**1.3 Risk factors of T2DM**

Several factors contribute to the high incidence of DM, such as population growth rate, ageing population, age structures, urbanization, unhealthy diet habits, obesity, sedentary lifestyles, lack of physical activities, failure to access to healthcare facilities both in rural and urban areas in addition to the economic and health transition of the country. Moreover, the increased case of DM is also triggered by the positive family history of the disease [16]. The literature reveals three interrelated spheres of risk factors that contribute to the development of T2DM: (1) genetics, (2) environment or lifestyle, and (3) metabolic abnormalities. It is imperative to implement appropriate interventions for the prevention and treatment of T2DM among adult patients, where there is an understanding of the risk factors predisposing adults to this disease [17].

#### *1.3.1 Genetic factors*

Although research has not clarified a single gene that is alone responsible for the development of T2DM, there are many findings in literature that support the genetic hypothesis. Higher concordance rates are found among identical (96%) than dizygotic twins in some but not all twin studies which have been a compelling evidence of a significant genetic component in T2DM. Moreover, 40% of firstdegree relatives of T2DM patients may develop diabetes, whereas the incident rate is only 6% in the general population [5].

• Environmental or lifestyle factors:

There are a wide range of lifestyle factors which are of great importance to the development of T2DM disease, such as smoking, alcohol consumption, physical inactivity, obesity, obstructive sleep apnea, unhealthy diet (dietary fiber (a low-fiber diet with a high glycemic index), dietary fat (total and saturated fat intake) and frequent consumption of processed meat [5].

• Metabolic abnormalities or changes:

A recent study proved that resistance to insulin was the underlying abnormality in most people who develop T2DM. Such resistance resulted from an interaction between both genetic and environmental factors. Those factors were associated with the development of insulin resistance. The initial reaction of the beta cells was to increase output of insulin in order to overcome the insulin resistance and to maintain normal blood glucose levels. Unless insulin resistance was reversed, hyper secretion of insulin was insufficient to maintain normoglycemia indefinitely and progression to the states of impaired glucose metabolism (impaired fasting glucose (IFG), impaired glucose tolerance (IGT) and eventually T2DM) [18].

#### **1.4 Pathophysiology of T2DM**

The main pathophysiological cause of T2DM is the failure of pancreatic beta cells which leads to inadequate secretion of insulin and increased insulin resistance which refers to decreased tissue (especially the liver, adipose tissues and muscle) sensitivity to insulin. Normally, insulin binds to special receptors on cell surfaces and initiates a series of reactions involved in glucose metabolism. In T2DM; intracellular reactions are diminished, making insulin less effective at stimulating glucose uptake by the liver. Physical inactivity and obesity lead to insulin resistance, increased production of glucose by the liver and decreased glucose uptake in skeletal muscles. In order to compensate beta cells, increase insulin secretion, but the progressive failure of beta cells leads to hyperglycemia and finally T2DM [19, 20].

The inappropriately increased alpha-cell function and consequent hyperglucagonemia, in addition to insulin resistance and beta cell dysfunction, they all have long contributed to hyperglycemia in diabetic patients, by stimulating hepatic glucose production. In fasting state, hyperglycemia is directly related to increase hepatic glucose production while in postprandial state, hyperglycemia results from the combination of insufficient suppression to glucose output and defective insulin stimulation of glucose disposal in target tissues, mainly skeletal muscles. Antihyperglycemic agents are directed to one or more of the pathophysiological defects of T2DM; they modify physiological processes related to appetite, nutrient absorption or excretion [21, 22].

### **1.5 Clinical manifestation of T2DM**

It is almost traditionally known that classic symptoms of diabetes are polyuria (the need to urinate frequently), polydipsia (increased thirst & fluid intake), polyphagia (increased appetite) and weight loss and the symptoms that may provide cause for testing T2DM include increased thirst or urination, numbing of extremities, impotence, blurred vision and fatigue [23]. Other symptoms that are commonly present at diagnosis include; a history of blurred vision, itchiness, peripheral neuropathy, recurrent vaginal infections, poor healing skin wounds and fatigue. Patients with T2DM may rarely present with non-ketonic hyperosmolar coma, a condition of very high blood sugar associated with a decreased level of consciousness and low blood pressure. Many people however have no symptoms during the first few years which are diagnosed on routine testing [24].

#### **1.6 Diagnosis of T2DM**

The diagnostic criteria for diabetes mellitus are at least one of the following: [1] Glycated hemoglobin test (HbA1c) ≥ 6.5%. That test should be performed in a laboratory using the National Glycohemoglobin Standardization Program (NGSP) method which was certified by the NGSP standardized to the Diabetes Control and Complications Trial (DCCT) assay; [2] The Fasting Plasma Glucose Test (FPG) ≥ 126 mg/dl. Fasting is defined as no caloric intake for at least 8h; [3] 2-hour plasma glucose ≥ 200 mg/dl during an Oral Glucose Tolerance Test (OGTT). This test should be performed as described by the WHO, using a glucose load containing the equivalent of 75 g, anhydrous glucose dissolved in water; or [4]. In a patient with classic symptoms of hyperglycemia (polyuria, polydipsia, weight loss) or hyperglycemic crisis (Diabetic ketoacidosis (DKA), Hyperglycemic Hyperosmolar State (HHS)), a random plasma glucose ≥200mg/dL (11.1mmol/L). In the absence of unequivocal hyperglycemia, results should be confirmed by repeat testing [25].

