[vc_row full_width="0" full_height="0" particles="0"][vc_column margin="margin_bottom_grid" offset="vc_col-md-6"][vc_text_separator title="EPIDEMIOLOGY" title_align="separator_align_left"][vc_column_text]<strong>EPIDEMIOLOGY</strong>

According to WHO, the number of people with diabetes has risen from 108 million in 1980 to 422 million in 2014. The global prevalence of diabetes among adults over 18 years of age has risen from 4.7% in 1980 to 8.5% in 2014. In 2012, an estimated 1.5 million deaths were directly caused by diabetes and another 2.2 million deaths were attributable to high blood glucose.<sup>(1)</sup> WHO projects that diabetes will be the 7th leading cause of death in 2030.<sup>(2)</sup>[/vc_column_text][vc_text_separator title="Our Vision" title_align="separator_align_left"][/vc_column][vc_column offset="vc_col-md-6"][vc_video link="https://www.youtube.com/watch?v=JAjZv41iUJU"][/vc_column][vc_column][vc_column_text]In 2015, the International Diabetes Federation’s (IDF) Diabetes Atlas estimates that:<sup>(3)</sup>
<ul>
 	<li>One in 11 adults has diabetes (415 million)</li>
 	<li>One in two (46.5%) adults with diabetes is undiagnosed</li>
 	<li>One in seven births is affected by gestational diabetes</li>
 	<li>Three-quarters (75%) of people with diabetes live in low- and middle-income countries</li>
 	<li>Every six seconds a person dies from diabetes (5.0 million deaths)</li>
</ul>
Pakistan ranks at number six in terms of number of people with diabetes worldwide. It was estimated that in 2000 there were 5.2 million diabetic patients and this will rise to 13.9 million by 2020, leading Pakistan to 4th most populous country for patients with diabetes mellitus.<sup>(4) </sup>According to WHO prevalence of diabetes in Pakistan is 9.8%.<sup>(5)</sup> According to diabetes international federation, there were over 7 million cases of diabetes in Pakistan in 2015.<sup>(6)</sup>

Type II diabetes is a worldwide health problem and affecting more than 415 million individual and expected to reach 642 million individuals by end of 2040.<sup>(7)</sup>

It is reported that 120,000 people die in Pakistan every year as a result of type II diabetes and its related complications.<sup>(8)</sup>

Prevalence of Type 2 diabetes in Pakistan is high ranging from 7.6 % (5.2 million populations) to 11 %<sup>(9-11)</sup> and for 2030 it will increase to around 15% (14 million populations).

<strong>PATHOPHYSIOLOGY:</strong>

Type 2 diabetes is characterized by a combination of peripheral insulin resistance and inadequate insulin secretion by pancreatic beta cells. Insulin resistance, which has been attributed to elevated levels of free fatty acids and proinflammatory cytokines in plasma, leads to decreased glucose transport into muscle cells, elevated hepatic glucose production, and increased breakdown of fat.

A role for excess glucagon cannot be underestimated; indeed, type 2 diabetes is an islet paracrinopathy in which the reciprocal relationship between the glucagon-secreting alpha cell and the insulin-secreting beta cell is lost, leading to hyperglucagonemia and hence the consequent hyperglycemia.<sup>(12)</sup>

For type 2 diabetes mellitus to occur, both insulin resistance and inadequate insulin secretion must exist. For example, all overweight individuals have insulin resistance, but diabetes develops only in those who cannot increase insulin secretion sufficiently to compensate for their insulin resistance. Their insulin concentrations may be high, yet inappropriately low for the level of glycemia.

With prolonged diabetes, atrophy of the pancreas may occur. This may also explain the associated exocrine deficiency seen in prolonged diabetes.
<strong>BETA-CELL DYSFUNCTION:</strong> Beta-cell dysfunction is a major factor across the spectrum of prediabetes to diabetes. Beta-cell dysfunction develops early in the pathologic process and does not necessarily follow the stage of insulin resistance.<sup>(13) </sup>Singular focus on insulin resistance as the "be all and end all" is gradually shifting, and hopefully better treatment options that address the beta-cell pathology will emerge for early therapy.

