Juan Antonio Baena-Fustegueras

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. A group of 34 patients with morbid obesity and 22 nonobese subjects were recruited. Initial hypothalamus-pituitary-adrenal (HPA) basal activity and 11βHSD1 mRNA expression in liver, subcutaneous (SAT), and visceral adipose tissue (VAT) were evaluated. A year after bariatric surgery (weight loss of 48 kg), these parameters were reappraised in plasma, SAT, and liver. Body weight loss was accompanied by a downshift in basal HPA activity and 11βHSD1 expression in SAT. In patients with morbid obesity, 11βHSD1 expression correlated positively with BMI in VAT and negatively in liver at 6 and 12 months after surgery. In SAT, a correlation was observed with body weight only when patients showed type 1 obesity. Insulin, glucose, and HOMA correlated positively with all the HPA indicators and 11βHSD1 expression in SAT. Body weight loss after bariatric surgery is accompanied by a downshift in basal HPA activity. Hepatic and VAT 11βHSD1 expressions in morbid obesity are predictors of body weight loss.

We have investigated the differences between metabolically “healthy” morbidly obese patients and those with comorbidities. Thirty-two morbidly obese patients were divided by the absence (“healthy”: DM−DL−) or presence of comorbidities (dyslipidemic: DM−DL+, or dyslipidemic and with type 2 diabetes: DM+DL+). We have studied various plasma parameters and gene expression adipose tissue, before and after gastric bypass. The group DM+DL+ tends to have lower values than the other two groups for anthropometric parameters. Regarding the satiety parameters, only leptin (p = 0.0024) showed a significant increase with comorbidities. Lipid parameters showed significant differences among groups, except for phospholipids and NEFA. For insulin resistance parameters, only glucose (p < 0.0001) was higher in DM+DL+ patients, but not insulin or homeostasis model assessment of insulin resistance (HOMA-IR). The gene expression of adiponectin, insulin receptor (INSR) and glucose receptor-4 (GLUT4), in the subcutaneous fat, decreased in all groups vs. a non-obese control. Interleukin-6 (IL6) and the inhibitor of plasminogen activator type 1 (PAI-1) genes decreased only in DM−DL+ and DM+DL+, but not in “healthy” patients. Leptin increased in all groups vs. the non-obese control. The visceral fat from DM+DL+ patients showed a sharp decrease in adiponectin, GLUT4, IL6 and PAI-1. All parameters mentioned above improved very significantly by surgery, independent of the occurrence of comorbidities. The morbidly obese “healthy” individual is not really metabolically healthy, but morbidly obese individuals with diabetes and dyslipidemia are more metabolically imbalanced.

Objective The possible differences were investigated in 32 morbidly obese patients depending on whether they were “healthy” or had dyslipidemia and/or type 2 diabetes. Methods Lipid metabolism and insulin resistance were analyzed in subcutaneous (SAT) and visceral adipose tissue (VAT) before and during 6 and 12 months after Roux‐en‐Y gastric bypass. Results Significant differences have been found in lipoprotein lipase (LPL) and hormone‐sensitive lipase (HSL) activities in SAT from the different obese group versus normal weight (control) but not between them. The reduced lipase activities in VAT were 43 and 19% smaller (22 and 4% smaller, respectively, vs. control) than the “healthy” obese group for LPL and HSL, respectively, and were accompanied with a reduced expression of these lipases, as well as decreased expression of FAT/CD36, FABP4, and AQ7 in that tissue. In addition, the expression of the other genes measured showed a downregulation not only versus the “healthy” obese but also versus the normal weight group. Conclusions Being obese is not “healthy,” but it is even less so if morbidly obese patients with diabetes and dyslipidemia were considered. The reduced fat accumulation in these patients may be attributed to the decrease of the expression and activity of the lipases of their adipose tissue.

Iodine deficiency and obesity are worldwide-occurring health problems. Our purpose was to investigate the relationship between morbid obesity and iodine status, including subjects who lost weight after bariatric surgery. 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. 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; R ² = 0.166). 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.