**1. Introduction**

#### **1.1. General overview of diabetic mellitus**

Diabetes mellitus is a metabolic disorder that is characterized by hyperglycemia associat‐ ed with impairment in insulin secretion and/or insulin action as well as aberrations in intermediary metabolism of carbohydrates, proteins and lipids. Several reports indicate that annual incidence rate of diabetes mellitus will increase in the future worldwide, especial‐ ly in the developing countries [1]. The effects of diabetes mellitus include long-term damage, dysfunction and failure of various organs. Diabetes mellitus may present with classical characteristic features such as blurring of vision, excessive thirst (polydypsia), excessive feeding (polyphagia) excessive urination (polyuria), and weight loss. In its most severe forms, ketoacidosis may develop leading to stupor, coma and, in absence of effective treatment death ensues [2].

Often symptoms are not severe, or may be absent, and consequently hyperglycaemia sufficient to cause pathological and functional changes may be present for a long time before the diagnosis is made. On the other hand, other chronic features of diabetes mellitus include progressive development of the specific complications of retinopathy with potential blindness. Nephropathy that may lead to renal failure with risk of foot ulcers, amputation, including reproductive dysfunction [3-6]. People with diabetes are at increased risk of developing cardiovascular, peripheral vascular and cerebrovascular disease [7-8]. These include processes which destroy the beta cells of the pancreas with consequent insulin deficiency and ultimately

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resulting in insulin resistance. The abnormalities of carbohydrate, fat and protein metabolism have also been shown to result in deficient action of insulin on target tissues resulting from insensitivity or lack of insulin [9-10].

**2.1. Type 1 diabetes mellitus**

**2.2. Type 2 diabetes mellitus**

impaired glucose tolerance [19].

15-16].

DM [22-24].

Type 1 diabetes mellitus is caused by insulin deficiency due to destruction of pancreatic β-cells principally via an autoimmune reaction that can be triggered by different factors [14]. It can also develop in association with certain hereditary factors, such as Human Leukocyte Antigen (HLA) alleles. Typically, destruction of pancreatic β-cells progresses to absolute deficiency in insulin. This condition develops rapidly in young people and has been found to occur in any age group [14]. Similarly, autoantibodies against islet anti‐ gens (islet-associated antibodies) have been shown to increase in the early phase of the disease. Hence, pancreatic β-cell destruction involves autoimmune mechanisms. There‐ fore, type 1 diabetes mellitus is also known as 'autoimmune' type 1 diabetes mellitus [14,

Some Selected Medicinal Plants with Antidiabetic Potentials

http://dx.doi.org/10.5772/57230

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Type 2 diabetes mellitus is one of the most common diseases of the western world and is associated with cardiovascular disease [17]. Type 2 diabetes mellitus (formerly called NIDDM, type II or adult-onset) is characterized by insulin resistance in peripheral tissue and an insulin secretory defect of the beta cell. This is the most common form of diabetes mellitus and is highly associated with a family history of diabetes, old age, obesity and lack of exercise. It is more common in women, especially women with a history of gestational diabetes. Type 2 diabetes mellitus is characterized by derangement of carbohydrate, protein and fat metabolism [18]. Insulin resistance and hyperinsulinemia eventually lead to

Defective beta cells become exhausted, further fuelling the cycle of glucose intolerance and hyperglycaemia. The aetiology of type 2 diabetes mellitus is multifactorial with evidence of genetic involvement [20-21]. Types of diabetes mellitus of various known aetiologies are grouped together to form the classification called "other specific types." This group includes persons with genetic defects of beta-cell function (this type of diabetes was formerly called MODY or maturity-onset diabetes in youth) or with defects of insulin action; persons with diseases of the exocrine pancreas, such as pancreatitis or cystic fibrosis; persons with dysfunc‐ tion associated with other endocrinopathies (e.g., acromegaly); and persons with pancreatic dysfunction caused by drugs, chemicals or infections. Diabetic cardiomyopathy (DCM) has also been extensively reported in type 2 diabetes mellitus [22-25]. DCM is recognized as asymptomatic progressing structural and functional remodelling in the heart of diabetics, in the absence of coronary atherosclerosis and hypertension. Diabetic cardiomyopathy is a fairly common cause of heart failure in the native population with type-2 diabetes mellitus and results in high morbidity and mortality [22]. Few of the classical symptoms of DCM include marked left ventricular (LV) systolic dysfunction, dysfunction of coronary microcirculation, in relation with glycaemic levels, insulin resistance, sympathetic overdrive, endothelial dysfunction, abnormalities of the angiotensin-renin system, and remodelling/hypertrophy, diastolic dysfunction and impairment of coronary flow reserve (CFR) may be associated in

**Figure 1.** The structure of the pancreas which houses islets of Langerhans

Insulin resistance was recently reported to be associated with obesity and type 2 diabetes[11]. Recent studies suggest that a complex interaction between inflammation, endoplasmic reticulum stress, oxidative stress, mitochondrial dysfunction and autophagy dysregulation play an important role in insulin resistance. The stress-activated c-Jun N-terminal kinase (JNK) has been increasingly recognized as a central mediator of insulin resistance [11] and suppres‐ sion of the JNK pathway has been shown to improve insulin resistance and glucose tolerance. Also, hyperhomocysteinemia (HHcy) was found to induce insulin resistance in adipose tissue via activation of JNK pathway [12].