<strong>INSULIN RESISTANCE:</strong> In the progression from normal to abnormal glucose tolerance, postprandial blood glucose levels increase first. Eventually, fasting hyperglycemia develops as suppression of hepatic gluconeogenesis fails.
During the induction of insulin resistance (such as occurs with a high-calorie diet, steroid administration, or physical inactivity), increased glucagon levels and increased glucose-dependent insulinotropic polypeptide (GIP) levels accompany glucose intolerance. However, the postprandial glucagon like peptide-1 (GLP-1) response is unaltered.<sup>(14)</sup>

<strong>GENOMIC FACTORS:</strong> Genome-wide association studies of single-nucleotide polymorphisms (SNPs) have identified a number of genetic variants that are associated with beta-cell function and insulin resistance. Some of these SNPs appear to increase the risk for type 2 diabetes. Over 40 independent loci demonstrating an association with an increased risk for type 2 diabetes have been shown.<sup>(15) </sup>A subset of the most potent are shared below:<sup>(16)</sup>
<ul>
 	<li>Decreased beta-cell responsiveness, leading to impaired insulin processing and decreased insulin secretion (TCF7L2)</li>
 	<li>Lowered early glucose-stimulated insulin release (<em>MTNR1B, FADS1, DGKB</em>,<em>GCK</em>)</li>
 	<li>Altered metabolism of unsaturated fatty acids (<em>FSADS1</em>)</li>
 	<li>Dysregulation of fat metabolism (<em>PPARG</em>)</li>
 	<li>Inhibition of serum glucose release (<em>KCNJ11</em>)<sup>(17)</sup></li>
 	<li>Increased adiposity and insulin resistance (<em>FTO</em> and <em>IGF2BP2</em>)<sup>(18,19)</sup></li>
 	<li>Control of the development of pancreatic structures, including beta-islet cells (<em>HHEX</em>)<sup>(20)</sup></li>
 	<li>Transport of zinc into the beta-islet cells, which influences the production and secretion of insulin (<em>SLC30A8</em>)<sup>(20)</sup></li>
 	<li>Survival and function of beta-islet cells (<em>WFS1</em>)<sup>(21)</sup></li>
</ul>
Susceptibility to type 2 diabetes may also be affected by genetic variants involving incretin hormones.For example, reduced beta-cell function has been associated with a variant in the gene that codes for the receptor of gastric inhibitory polypeptide (<em>GIPR</em>).<sup>(22)</sup>

<strong>AMINO ACID METABOLISM:</strong> Amino acid metabolism may play a key role early in the development of type 2 diabetes. Wang et al reported that the risk of future diabetes was at least 4-fold higher in normoglycemic individuals with high fasting plasma concentrations of 3 amino acids (isoleucine, phenylalanine, and tyrosine). Concentrations of these amino acids were elevated up to 12 years prior to the onset of diabetes.<sup>(23) </sup>

<strong>DIABETES COMPLICATIONS:</strong> Although the pathophysiology of the disease differs between the types of diabetes, most of the complications, including microvascular, macrovascular, and neuropathic, are similar regardless of the type of diabetes. Hyperglycemia appears to be the determinant of microvascular and metabolic complications. Macrovascular disease may be less related to glycemia.

<strong>CARDIOVASCULAR RISK:</strong> Cardiovascular risk in people with diabetes is related in part to insulin resistance, with the following concomitant lipid abnormalities:
<ul>
 	<li>Elevated levels of small, dense low-density lipoprotein (LDL) cholesterol particles</li>
 	<li>Low levels of high-density lipoprotein (HDL) cholesterol</li>
 	<li>Elevated levels of triglyceride-rich remnant lipoproteins</li>
</ul>
Thrombotic abnormalities (i.e. elevated type-1 plasminogen activator inhibitor [PAI-1], elevated fibrinogen) and hypertension is also involved. Other conventional atherosclerotic risk factors (e.g. family history, smoking, elevated LDL cholesterol) also affect cardiovascular risk.

Insulin resistance is associated with increased lipid accumulation in liver and smooth muscle, but not with increased myocardial lipid accumulation.<sup>(24) </sup>Persistent lipid abnormalities remain in patients with diabetes despite the use of lipid-modifying drugs, although evidence supports the benefits of these drugs. Statin dose up-titration and the addition of other lipid-modifying agents are needed.<sup>(25)</sup>

Increased cardiovascular risk appears to begin prior to the development of frank hyperglycemia, presumably because of the effects of insulin resistance.

<strong>COGNITIVE DECLINE:</strong> Diabetic individuals aged 55 years and more are more likely to have brain atrophy than cerebrovascular lesions, with patterns resembling those of preclinical Alzheimer disease.<sup> </sup>Type 2 diabetes was associated with hippocampal atrophy; temporal, frontal, and limbic gray-matter atrophy; and, to a lesser extent, frontal and temporal white-matter atrophy.

