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Insulin Resistance in Gastroesophageal Reflux Disease REVIEW ARTICLE Insulin Resistance in Gastroesophageal Reflux Disease Laras Budiyani, Dyah Purnamasari, Marcellus Simadibrata, Murdani Abdullah Department of Internal Medicine, Faculty of Medicine Universitas Indonesia - Cipto Mangunkusumo Hospital, Jakarta, Indonesia. Corresponding Author: Dyah Purnamasari, MD., PhD., Endocrinologist. Division of Endocrinology and Metabolism, Department of Internal Medicine, Faculty of Medicine Universitas Indonesia - Cipto Mangunkusumo Hospital. Jl Salemba Raya No 6, Jakarta 10430, Indonesia. email: [email protected]. ABSTRAK Resistensi insulin merupakan gangguan dalam regulasi glukosa yang ditandai dengan peningkatan kadar insulin. Dalam konteks klinik, resistensi insulin dapat bermanifestasi sebagai sindrom metabolik yang memiliki risiko kejadian kardivaskular yang tinggi. Beberapa studi telah melaporkan bahwa resistensi insulin berhubungan langsung terhadap adanya esofagitis erosif pada pasien dengan penyakit refluks gastroesofageal (GERD). Dalam tinjauan pustaka ini, kami akan menelaah pemahaman terbaru yang dapat menjelaskan adanya resistensi insulin pada pasien dengan penyakit refluks gastroesofageal. Kata kunci: resistensi insulin, GERD, sindrom metabolik, esofagitis erosif. ABSTRACT Insulin resistance is the disturbance of glucose regulation characterized by higher insulin level. In clinical context, insulin resistance can manifest as abnormalities that are related with cardiovascular event risk, known as metabolic syndrome. Several studies had reported that insulin resistance was associated with erosive esophagitis in patients with gastroesophageal reflux disease (GERD). Keywords: insulin resistance, GERD, metabolic syndrome, erosive esophagitis. INTRODUCTION syndrome had reached 28.6%.4 Insulin sensitivity is the ability of insulin In addition to the risk of cardiovascular to exert normal physiologic effects in glucose events, insulin resistance may also be associated regulation. In clinical context, insulin resistance with other conditions such as polycystic may manifest as obesity, dyslipidemia, and ovary syndrome, non-alcoholic fatty liver hyperglycemia. These related abnormalities disease, and gastroesophageal reflux disease.1 carry high risk of cardiovascular events, known Gastroesophageal Reflux Disease (GERD) is as metabolic syndrome.1,2 quite common in daily practice. The prevalence The rising prevalence of metabolic syndrome of GERD in Jakarta in 2002 was 25.18%.5 This carries a public health issue that needs attention. disease has a wide clinical spectrum and may Based on Riskesdas 2013, the proportion of cause complications related to gastric reflux to high triglyceride levels in Indonesia, low HDL, the esophagus, oral cavity, and / or lung and are and hypertension had reached 13%, 22.9%, and associated with decreased quality of life.6,7 This 25.8%, respectively.3 A survey in Jakarta in paper will discuss the current understanding of 2006 showed that the prevalence of metabolic the relationship between gastroesophageal reflux 336 Acta Med Indones - Indones J Intern Med • Vol 50 • Number 4 • October 2018 Vol 50 • Number 4 • October 2018 Insulin resistance in GERD disease and insulin resistance. protein O (FOXO) which may elevate hepatic gluconeogenesis.8-10 INSULIN RESISTANCE AND ITS When there is an increase in adipocytes, MECHANISM especially abdominal visceral fat, the body’s Insulin sensitivity is the ability of insulin to insulin sensitivity decreases. The target tissue work in glucose regulation, to increase glucose reduces the number of insulin receptors on absorption, lower glucose levels and increase the cell surface in response to prolonged high the conversion of glucose into a form that is insulin levels. Adipose tissue can affect insulin stored by the body. Insulin resistance can be sensitivity to other tissues by secreting adipokine defined as decreased tissue responsiveness to molecules (TNFα, IL-6) that inhibit insulin insulin with an increased production of insulin signals locally or on remote target tissues.11 to provide a normal biological response. Insulin Measurement of Insulin Resistance resistance syndrome is a group of abnormalities Insulin resistance is measured by two and interrelated physical manifestations that approaches, dynamic intervention and steady occur in individuals with insulin resistance. state assessment using mathematical calculations. Meanwhile, the metabolic syndrome represents a The first approach includes examination of clinical diagnostic entity associated with insulin hyperinsulinemic glucose clamp, which is resistance that identifies an individual as having the gold standard. While the second approach a high risk of cardiovascular morbidity.1 includes assessment of Homeostasis Model