**1. Introduction**

Changing food habits, sedentary lifestyle and obesity has made type 2 diabetes (T2D) a global epidemic. T2D has various characteristic features such as insulin resistance caused when peripheral tissues such as liver, muscle and adipocytes have a decreased response to insulin. The progression from normal glucose tolerance to type 2 diabetes involves several transitional stages of impaired fasting glucose and impaired glucose tolerance which is known as prediabetes. The mechanism leading to the development of these glucose metabolic alterations is multifactorial. The most prevalent factor of T2D is insulin resistance that occurs when peripheral tissues such as liver, muscle and adipocytes, the main target organs of Insulin hormone, loses the ability to respond to insulin [1]. Generally in the obese patients without T2D and initially in people who develop insulin resistance, pancreatic β-cells are able to compensate for insulin resistance by increasing insulin secretion by increasing β-cell mass via increased proliferation and hypertrophy [2, 3].

Increasing of β-cells in a compensatory mechanism to avoid the complications caused due to insulin resistance and henceforth prevents diabetes [4]. This unique mechanism of β-cell mass expansion has been observed in normal individuals during physiological growth [5] as well as in insulin resistant patients, especially pregnant women [6] and obese people [7]. In patients having T2D the initial stage of β-cell compensation is followed by dysfunction or failure of β-cells due to less proliferation and increased apoptosis [1, 8].

Pancreatic β-cell dysfunction plays a critical role in progression of T2D. Insulin is produced as preproinsulin and then processed to proinsulin. Proinsulin is then converted to insulin and C-peptide and stored in secretory granules. Synthesis of insulin is regulated at both transcription and translational level. Several transcription factors in the cis-acting sequences within the 5′ region and trans-activators regulate insulin gene transcription. These transcription factors are paired homeobox gene 6 (PAX6), pancreatic and duodenal homeobox-1 (Pdx-1), MafA and B-2/ Neurogenic differentiation 1 (NeuroD1). Insulin secretion from β-cells contains a series of events and is controlled by variety of factors and signaling pathways that ultimately leads to the fusion of secretory granules with the plasma membrane. The various stimulants that regulate insulin secretion are glucose, free fatty acids, amino acids, also various hormones like melatonin, estrogen, leptin, growth hormone and glucagon like peptide-1 [9].
