**2.1 Pathophysiology of GERD in obesity**

Since obesity has contributed largely to the increased of GERD prevalence, there has been a substantial attention to explore the possible mechanisms of GERD development in obesity [17]. The essential pathology in the development of GERD is excessive acid and bile salt exposure on the gastric mucosa [3]. This abnormal exposure may lead to distressing symptoms of GERD when the number of reflux events is enormous, the period of mucosal exposure to gastric content is prolonged, there is concomitant defect in mucosal integrity, or hypersensitivity to refluxate [3]. The integrity of the esophagogastric junction (EGJ), both structural and functional, is an important antireflux barrier [3]. Major mechanisms of EGJ incompetence that discovered in GERD are anatomical derangement of the EGJ including hiatal hernia, decreased pressure of lower esophageal sphincter (LES), and transient lower esophageal sphincter relaxation (TLESR). Delayed gastric emptying and prolonged esophageal clearance time has been found in subsets of patients as mechanism that may exacerbate GERD [3].

Several factors that could increase acid exposure time on the esophagus was found more often in patients with obesity than in individuals with normal weight [12]. The development of GERD in obese individuals was previously thought to be mainly structural, owing to the weight of abdominal fat that increase intraabdominal pressure, thereby increased the likelihood reflux occurrence. Recent evidence also suggest that obesity may alter the physiologic function of lower esophageal sphincter (decreased LES pressure, increased frequency of transient LES relaxation), and/or gastroesophageal motility (delayed esophageal clearing time, impaired gastric emptying) [9, 13].

The development of a hiatal hernia is the main factor that disrupts the integrity of the EGJ in patients with excess body weight [9]. The prevalence of hiatal hernia is
