Structure-effect relation of C18 long-chain fatty acids in the reduction of body weight in rats.

OBJECTIVE: To investigate the relationship between chemical structure and physiological effect, the efficacy and the molecular mechanisms involved in the reduction of body weight by C18 fatty acids (stearic, elaidic, oleic, linoleic and 2-hydroxyoleic acids (2-OHOA)). DESIGN: Ad libitum fed, lean Wistar Kyoto rats treated orally with up to 600 mg kg(-1) of the fatty acids or vehicle every 12 h for 7 days. Besides, starved rats and rats pairfed to the 2-OHOA-treated group served as additional controls under restricted feeding conditions. MEASUREMENTS: Body weight, food intake, weight of various fat depots, plasma leptin, hypothalamic neuropeptides, uncoupling proteins (UCP) in white (WAT) and brown adipose tissue (BAT) and phosphorylation level of cyclic AMP (cAMP) response element-binding protein (CREB) in WAT. RESULTS: Only treatment with oleic acid and 2-OHOA induced body weight loss (3.3 and 11.4%, respectively) through reduction of adipose fat mass. Food intake in these rats was lower, although hypothalamic neuropeptide and plasma leptin levels indicated a rise in orexigenic status. Rats pairfed to the 2-hydroxyoleic group only lost 6.3% body weight. UCP1 expression and phosphorylation of CREB was drastically increased in WAT, but not BAT of 2-OHOA-treated rats, whereas no UCP1 expression could be detected in WAT of rats treated with oleic acid. CONCLUSION: Both cis-configured monounsaturated C18 fatty acids (oleic acid and 2-OHOA) reduce body weight, but the introduction of a hydroxyl group in position 2 drastically increases loss of adipose tissue mass. The novel molecular mechanism unique to 2-hydroxyoleic, but not oleic acid, implies induction of UCP1 expression in WAT by the cAMP/PKA pathway-dependent transcription factor CREB, most probably as part of a transdifferentiation process accompanied by enhanced energy expenditure.

Critical assessment of the current guidelines for the management and treatment of morbidly obese patients.

An interdisciplinary panel of specialists met in Mallorca in the first European Symposium on Morbid Obesity entitled; "Morbid Obesity, an Interdisciplinary Approach". During the two and half days of the meeting, the participants discussed several aspects related to pathogenesis, evaluation, and treatment of morbid obesity. The expert panel included basic research scientists, dietitians and nutritionists, exercise physiologists, endocrinologists, psychiatrists, cardiologists, pneumonologists, anesthesiologists, and bariatric surgeons with expertise in the different weight loss surgeries. The symposium was sponsored by the Balearic Islands Health Department; however, this statement is an independent report of the panel and is not a policy statement of any of the sponsors or endorsers of the Symposium. The prevalence of morbid obesity, the most severe state of the disease, has become epidemic. The current recommendations for the therapy of the morbidly obese comes as a result of a National Institutes of Health (NIH) Consensus Conference held in 1991 and subsequently reviewed in 2004 by the American Society for Bariatric Surgery. This document reviews the work-up evaluation of the morbidly obese patient, the current status of the indications for bariatric surgery and which type of procedure should be recommended; it also brings up for discussion some important real-life clinical practice issues, which should be taken into consideration when evaluating and treating morbidly obese patients. Finally, it also goes through current scientific evidence supporting the potential effectiveness of medical therapy as treatment of patients with morbid obesity.

Comments to SEOM clinical guidelines for the treatment of thyroid cancer

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Novedades en terapia hipoglucemiante. Fármacos con acción incretina / Advances in glucose-lowering therapy. Drugs that enhance incretin action

Las hormonas incretinas son péptidos liberados en el tracto gastrointestinal en respuesta a la ingesta de nutrientes, que potencianl a liberación de insulina y ayudan en el mantenimiento homeostático de la glucemia. El concepto de esta acción incretina se basó en la observación de quela respuesta secretora de insulina a la administración oral de glucosa era superior a la respuesta a cantidades equivalentes de glucosa administrada intravenosa. El efecto incretina se estima que es responsable de hasta el 70% de la secreción de insulina en respuesta a la glucosa oral y es causado principalmente por 2 hormonas intestinales: glucagon-like peptide (GLP-1) y glucose-dependent insulinotropic peptide (GIP).En la diabetes tipo 2, además del efecto deficiente de las incretinas, también se ha encontrado una alteración en la secreción de GLP-1.La administración exógena de GLP-1 ayuda a la normalización de la glucemia tanto basal como posprandial; sin embargo, el GLP-1 es rápidamente degradado por la enzima dipeptidil peptidasa (DPP-IV).Esta circunstancia ha llevado al desarrollo de fármacos análogos deGLP-1, con mayor resistencia a la degradación enzimática o a fármacos inhibidores de DPP-IV. El mecanismo por el cual las incretinas causan su efecto regulador sobre la homeostasis energética es en parte todavía desconocido y es actualmente un área de intensa investigación (AU)

The incretin hormones are peptides released in the gastrointestinal tract in response to nutrient ingestion. These hormones enhance insulin release and help to maintainglycemic homeostasis. The concept of incretin action was based on the observation that the secretory response of insulin to oral glucose administration is greater than that to equivalent quantities of intravenous glucose. The incret in effect is estimated to be responsible for up to 70% of insulin secretion in response to oral glucose and is mainly caused by two gastrointestinal hormones: glucagon-like peptide (GLP-1) y glucose-dependent insulinotropic peptide(GIP). In type 2 diabetes, in addition to a deficiency in incretin-mediated insulinsecretion, alterations in GLP-1 secretion have also been found. Exogenous GLP-1secretion helps to restore normal levels of both basal and postprandial blood glucose. However, GLP-1 is rapidly degraded by the dipeptidyl peptidase enzyme (DPP-IV). This phenomenon has led to the development ofGLP-1 analogs, which are more resistant to enzyme degradation or DPP-IV inhibitors. The mechanism through which the incretin hormones exert their regulatory effect onenergy homeostasis remains unknown and is currently the subject of intense research (AU)