Under normal circumstances, insulin release Assessment for Insulin Resistance (HOMA- from pancreatic β cells will induce the entry IR) and quantitative insulin sensitivity check of glucose into cells when binding to insulin index (QUICKI). This calculation is processed receptors on the cell surface. The insulin receptor using a mathematical formula that represents will undergo autophosphorylation initiating fasting insulin kinetic and fasting glucose a cascade in the translocation of glucose measurement.12 transporters types 1 and 4 (GLUT 1 and GLUT This mathematical equation was often used 4) to the membrane in facilitating the entry in epidemiology study due to the practical of glucose into the cell.8.9 The circumstances and easy method using one blood sample. that cause insulin receptor disorders, both in Nevertheless, this simple method could not activity and concentration, will affect the action be used in determining insulin resistance in of insulin. Molecular mechanism disturbances certain population, such as in elderly and type associated with glucose transport activity through 1 diabetes. This is due to insulin levels that insulin receptor substrate serine phosphorylation will not accurately represent insulin resistance (IRS) -1 and mitochondrial disorders may cause because β cells do not secrete sufficient insulin.12 insulin resistance.8 Nevertheless, in one multivariate study in The mechanisms of insulin resistance in patients with hypertension and type 2 diabetes obesity begin with increased fatty acyl CoA mellitus comparing HOMA-IR, QUICKI and and diacylglycerol in plasma and / or decreased McAulay index against insulin resistance using oxidation due to mitochondrial dysfunction that clamp technique, HOMA IR and QUICKI had activates protein kinase C in skeletal muscle. good validity in estimating insulin resistance, Furthermore, activation of serine residue on with HOMA IR was being the most appropriate IRS-1 will decrease GLUT4 translocation. value.13 In addition, there was a good correlation In the liver, elevated hepatic diacylglycerol between the estimated value of insulin resistance content due to increased fatty acids from from HOMA and from the Clamp technique.8 plasma will lead to decreased insulin kinase The model of insulin resistance homeostasis receptor activity and decrease IRS-2 tyrosine (HOMA-IR) is used to estimate insulin resistance phosphorylase, resulting in decreased insulin and β cell function using plasma insulin and stimulation of glycogen synthase activation fasting glucose concentration. The relationship and decreased phosphorylation of forkhead box between glucose and insulin in the basal state 337 Laras Budiyani Acta Med Indones-Indones J Intern Med reflects the balance between liver glucose output irritating substance entering the esophagus, and and insulin secretion maintained by the feedback the mechanism of excreting irritating materials mechanism between the liver and β cells. There is through normal esophageal motility. If there is no cut off value that applied globally to determine a disturbance in this defense mechanism, the insulin resistance. The higher the HOMA-IR esophagus will be irritated by prolonged acidic index, the higher the insulin resistance in one liquids, resulting in GERD conditions. In patients individual.11,13 One study in Japan determined with GERD, temporary relaxation of LES the value of HOMA-IR > 1.7 as a reference point occurs more frequently than normal conditions. for identifying subjects with a high risk of the Defects in LES, such as hypotonicity in LES, presence of the metabolic syndrome.14 Indonesia and the effects of a hiatal hernia can cause the does not have data on the average value of insulin condition.20,21 resistance in the general population, but study in obese adolescents revealed HOMA-IR mean was INSULIN RESISTANCE AND 3.92 and in elderly women had a mean HOMA- GASTROESOFAGEAL REFLUX DISEASE IR level of 2.87.15,16 There are many studies that linking gastroesophageal reflux disease with metabolic GASTROESOPHAGEAL REFLUX DISEASE syndrome. A study by Park et al.22 showed an Gastroesophageal reflux disease (GERD) association between erosive esophagitis and is defined as symptoms of reflux or mucosal metabolic syndrome.Another study by Wu et damage due to reflux of gastric contents into the al.23 showed that the prevalence of metabolic esophagus or higher, to the oral or lung cavity, syndrome in patients with reflux esophagitis causing symptoms or related complications. was significantly higher than that of the control This gastroesophageal reflux disease may be group and parameters associated with reflux classified as a non-erosive reflux disease (NERD) esophagitis were peripheral circumference, and or erosive reflux disease (ERD) based on the fasting
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