Type 2 diabetes was also linked with poorer performance on certain cognitive tests. Patients with type 2 diabetes were more likely to have gray-matter atrophy in several bilateral regions of the cortices, especially in the left hemisphere, similar to the distribution of cortical atrophy described in early Alzheimer disease.<sup>(26)</sup>

<strong>SECONDARY DIABETES:</strong> Various other types of diabetes, previously called secondary diabetes, are caused by other illnesses or medications. Depending on the primary process involved (e.g. destruction of pancreatic beta cells or development of peripheral insulin resistance), these types of diabetes behave similarly to type 1 or type 2 diabetes.
The most common causes of secondary diabetes are as follows:
<ul>
 	<li>Diseases of the pancreas that destroy the pancreatic beta cells (e.g. hemochromatosis, pancreatitis, cystic fibrosis, pancreatic cancer)</li>
 	<li>Hormonal syndromes that interfere with insulin secretion (e.g. pheochromocytoma)</li>
 	<li>Hormonal syndromes that cause peripheral insulin resistance (e.g. acromegaly, Cushing syndrome, pheochromocytoma)</li>
 	<li>Drugs (e.g. phenytoin, glucocorticoids, estrogens)</li>
</ul>
<strong>GESTATIONAL DIABETES:</strong> Gestational diabetes mellitus is defined as any degree of glucose intolerance with onset or first recognition during pregnancy. A steady decline in insulin sensitivity as gestation progresses is a normal feature of pregnancy; gestational diabetes mellitus results when maternal insulin secretion cannot increase sufficiently to counteract the decrease in insulin sensitivity.

<strong>NATURAL HISTORY:</strong>

Type 2 diabetes, previously referred to as adult-onset or non-insulin-dependent diabetes, progresses from an early asymptomatic stage with insulin resistance to mild postprandial hyperglycemia to frank diabetes requiring pharmacological intervention. Understanding this natural history of type 2 diabetes will guide primary care providers in formulating effective treatment regimens that reflect the pathological differences between these stages of the disease. The optimal medication regimen, when used in conjunction with dietary changes and exercise, will require modifications for each patient as the disease progresses.

This stage of mild postprandial hyperglycemia is an extremely useful marker of patients at risk for the eventual development of type 2 diabetes. Patients with Impaired Glucose Tolerance (IGT) may benefit from timely patient education and perhaps even more aggressive forms of intervention, such as diet, exercise, or medication.

<strong>SIGN AND SYMPTOMS:</strong>

Type 2 DM may present to the clinician in one of 4 ways:
<ul>
 	<li>Classical symptoms</li>
 	<li>Incidental diagnosis</li>
 	<li>Hyperosmolar nonketotic coma.</li>
 	<li>Complications of diabetes mellitus</li>
</ul>
<strong>CLASSICAL SYMPTOMS:</strong>

Symptoms of type 2 DM that may be seen at diagnosis are increased thirst, polyuria, increased hunger, weight loss, fatigue, blurred vision, slow healing sores or frequent infections and acanthosis nigricans.
<ul>
 	<li><strong>Increased thirst and polyuria: </strong>Excess sugar building up in blood stream causes fluid to be pulled from the tissues. Due to which patient may feel thirsty. As a result, patient may drink and urinate more than usual.</li>
 	<li><strong>Increased hunger: </strong>Without enough insulin to move sugar into cells, patient’s muscles and organs become depleted of energy. This triggers intense hunger.</li>
 	<li><strong>Weight loss: </strong>Despite eating more than usual to relieve hunger, patient may lose weight. Without the ability to metabolize glucose, the body uses alternative fuels stored in muscle and fat. Calories are lost as excess glucose is released in the urine.</li>
 	<li><strong>Fatigue: </strong>If cells are deprived of sugar, patient may become tired and irritable.</li>
 	<li><strong>Blurred vision: </strong>If blood sugar is too high, fluid may be pulled from the lenses of eyes. This may affect patient’s ability to focus.</li>
 	<li><strong>Slow-healing sores or frequent infections: </strong>Type 2 diabetes affects ability to heal and resist infections. Elevated glucose levels may make it harder for body to heal. Therefore, injuries like cuts and sores stay open longer. This makes them more susceptible to infection.</li>
 	<li><strong>Acanthosis nigricans: </strong>Some people with type 2 diabetes have patches of dark, velvety skin in the folds and creases of their bodies, usually in the armpits and neck. This condition, called acanthosis nigricans, may be a sign of insulin resistance.</li>
</ul>
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