Effect of exercise on circulating levels of brain-derived neurotrophic factor (BDNF) in overweight and obese subjects.

Exercise increases the expression of brain-derived neurotrophic factor (BDNF) in rodents and in healthy humans. Its relationship with weight loss and improvement in metabolic parameters, in obese human subjects, has not been elucidated. The aim of the study was to evaluate the effect of an aerobic exercise program on circulating levels of BDNF in overweight and obese subjects. We measured anthropometric and metabolic parameters in 15 male and female nondiabetic outpatients (age 38.3±9.5 years, BMI 27-35 kg/m2), before and after 30 sessions of aerobic exercise (3 sessions per week). Plasma (p), serum (s), and platelet (plat) BDNF concentrations were measured at basal condition and after completing 15 and 30 sessions of exercise. Subjects were advised to continue their usual food intake. A significant decrease in weight, BMI, waist circumference, diastolic blood pressure and total cholesterol was observed at the end of the study (p<0.02). Serum and platBDNF showed a significant increase during the training period (p=0.005 and 0.04 respectively). However, pBDNF showed no significant increase. Area under the curve of glucose at baseline, was inversely correlated with sBDNF (r= - 0.53, p=0.04) and platBDNF (r= - 0.6, p=0.01) after session 15. Also, platBDNF was correlated inversely with post load insulin and HOMA2-IR at the end of the training program (r= - 0.53, p=0.03 and r= - 0.52, p=0.04, respectively). In overweight and obese subjects, serum and platBDNF levels increase after 30 sessions of aerobic exercise. This is accompanied with the improvement of anthropometric and metabolic parameters and modest weight loss.

Association of the intronic polymorphism rs891512 (G24943A) of the endothelial nitric oxide synthase gene with hypertension in Chilean type 2 diabetes patients.

We investigated two single nucleotide polymorphisms of the NOS3 gene in type 2 diabetic patients (n=93) and healthy non-diabetic controls (n=76) and their relationship with smoking habits, body mass index, hypertension and dyslipidemia. Results showed that eNOS polymorphism rs891512 (G24943A) is associated with hypertension in Chilean individuals (p<0.05).

Early response to venlafaxine antidepressant correlates with lower ACTH levels prior to pharmacological treatment.

A link between stressful life events and development or exacerbation of depression has been established via a large body of evidence. An alteration in the regulation of the hypothalamic-pituitary-adrenal (HPA) axis in depression has also been associated with an increase in cortisol secretion. As arginine-vasopressin (AVP) plays an important role in the activation of HPA axis during stress, the present study investigated ACTH and cortisol secretory response induced by an AVP-related peptide desmopressin (ddAVP) in patients with major depression. Prior to antidepressant treatment, endocrinological parameters were evaluated and correlated with the clinical response to venlafaxine treatment, which offers a dual antidepressant action. Depressive patients with no other psychiatric pathology were evaluated with 17-item Hamilton Depression Scale (HAM-D) in order to follow-up the response to venlafaxine. After 1 wk of treatment, 60% of patients reduced their initial HAM-D score to at least 25%; this group was classified as early responders. The other group (40%) started to reduce significantly their HAM-D score after 3 wk of treatment and was classified as late responders. After 6 wk of treatment both groups have reduced HAM-D score to at least 25% of the baseline score. Prior to the pharmacological treatment, both early and late responders showed salivary cortisol rhythm and urinary free cortisol (UFC) in 24-h similar to healthy subjects. However, we did observe differences in basal ACTH secretion, showing that the late responder group had higher basal ACTH than both early responders and controls. The ddAVP challenge promoted a robust secretion of ACTH only in late responders, suggesting a different sensitivity of pituitary vasopressin receptor. The differences in clinical response to venlafaxine among depressive patients seem to be related to endocrinological parameters.

Role of stress and sympathetic innervation in the development of polycystic ovary syndrome

This work attempts to give a review of ovarian innervation, the mechanism of regulation of nerve activity and the role of the sympathetic activity in ovarian pathologies affecting reproductive function. We provide a succinct outline of the findings of our group in this area. The participation of stress as an etiological factor for ovarian pathologies throughout animal models and preliminary data in patients with polycystic ovary syndrome give strong support for a participation of sympathetic nerves in the ovary function both in normal and pathological states.

Evaluation of insulin resistance in two kinds of South American camelids: llamas and alpacas.

Insulin resistance was evaluated in South American camelids, llamas and alpacas, by use of the minimal model test and the insulin tolerance test. Animals were catheterized for long-term studies and tamed to minimize stress during evaluation. Results indicated a low insulin sensitivity index (SI) = 0 to 0.97, median = 0.39 x 10(-4) min/uIU x ml, about a fifth the value in other mammals and humans. The KITT was between 1.43 and 3.19 %/min, also significantly lower than that reported for humans. Glycosylated hemoglobin concentration was 6%, and HbAlc concentration was 5.5%; red blood cell lifetime, as measured by use of the 51Cr method, was 120 days, similar to the value in humans. We concluded that llamas and alpacas have naturally higher blood glucose concentration than do humans and other mammals during the glucose tolerance test. Using the same mathematical tools to evaluate glucose metabolism as those used in people, South American camelids appear to be resistant to insulin. Thus, the South American camelid may be a useful new animal model for the study of sugar metabolism and various facets of diabetes mellitus, especially protection from the deleterious effects of glycosylation.

[Primary hyperparathyroidism caused by a mediastinal adenoma with intermittent hypercalcemia and severe bone disease]. / Hiperparatiroidismo primario por adenoma mediastínico, con hipercalcemia intermitente y enfermedad ósea acentuada.

We report the case of a 33-year-old woman who was operated on with the diagnosis of primary hyperparathyroidism (PHP) in 1986. She had bone disease and slight hypercalcemia. Two parathyroid glands were removed with a lack of clinical improvement. Subsequently, the serum calcium levels were normal with occasional slight increases. Depressed phosphorus values and elevated alkaline phosphatases and PTH levels were also present, associated with severe bone involvement and muscular weakness. A second cervical exploration performed in 1989 disclosed only a normal parathyroid gland, which was not removed. In 1990, a thoracic CT scan showed the presence of a 1 cm mediastinal nodule close to the great vessels. A thoracotomy was performed to remove this nodule, which proved to be a parathyroid adenoma. After surgery, the patient presented with a "hungry bone" syndrome, characterized by very low levels of calcium, phosphorus and magnesium, which required enteral and parenteral calcium and magnesium supplements, plus dihydroxyvitamin D. The association of normocalcemia and intermittent hypercalcemia with severe bone disease is very rare, as is the presence of a mediastinal adenoma. This could explain the difficulty in the diagnosis in this case.