The effect of H. pylori eradication on meal-associated changes in plasma ghrelin and leptin

New York University Langone Medical Center, New York, NY, USA.
BMC Gastroenterology (Impact Factor: 2.37). 04/2011; 11(1):37. DOI: 10.1186/1471-230X-11-37
Source: PubMed


Appetite and energy expenditure are regulated in part by ghrelin and leptin produced in the gastric mucosa, which may be modified by H. pylori colonization. We prospectively evaluated the effect of H. pylori eradication on meal-associated changes in serum ghrelin and leptin levels, and body weight.
Veterans referred for upper GI endoscopy were evaluated at baseline and ≥8 weeks after endoscopy, and H. pylori status and body weight were ascertained. During the first visit in all subjects, and during subsequent visits in the initially H. pylori-positive subjects and controls, blood was collected after an overnight fast and 1 h after a standard high protein meal, and levels of eight hormones determined.
Of 92 enrolled subjects, 38 were H. pylori-negative, 44 H. pylori-positive, and 10 were indeterminate. Among 23 H. pylori-positive subjects who completed evaluation after treatment, 21 were eradicated, and 2 failed eradication. After a median of seven months following eradication, six hormones related to energy homeostasis showed no significant differences, but post-prandial acylated ghrelin levels were nearly six-fold higher than pre-eradication (p=0.005), and median integrated leptin levels also increased (20%) significantly (p<0.001). BMI significantly increased (5 ± 2%; p=0.008) over 18 months in the initially H. pylori-positive individuals, but was not significantly changed in those who were H. pylori-negative or indeterminant at baseline.
Circulating meal-associated leptin and ghrelin levels and BMI changed significantly after H. pylori eradication, providing direct evidence that H. pylori colonization is involved in ghrelin and leptin regulation, with consequent effects on body morphometry.

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    • "Elevated levels of inflammatory cytokines may lead to phosphorylation of serine residues on the insulin receptor substrate, which prevents its interaction with insulin receptors, inhibiting insulin action.[2] Mammalian stomach produces leptin and ghrelin, two hormones involved in energy homeostasis and whose interactions affect obesity, insulin sensitivity, and glucose homeostasis. Increasing evidence indicates that H. pylori is involved in the regulation of these hormones.[3] The study was designed to study association of H. pylori infection in type 2 diabetes. "
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    ABSTRACT: Introduction:Helicobacter pylori (H. pylori) infection has been associated with increased levels of inflammatory cytokines and subsequent insulin resistance and epidemiologically linked to type 2 diabetes.Objectives:To study the prevalence rate of H. pylori infection in type 2 diabetes and its relation with HbA1C levels.Materials and Methods:In this cross-sectional case-control study, 80 patients (≥18 years) who met the Americans with Disabilities Act (ADA) criteria for diabetes were recruited. Similarly, 60 age, sex, and education matched healthy controls were taken. They were tested for H. pylori infection by rapid urease test, histological examination of antral endoscopic biopsy specimens and serology. The relationship between H. pylori infection and levels of plasma glucose and HbA1C was assessed.Results:Out of the 80 patients of type 2 diabetes, H. pylori infection was found in 62 (77.5%) while it was present in only 35 (58.3%) of 60 controls, which was found to be significant (Chi-square test: 5.919, df = 1, P value = 0.015). Mean HbA1C among diabetics with H. pylori infection was 8.19 ± 1.16% and without H. pylori infection was 6.9 ± 0.84% (t = 4.3872, P value = 0.0001).Conclusions:Prevalence of H. pylori infection was significantly higher in diabetes as compared to controls. Presence of H. pylori infection significantly correlated with the level of HbA1C.
    09/2014; 18(5):694-9. DOI:10.4103/2230-8210.139235
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    • "H. pylori gastritis and its role in mucosal activation of innate immunity and upregulation of IL-1β is also suggested in the pathogenesis of IR (25). H.pylori gastritis and its effects on ghrelin may also affect appetite and insulin sensitivity (26). "
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    ABSTRACT: Background: The association of HP and insulin resistance degree (IR) has not been evaluated in the diabetic patients so far. In this study, we evaluated the association between HP seropositivity and the homeostatic model assessment for insulin resistance (HOMA-IR) in diabetic patients. Methods: In this study, 211 diabetic patients admitted to the endocrinology clinic of Shahid Beheshti Hospital of Qom for routine diabetic check-ups were evaluated. The patients were divided into HP+ and HP- groups based on the seropositivity of helicobacter pylori IgG antibody. The serum H. pylori IgG antibody, blood sugar, serum insulin, HbA1c, LDL, HDL, cholesterol, triglyceride, HOMA-IR and BMI were measured. Seropositivity for H. pylori was detected based on the serum titers of >30 AU/mL. Results: We found that serum insulin (HP-=6.97±5.64 vs. HP+=10.12±7.72, P=0.002) and insulin resistance degree (HP-=3.160±3.327 vs. HP+=4.484±3.781, P=0.013) is significantly higher in HP+ group. We also found that there is no significant difference between these groups according to the short-term or the long-term indices of glycemic control as well as most of the diabetic risk factors or complications. The treatment type was also not significantly different between these groups. Conclusion: It seems that the HP+ diabetic patients require higher levels of serum insulin to reach the same degree of glycemic control compared to the HP- ones. Keywords: Keywords: Diabetes, Helicobacter pylori, Insulin Resistance,
    Caspian Journal of Internal Medicine 05/2014; Volume 5, Number 3 (5-2014)(3).
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    • "However this study recommended, that further studies are needed to define whether this is a fundamental association (15). In agreement to these mentioned studies and our results, some authors indicated that the HP infection is related to HbA1c and a possible mechanism for the association is the role of HP in the host metabolic homeostasis by disturbing the ghrelin and leptin production that affects the blood glucose level in diabetes patients (16–18). Moreover other studies revealed that HP infection is related to a various complications such as peptic ulcer as carcinoma, anaemia and gastric motor dysfunction (14). "
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    ABSTRACT: To evaluate the possible long-term effects of Helicobacter pylori infection on Hemoglobin A1c and fasting blood sugar levels in patients with type 2 diabetes. Helicobacter pylori causes the gastrointestinal tract inflammation, which it plays an important role in distortion of glucose and lipids absorption that altered lipid metabolism and energy harvesting and develops type 2 diabetes, insulin resistance and has been linked to impaired blood glucose. In this clinical trial, patients with type 2 diabetes and confirmed Helicobacter pylori infection were recruited from the endocrinology clinic of the Shahid Beheshti University Tehran, Iran. Before and after 3 months of eradication therapy fasting blood samples were taken and glycalated hemoglobin levels and fasting blood sugar levels were measured. 85 (27 male 31.8%, 58 female 68.2%) patients with the mean age of 52.±4.7 years were recruited. 52 (62%) had successful Helicobacter pylori eradication (16 male, 30.8% and 36 female, 69.2%). The mean glycalated haemoglobin levels before successful treatment was 8.7±1.1 and after treatment was 8.3±0.9 and difference was significant (p<0.001). Mean IgG level of serology was 3.3±1.1 and the correlation with glycalated haemoglobin was significant (p=0.02) (r=0.4). Our results indicate that the Helicobacter pylori treatment can improve the mean glycalated haemoglobin in patients with type 2 diabetes. More investigations will be required to evaluate the effects of Helicobacter pylori eradication among different age groups and in relation to obesity status, diabetes and other disease, and it may be beneficial for patients at risk of diabetes to be checked for the presence of Helicobacter pylori infection.
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