Background: Ghrelin is a peptide mainly secreted by gastric mucosa and has been implicated in the regulation of eating behavior and weight balance. Obesity and Helicobacter pylori infection are associated with changes in plasma ghrelin levels. Objective: This study was designed to evaluate the density of ghrelin-producing cells in the gastric mucosa of morbidly obese and dyspeptic non-obese patients, with and without H. pylori infection. Methods: Gastric biopsies of the antral and oxyntic mucosa were obtained from 50 morbidly obese patients (BMI O40, 21 with metabolic syndrome (MS)), 17 dyspeptic overweight subjects (25!BMI!30), and 33 lean individuals (BMI!25) and processed for histology and immunohistochemistry. Results: Ghrelin-immunoreactive cell densities in the oxyntic mucosa were similar in morbidly obese patients with MS and in overweight and lean patients, whereas morbidly obese patients without MS presented higher ghrelin-immunoreactive cell density. The number of ghrelin cells in the oxyntic mucosa was significantly lower in obese and non-obese H. pylori-infected subjects. Ghrelin-immunoreactive cells, although sparse in the antral mucosa, were found more frequently in obese patients and their numbers did not seem to be affected by H. pylori infection. Conclusions: The higher expression of ghrelin-immunoreactive cells in the oxyntic mucosa of morbidly obese patients compared with non-obese subjects or with morbidly obese subjects with MS and the finding of a higher number of small foci of ghrelin cells in the antral mucosa of obese patients may indicate an adaptive mechanism or an individual factor to be considered in the pathogenesis of obesity.

Introduction: Osteoporosis and vitamin B12 defi ciency are conditions with an increasing prevalence over time. It has been described an association between low serum vitamin B12, osteoporosis and increased risk of bone fractures, but the studies are heterogeneous and the results are controversial. Objective: To investigate the association between plasma levels of vitamin B12 and bone mineral density in a group of asymptomatic women after menopause. Methods: Asymptomatic postmenopausal women were consecutively invited to participate in this cross-sectional study. Bone mineral density (lumbar spine and femur) was measured by DXA Lunar Prodigy Vision, and blood levels of vitamin B12, calcium, phosphorus, bone alkaline phosphatase (BAF), and parathyroid hormone were determined. For the diagnostic of osteoporosis the World Health Organization criteria were considered. Results: Seventy women were included, mean age 62.5 ± 7 years. Eighteen (25.7%) women had normal bone mineral density, 33 (47.1%) had osteopenia and 19 (27.1%) had osteoporosis. Six (8.6%) patients had wrist fracture; two (2.8%) reported a diagnosis of vertebral fracture and only one (1.4%) patient had suffered a hip fracture. The levels of vitamin B12 (mean ± SD, pg/mL) of women with normal bone mineral density, osteopenia and osteoporosis were 590.2 ± 364.3, 536.6 ± 452.3, and 590.2 ± 497.9, respectively (P = 0.881). Multiple regression analysis showed that body mass index and BAF were the main predictors of lumbar spine bone mineral density. Conclusion: The results indicate that vitamin B12 serum levels are not related to bone mineral density in this group of Brazilian postmenopausal women.

Generalized bone loss can be considered an extra-articular manifestation of rheumatoid arthritis (RA) that may lead to the occurrence of fractures, resulting in decreased quality of life and increased healthcare costs. The peptide ghrelin has demonstrated to positively affect osteoblasts in vitro and has anti-inflammatory actions, but the studies that correlate ghrelin plasma levels and RA have contradictory results. We aimed to evaluate the correlation between total ghrelin plasma levels, density of ghrelin-immunoreactive cells in the gastric mucosa, and bone mineral density (BMD) in twenty adult women with established RA with 6 months or more of symptoms (mean age of 52.70±11.40 years). Patients with RA presented higher ghrelin-immunoreactive cells density in gastric mucosa (P=0.008) compared with healthy females. There was a positive relationship between femoral neck BMD and gastric ghrelin cell density (P=0.007). However, these same patients presented a negative correlation between plasma ghrelin levels and total femoral BMD (P=0.03). The present results indicate that ghrelin may be involved in bone metabolism of patients with RA. However, the higher density of ghrelin-producing cells in the gastric mucosa of these patients does not seem to induce a corresponding elevation in the plasma levels of this peptide.

Obesity is a multifactorial disorder often associated with many important diseases such as diabetes, hypertension and other metabolic syndrome conditions. Argyrophil cells represent almost the total population of endocrine cells of the human gastric mucosa and some reports have described changes of specific types of these cells in patients with obesity and metabolic syndrome. The present study was designed to evaluate the global population of argyrophil cells of the gastric mucosa of morbidly obese and dyspeptic non-obese patients. Gastric biopsies of antropyloric and oxyntic mucosa were obtained from 50 morbidly obese patients (BMI >40) and 50 non-obese patients (17 dyspeptic overweight and 33 lean individuals) and processed for histology and Grimelius staining for argyrophil cell demonstration. Argyrophil cell density in the oxyntic mucosa of morbidly obese patients was higher in female (238.68 ± 83.71 cells/mm2) than in male patients (179.31 ± 85.96 cells/mm2) and also higher in female (214.20 ± 50.38 cells/mm2) than in male (141.90 ± 61.22 cells/mm2) morbidly obese patients with metabolic syndrome (P = 0.01 and P = 0.02, respectively). In antropyloric mucosa, the main difference in argyrophil cell density was observed between female morbidly obese patients with (167.00 ± 69.30 cells/mm2) and without (234.00 ± 69.54 cells/mm2) metabolic syndrome (P = 0.001). In conclusion, the present results show that the number of gastric argyrophil cells could be under gender influence in patients with morbid obesity. In addition, gastric argyrophil cells seem to behave differently among female morbidly obese patients with and without metabolic syndrome.

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