الفهرس 
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Abstract
Obesity is a disease in which excess body fat has accumulated to an extent that health is adversely affected .The World Health Organization (WHO) defines obesity as a BMI (body mass index) of 30 kg/m2
Obesity is the most common nutritional disorder in the world. According to the World Health Organization (WHO), recent research data suggest that obesity has tripled in developing countries and particularly, in low-income countries.. Egypt is the 14th fattest country in the world, according to the most recent World Health Organization statistics issued for the year 2010. Obesity results from imbalance between energy consumed and energy expended, with excess energy stored as fat, and it has numerous health consequences .
Helicobacter pylori (H. pylori) is one of the most prevalent human infections representing the major cause of chronic gastritis. Its prevalence in developed countries is rare in children, and less than 50% of the population is infected at age 60. In contrast, in developing countries more than 20% of children younger than 5 years are infected, rising to 80% at age 25.
The relationship between obesity and H pylori infection and eradication is controversial. According to some studies, the risk of H pylori infection does not increase in overweight young persons and H pylori seropositivity are not associated with the BMI or fasting serum leptin levels .In contrast, other studies showed that obesity and/or an elevation of the BMI may be associated with an increased incidence of H pylori colonization, probably as a result of reduced gastric motility.
It was hypothesized that gastric H. pylori colonization affects the physiologic regulation of gut hormones involved in food intake, energy expenditure, and body weight maintenance. The hormones that affect overall metabolic function include ghrelin, leptin, amylin, insulin, active glucagon-like peptide-1, gastric inhibitory polypeptide, peptide YY, and pancreatic polypeptide.
Ghrelin and obestatin are both important peptides that regulate appetite and play roles as orexigenic signals and in satiety pathways. Both are secreted mainly from gastric oxyntic mucosa and are thought to be influenced by Helicobacter pylori (H. pylori) . However, the influences of H. pylori on serum concentrations of ghrelin are contradictory, since multiple factors interfere with its serum level. Further, and only a limited number of studies have focused on interaction between obestatin and H. pylori .
Serum leptin, which is primarily synthesized by adipose tissue, regulates food intake and body weight homeostasis. Leptin is now known to be synthesized in the stomach
as well , and this source may also be involved in the regulation of food intake and satiety.
The aim of this study is to evaluate ghrelin /obestatin balance and leptin in obese subjects with h. pylori infection.
Sixty healthy volunteer aged between 25 – 55 years were divided into two equal groups: obese and non obese. Each group was divided into H. Pylori positive (+) or H. Pylori negative (-) according to the presence of H. pylori in their stool .
Anthropometric parameters; including Body mass index (BMI), Waist circumference (WC) and waist to hip ratio (WHR) were measured . Blood samples were taken from each subject, centrifuged and sera were separated for evaluation of: Fasting serum glucose, Total cholesterol, triglycerides (TG), high density cholesterol (HDL), and low density cholesterol (LDL). In addition fasting serum insulin with calculation of Homeostasis Model Assessment Insulin Resistance (HOMA-IR). H. Pylori status by evaluating IgG antibodies against H. Pylori by ELISA are measured.
Serum levels of ghrelin , obestatin and leptin were evaluated using ELISA technique and Ghrelin / obestatin ratio was estimated
Findings demonstrated significant increase in serum glucose, insulin and HOMA-IR ratio in obese subjects with positive H .pylori as compared to other groups. Disturbed lipid profile including serum cholesterol , triglycerides, HDL and LDL cholesterol in obese subjects as compared to non obese.
As regards hormonal results, H. pylori positive subjects showed significant increased ghrelin and ghrelin / obestatin balance and a significant decreased obestatin as compared to negative subjects. The most significant changes were observed in obese subjects.
In obese subjects with negative H. pylori , ghrelin/ obestatin ratio was negatively associated with weight, BMI ,glucose, insulin, HOMA-IR, cholesterol ,triglycerides LDL, Leptin and H. pylori Ag .However, these correlation were reversed in obese subjects with positive H. pylori as ghrelin / obestatin ratio was positively correlated with weight, BMI, waist, glucose, insulin, HOMA, leptin, cholesterol, trigycerides, LDL and also with
H. pylori Ag.
from the data obtained in this study we can conclude that:
• Stomach hormones ghrelin, obestatin and leptin are affected by presence of h.pylori seropositivity in obese subjects.
• The higher ghrelin levels and ghrelin / obestatin ratio with lowered obestatin could be considered as a gastroprotectve effect against inflammation induced by H. pylori .
• Ghrelin, obestatin hormones and ghrelin / obestatin ratio could be considerd as markers for gastric mucosal progression in infected subjects and may also reflect the effectiveness of treatment
• This hormonal imbalance may have a role in metabolic alterations. .However , the discrepancies between our findings and other reported data indicate that further research is needed.
• Early eradication of H. pylori is recommended to control the associated metabolic consequences