No abstract

RYGB is associated to high bone resorption and hyperparathyroidism prevalence in postmenopausal women in the long-term. This occurs independently of the intake of calcium, vitamin D status, or ghrelin and does not seem to affect BMD after RYGB.

Context:The effects of medical and surgical treatments for obesity on peptide YY (PYY) levels, in patients with similar weight loss, remain unclear.Objective: The objective of the study was to assess PYY and appetite before and after Roux-en-Y gastric bypass (RYGB), sleeve gastrectomy (SG), and medical treatment (MED).Design: This was a prospective, controlled, nonrandomized study. Setting:The study was conducted at the Departments of Nutrition and Digestive Surgery at a university hospital.Participants: Participants included three groups of eight patients with similar body mass indexes (RYGB 37.8 Ϯ 0.8, SG 35.3 Ϯ 0.7, and MED 39.1 Ϯ 1.7 kg/m 2 , P ϭ NS) and eight lean controls (body mass index 21.7 Ϯ 0.7 kg/m 2 ). Main Outcome Measures:Total plasma PYY, hunger, and satiety visual analog scales in fasting and after ingestion of a standard test meal were measured.Results: At baseline there were no differences in the area under the curve (AUC) of PYY, hunger, or satiety in obese groups. Two months after the interventions, RYGB, SG, and MED groups achieved similar weight loss (17.7 Ϯ 3, 14.9 Ϯ 2.4, 16.6 Ϯ 4%, respectively, P ϭ NS). PYY AUC increased in RYGB (P Ͻ 0.001) and SG (P Ͻ 0.05) and did not change in MED. PYY levels decreased at fasting, 30 min, and 180 min after a standard test meal in MED (P Ͻ 0.05). Hunger AUC decreased in RYGB (P Ͻ 0.05). Satiety AUC increased in RYGB (P Ͻ 0.05) and SG (P Ͻ 0.05). Appetite did not change in MED. PYY AUC correlated with satiety AUC (r ϭ 0.35, P Ͻ 0.05).Conclusion: RYGB and SG increased PYY and reduced appetite. MED failed to produce changes. Different effects occur despite similar weight loss. This suggests that the weight-loss effects of these procedures are enhanced by an increase in PYY and satiety. O ver the last 30 yr, the prevalence of obesity has increased worldwide, becoming one of the world's most important public health problems and resulting in great efforts toward the development of strategies to treat this condition (1). However, medical interventions for obesity, including diet, physical activity, behavioral therapy, and weight loss drugs, are associated with poor weight reduction and are difficult to sustain in the long term (2). These modest results can be explained by several factors, one being that the human body responds to weight

Our results showed differences in glucose metabolism between PA patients and those with hypertension suggesting that these findings could probably be determined by a lower beta-cell function influenced by aldosterone. These findings highlight the importance of aldosterone in glucose metabolism.

Acarbose avoided postprandial hypoglycaemia following RYGBP by decreasing the hyperinsulinemic response. This was associated with a decrease in early GLP-1 secretion, in contrast to that observed in non-surgical subjects. This finding could be explained by the reduction of glucose load in the jejunum produced by the α-glucosidase inhibition, which is the main stimulus for GLP-1 secretion.

The rs17782313 variant may influence eating behavior in obese children.

No abstract

Cholesterol has evolved to fulfill sophisticated biophysical, cell signalling, and endocrine functions in animal systems. At the cellular level, cholesterol is found in membranes where it increases both bilayer stiffness and impermeability to water and ions. Furthermore, cholesterol is integrated into specialized lipid-protein membrane microdomains with critical topographical and signalling functions. At the organismal level, cholesterol is the precursor of all steroid hormones, including gluco- and mineralo-corticoids, sex hormones, and vitamin D, which regulate carbohydrate, sodium, reproductive, and bone homeostasis, respectively. This sterol is also the immediate precursor of bile acids, which are important for intestinal absorption of dietary lipids as well as energy homeostasis and glucose regulation. Complex mechanisms maintain cholesterol within physiological ranges and the dysregulation of these mechanisms results in embryonic or adult diseases, caused by either excessive or reduced tissue cholesterol levels. The causative role of cholesterol in these conditions has been demonstrated by genetic and pharmacological manipulations in animal models of human disease that are discussed herein. Importantly, the understanding of basic aspects of cholesterol biology has led to the development of high-impact pharmaceutical therapies during the past century. The continuing effort to offer successful treatments for prevalent cholesterol-related diseases, such as atherosclerosis and neurodegenerative disorders, warrants further interdisciplinary research in the coming decades.