International Journal of Endocrinology and Metabolism
Year:2012 | Volume:10 | Issue:2|Papers Count:10

Background: Postprandial lipemia has been found to be strongly associated with atherosclerosis due to its atherogenic and thrombogenic lipoprotein changes. This phenomenon occurs even in normal subjects especially after high fat meals. Orlistat, an anti- obesity drug, has been shown to address postprandial lipemia after a single high fat meal.Objectives: To compare the effects of orlistat and placebo on the postprandial lipid levels after sequential high-fat meals in healthy individuals with normal fasting lipid levels.Patients and Methods: Thirty-one healthy adult volunteers with normal fasting lipid levels were fed 50% fat meals (3 meals and 2 snacks of pre-weighted butter and bread). The subjects were blindly randomized to receive either placebo or orlistat 120 mg before each main meal. The outcome parameters were total cholesterol (TC), triglyceride (TG), high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, and very-low–density lipoprotein (VLDL) cholesterol levels measured at fasting (0 h) and every 2 h thereafter, until the sixteenth hour. Additionally, we estimated the lipid levels at the fifth and ninth hour.Results: The non-orlistat group showed a significant postprandial rise in the levels of TG and VLDL, which began 4 h after breakfast (P<0.05); this rise in levels was sustained until 9 h after breakfast for TG and up to 10 h after breakfast for VLDL. In contrast, only one significant rise in both TG and VLDL levels (at 4 h after breakfast) was noted in the orlistat group. The maximum mean difference from the baseline TG level for the orlistat group was lower than that for the non-orlistat group (0.22 mmol/L vs.0.756 mmol/L, respectively). Similarly, the maximum mean difference from the baseline VLDL level from baseline in the orlistat group was only 0.099 mmol/L, which was lower than that in the non-orlistat group (0.588 mmol/L). LDL levels rose to a lesser extent in the orlistat group than in the non-orlistat group (0.268 vs. 0.362 mmol/L). The TC levels did not show a postprandial rise; instead, the levels reduced in both groups, with the orlistat group showing a higher reduction than the non-orlistat group (-0.288 vs. -0.188 mmol/L). The orlistat group did not show any significant differences in the HDL measurements.Conclusions: Administration of orlistat abolished the significantly sustained postprandial rise of TG and VLDL levels in healthy individuals who were fed sequential 50% fat meals.

Background: Osteoporosis and chronic kidney disease are common conditions in older adults, and often occur concurrently. Bone disease is caused by increased bone turnover accompanying secondary hyperparathyroidism, and by factors such as bone metabolic disorder accompanying kidney disease and postmenopausal or age-related osteoporosis, even in hemodialysis patients. Raloxifene is commonly used for the treatment of postmenopausal osteoporosis in the general population, and may be a treatment option for osteoporosis in hemodialysis patients. However, the effects of raloxifene in hemodialysis patients with type 2 diabetes have not been examined in detail.Objectives: This study was performed to investigate the effects of raloxifene on bone turnover markers and bone density in postmenopausal women with type 2 diabetes mellitus who were undergoing hemodialysis in Japan. Patients and Methods: The subjects were 60 female patients on maintenance hemodialysis (non-diabetic, n=30; diabetic, n=30). Raloxifene hydrochloride (60 mg) was administered to 14 diabetic patients and 14 non-diabetic patients for one year, and these patients were compared with control groups (no raloxifene) of 16 diabetic patients and 16 non-diabetic patients. Serum levels of N-terminal cross-linking telopeptide of type I collagen (NTx), bone alkaline phosphatase, and intact parathyroid hormone (iPTH) were measured, and bone density was determined by quantitative heel ultrasound at the speed of sound (SOS) in the calcaneus during this period.Results: There were no significant differences in the levels of bone turnover markers except for iPTH after treatment of diabetic and non-diabetic patients with raloxifene for one year. SOS increased after treatment with raloxifene, but was significantly decreased in the control groups. Treatment with raloxifene resulted in a significant decrease in NTx and a significant increase in SOS in both diabetic and non-diabetic patients. There were no significant differences between the diabetic and non-diabetic patients who received raloxifene.Conclusions: Treatment with raloxifene can suppress reduction in bone density in postmenopausal women with type 2 diabetes who are undergoing hemodialysis.

Background: The physiological link between ghrelin and growth hormone (GH) has not yet been fully clarified. Furthermore, the existence of a negative feedback mechanism between growth hormone–insulin-like growth factor (GH–IGF) -I axis and ghrelin and the influence of amino acids on ghrelin secretion in children remain matters of debate.Objectives: To understand the regulation of ghrelin secretion and clarify the relationship between ghrelin and GH secretion in GH-deficient (GHD) and GH-sufficient (GHS) children Patients and Methods: Ten GHD (male/female [M/F], 6/4; age [mean ± SEM], 10.7 ± 0.9 years) and 10 GHS prepubertal children (M/F, 6/4; age [mean ± SEM], 10.3 ± 0.6 years), underwent an arginine (ARG) test (infusion, 0.5 g/kg, iv). Levels of GH, total ghrelin, and acylated ghrelin (AG) were assayed every 30 min from 0 to+120 min.Results: Peak GH values were lower in GHD subjects than in GHS subjects (P< 0.0001). The baseline levels, peak levels, or area under the curves (AUC) for total ghrelin and AG were similar between GHD and GHS children. ARG infusion was followed by a slight to significant decrease in total ghrelin levels, but not AG levels, both in GHD and GHS subjects with a nadir at+30 min. No correlation was seen between GH, total ghrelin, or AG response and ARG infusion.Conclusions: Total ghrelin and AG levels seemed unaffected by GH status in prepubertal children. ARG infusion was unable to blunt ghrelin secretion irrespective of GH status in childhood. Moreover, since ARG influences GH secretion via modulation of somatostatin release, ghrelin secretion seems to be partially refractory to somatostatin action.