#### **1.7 Complications of T2DM**

T2DM is considered as one of the most leading causes of premature morbidity and mortality worldwide as a result of the long-term micro vascular and macro

#### *Effect of Lifestyle Modification on Glycemic Control of Type 2 Diabetic Patients at Suez Canal… DOI: http://dx.doi.org/10.5772/intechopen.97738*

vascular complications associated with this disease. For instance, diabetic retinopathy is the most leading cause of blindness among adults aged 20-74 years; diabetic nephropathy, which affects approximately 40% of type 2 diabetic patients, is the leading cause of chronic kidney disease in patients starting replacement therapy; and diabetic neuropathy, which affects up to 50% of individuals with diabetes, increases the risk of foot ulcers and limb amputation [26].

In fact, more than 80% of non-traumatic limb amputations follow a foot ulcer or injury, and the risk of amputation in individuals with diabetes is up to 25 times greater compared with patients without diabetes. Although micro vascular complications increase morbidity and lead to premature mortality, the major cause of death in individuals with diabetes is cardiovascular disease (CVD), which in turn accounts for approximately 65% of all diabetes-related deaths. For example, transient ischemic attacks are 2-6 times more common in patients with T2DM, while the risk of developing heart failure is a startling 2- to 8-fold higher [26].

The sudden development of short-term complications, such as hyperglycemic crisis (DKA, HHS and severe hypoglycemia) that can lead to coma and, if untreated, death, are a daily threat to the many people worldwide with diabetes who have major difficulty in accessing essential treatment supplies (including insulin) [27].

Recent studies have shed the light on "hypoglycemia" (blood glucose < 3.9 mmol/L or 70 mg/dL) as a common unwanted effect in people treated with insulin and occurs when there is an imbalance in insulin dose, food consumed and activity. Usually the condition is manageable, but occasionally, it can be severe or even life threatening, particularly if the patient fails to recognize the symptoms, especially while continuing to take insulin or other hypoglycemic drugs. The signs of hypoglycemia can vary from person to person and may occur suddenly such as: hunger, perspiration, rapid heartbeat, weakness, feeling sleepy, feeling drunk, difficulty speaking, trembling, dizziness, confusion, and anxiety [28, 29].

DKA results from absolute insulin insufficiency, leading to metabolic acidosis (pH <7.3), hyperglycemia (blood glucose >11 mmol/L). DKA may also be present in up to 25% of young people presenting with T2DM. DKA should be treated as a medical emergency by an experienced medical team [30]. Hyperglycemic Hyperosmolar Non ketonic Syndrome (HHNS) usually occurs with T2DM and can occur with T1DM. It is often triggered by a serious infection, another severe illness, or by medications that lower glucose tolerance or increase fluid loss (especially in people who are not drinking enough fluids). Symptoms of HHNS include; high blood sugar levels, dry mouth, extreme thirst, dry skin and high fever. HHNS leads to loss of consciousness, seizures, coma and death [31].

No doubt, early detection and good glycemic control can slow the progression of the acute and chronic complications of DM, which cause significant mortality and morbidity in both developing and developed countries. Such chronic complications of DM if once developed are irreversible except by early detection and management [4].

#### **1.8 Management of T2DM**

Both patients and health care professionals are partners in managing T2DM, in which the health professionals support the patients in self-managing their disease. Management of every patient should start with a detailed evaluation of the initial diagnosis including diabetes complications and its risk factors. This, of course, provides basis for continuing treatment plan, treatment administration, monitoring, and review [32]. The main goals of treatment of DM are to reduce complications through control of glycaemia, blood pressure, macro vascular (i.e., coronary,


**Table 1.**

*Oral antihyperglycemic agents for T2DM [35].*

cerebrovascular, peripheral vascular), control of lipids, hypertension and smoking cessation. Metabolic and neurological complications can be reduced through control of glycaemia [33].

The treatment of hyperglycemia should start with the establishment of a target HbA1c that, in most cases, will be ≤ 7.0%, as this has been shown to reduce longterm microvascular complications in newly diagnosed patients with T2DM. HbA1c targets may be higher (up to 8.5%) if the benefits of intensive glycemic control are unlikely to outweigh the risks and burden, such as in individuals with limited life expectancy, high risk of hypoglycemia, multimorbidity, or based on the values and preferences of the person with diabetes. It should be emphasized to people with T2DM that reductions in HbA1c levels are associated with better outcomes even if recommended glycemic targets cannot be reached, and inability to achieve HbA1c target should not be considered a treatment failure [34].

If the level of HbA1c at diagnosis is less than 1.5% above target and the person with T2DM, lacks metabolic decompensate and/or symptoms of hyperglycemia, the first step of treatment should be healthy lifestyle conduct. If healthy behavior interventions are insufficient to achieve target HbA1c levels within 3 months, they should be combined with oral antihyperglycemic medications (**Table 1**) [35].

In the face of significant hyperglycemia (i.e., HbA1c >1.5% above target), pharmacotherapy is usually required at diagnosis concurrent with healthy behavior interventions. People who have evidence of metabolic decompensation (e.g., marked hyperglycemia, ketosis or unintentional weight loss) and/or symptomatic hyperglycemia should be started immediately on insulin, regardless of HbA1c level. Insulin may later be tapered or discontinued once stability is achieved [34].

#### **2. Glycemic control**

Glycemic control is extremely fundamental to the management of T2DM. Diabetes management aims to delay the onset of disease complications, and to hinder its progression, mostly by improving glycemic control and controlling the risk of cardiovascular disease. Previous studies have provided evidence of the power of good glycemic control to restrict the micro-vascular and macro-vascular complications of diabetes [36].

#### **2.1 Assessment of glycemic control**

Glycemic control is a very important instrument that prevents or delays the complications associated with DM, such as peripheral vascular disease, vision loss, and renal failure. There are two primary techniques available for both health providers and patients to assess effectiveness of management plan on glycemic control: patient self-monitoring of blood glucose (SMBG) and HbA1c [37].
