The role of morbid obesity in the promotion of metabolic disruptions and non-alcoholic steatohepatitis by Helicobacter Pylori

Helicobacter pylory (HP) infection has been associated to an increased rate of type 2 diabetes (T2D) and liver disease through its effect on insulin resistance and systemic inflammation. However, results are inconstant and no studies exist in morbidly obese patients, in which both insulin resistance and inflammation coexist

Diabetes Is the Main Factor Accounting for Hypomagnesemia in Obese Subjects

OBJECTIVE: Type 2 diabetes (T2DM) and obesity are associated with magnesium deficiency. We aimed to determine whether the presence of type 2 diabetes and the degree of metabolic control are related to low serum magnesium levels in obese individuals. METHODS: A) Case-control study: 200 obese subjects [50 with T2DM (cases) and 150 without diabetes (controls)] prospectively recruited. B) Interventional study: the effect of bariatric surgery on serum magnesium levels was examined in a subset of 120 obese subjects (40 with type 2 diabetes and 80 without diabetes). RESULTS: Type 2 diabetic patients showed lower serum magnesium levels [0.75±0.07 vs. 0.81±0.06 mmol/L; mean difference -0.06 (95% CI -0.09 to -0.04); p<0.001] than non-diabetic patients. Forty-eight percent of diabetic subjects, but only 15% of non-diabetic subjects showed a serum magnesium concentration lower than 0.75 mmol/L. Significant negative correlations between magnesium and fasting plasma glucose, HbA1c, HOMA-IR, and BMI were detected. Multiple linear regression analysis showed that fasting plasma glucose and HbA1c independently predicted serum magnesium. After bariatric surgery serum magnesium increased only in those patients in whom diabetes was resolved, but remain unchanged in those who not, without difference in loss weight between groups. Changes in serum magnesium negatively correlated with changes in fasting plasma glucose and HbA1c. Absolute changes in HbA1c independently predicted magnesium changes in the multiple linear regression analysis. CONCLUSIONS: Our results provide evidence that the presence of diabetes and the degree of metabolic control are essential in accounting for the lower levels of magnesium that exist in obese subjects

Iodine deficiency is higher in morbid obesity in comparison with late after bariatric surgery and non-obese women

Background Iodine deficiency and obesity are worldwideoccurring health problems. Our purpose was to investigate the relationship between morbid obesity and iodine status, including subjects who lost weight after bariatric surgery. Methods Ninety morbidly obese women, 90 women with at least 18 months follow-up after bariatric surgery, and 45 healthy non-obese women were recruited. Urinary iodine concentration (UIC) was measured in a spot urinary sample and expressed as the iodine-to-creatinine ratio. Results Obese women showed a significantly lower UIC in comparison with non-obese women (96.6 (25.8–267.3) vs. 173.3 (47.0–493.6) μg/g; p<0.001), with a lesser proportion of subjects with adequate iodine status (46.6 vs. 83.3 %, p<0.001). The mean UIC significantly increased among women who underwent bariatric surgery before the collection of the urinary sample (96.6 (25.8–267.3) vs. 131.9 (62.9– 496.4) μg/g; p<0.001). No difference in UIC was detected between laparoscopic Roux-en-Y gastric bypass and laparoscopic sleeve gastrectomy. Univariate analysis showed that UIC negatively correlated with body mass index (BMI) (r=−0.278, p<0.001) and positively with age (r=0.206, p=0.002). Finally, multiple linear regression analyses showed that BMI was independently associated with UIC (beta=−0.312, p<0.001; R2=0.166). Conclusion Obesity is an independent risk factor to iodine deficiency, almost in women.Whether more obese population needs to be considered as a vulnerable group and whether bariatric surgery can reverse iodine deficiency still remain to be elucidated

Hepatic and Visceral Adipose Tissue 11bHSD1 Expressions are Markers of Body Weight Loss After Bariatric Surgery

Cortisolemia and 11βHSD1 in liver and adipose tissue are altered in obesity. However, their participation in the development of obesity remains unclear. This study analyzed these parameters in the transition from morbid to type 1 obesity after bariatric surgery