Metformin is a drug of choice for monotherapy or dual therapy in the management of type 2 diabetes because it is low cost, proven safe, promotes weight loss, decreases hepatic glucose production and intestinal glucose absorption, while increasing insulin sensitivity, with benefits on cardiovascular and renal outcomes. However, Metformin is contraindicated in patients with glomerular filtration rate (GFR) of less than 30ML/min or serum creatinine greater than 1.5 mg/dL in men or 1.4 mg/dLin women (Inzucchi et al., 2015).