Background: Ghrelin and obestatin are orexigenic and anorexigenic peptides, respectively. It appears that an accurate balance between theses peptides is important for regulating energy homeostasis and body weight.Objectives: The aim of this study was to identify the possible mechanisms by which circuit resistance training influences energy homeostasis and weight control. Patients and Methods: Twenty-seven female students with the mean age of 22 ± 1.54 years and mean body mass index (BMI) of 20.76 ± 1.86 kg/m2 were selected and randomly divided into experimental and control groups. Subjects performed circuit resistance training with 40% and 80% of 1 repetition maximum (1RM) for 4 weeks. Total plasma ghrelin, obestatin, and glucose levels and the ghrelin to obestatin ratio were measured for all subjects before and after training.Results: One-way ANOVA tests showed that, the plasma ghrelin to obestatin ratio increased significantly in the 80% 1RM group (P<0.05). Furthermore, a significant reduction of the plasma obestatin level was found in this group (P<0.05).Conclusions: It appears that an energy deficit caused by circuit resistance training in 80% of the 1RM group resulted in the ghrelin precursor being increasingly used for ghrelin production. Thus, obestatin secretion decreased and the ghrelin to obestatin ratio increased in order to stimulate food intake and lost energy resource consumption to eventually restore the energy balance in the body.

Introduction: Glucocorticoids taken orally increase the risk of fractures. It has been noted that a dose as low as 2.5 mg/day increases the risk of vertebral fracture. What is less clear is the possible influence of other risk factors for osteoporosis on the presence of non-vertebral fractures in patients taking glucocorticoids.Patients and Methods: A cross-sectional study, performed on 513 men and women from Spain, who were taking at least 7.5 mg/day of oral prednisone for a minimum of 3 months. A questionnaire was developed, through which information on risk factors was collected.Results: 28.3% of the patients who were taking glucocorticoids at a daily oral dose of 7.5 mg/ day for a minimum of 3 months had suffered at least one non-vertebral fracture. The risk increased with age, the number of months the glucocorticoids had been taken, the presence of falls in the last year and, above all, with a maternal history of hip fracture.Conclusions: In patients taking oral glucocorticoids for over 3 months at doses higher than 7.5 mg/day of prednisone or equivalent, the prevalence of non-vertebral fractures was 28.3%. Some risk factors associated with the presence of these fractures were identified. The duration of glucocorticoid use appears to be more strongly related to the presence of non-vertebral fractures than the daily dose.

Statistical errors are common in scientific literature and about 50% of the published articles have at least one error. The assumption of normality needs to be checked for many statistical procedures, namely parametric tests, because their validity depends on it. The aim of this commentary is to overview checking for normality in statistical analysis using SPSS.

The ideal approach for adequate management of subclinical hyperthyroidism (low levels of thyroid-stimulating hormone [TSH] and normal thyroid hormone level) is a matter of intense debate among endocrinologists. The prevalence of low serum TSH levels ranges between 0.5% in children and 15% in the elderly population. Mild subclinical hyperthyroidism is more common than severe subclinical hyperthyroidism. Transient suppression of TSH secretion may occur because of several reasons; thus, corroboration of results from different assessments is essential in such cases. During differential diagnosis of hyperthyroidism, pituitary or hypothalamic disease, euthyroid sick syndrome, and drug-mediated suppression of TSH must be ruled out. A low plasma TSH value is also typically seen in the first trimester of gestation. Factitial or iatrogenic TSH inhibition caused by excessive intake of levothyroxine should be excluded by checking the patient’s medication history. If these nonthyroidal causes are ruled out during differential diagnosis, either transient or long-term endogenous thyroid hormone excess, usually caused by Graves’ disease or nodular goiter, should be considered as the cause of low circulating TSH levels. We recommend the following 6-step process for the assessment and treatment of this common hormonal disorder: (1) confirmation, (2) evaluation of severity, (3) investigation of the cause, (4) assessment of potential complications, (5) evaluation of the necessity of treatment, and (6) if necessary, selection of the most appropriate treatment. In conclusion, management of subclinical hyperthyroidism merits careful monitoring through regular assessment of thyroid function. Treatment is mandatory in older patients (>65 years) or in presence of comorbidities (such as osteoporosis and atrial fibrillation).

Anti-androgens are an assorted group of drugs and compounds that reduce the levels or activity of androgen hormones within the human body. Disease states in which this is relevant include polycystic ovarian syndrome, hirsutism, acne, benign prostatic hyperplasia, and endocrine related cancers such as carcinoma of the prostate. We provide an overview and discussion of the use of anti-androgen medications in clinical practice and explore the increasing recognition of the benefits of plant-derived anti- androgens, forexample, spearmint tea in the management of PCOS, for which some evidence about efficacy is beginning to emerge. Other agents covered include red reishi, which has been shown to reduce levels 5-alpha reductase, the enzyme that facilitates conversion of testosterone to dihydrotestosterone (DHT); licorice, which has phytoestrogen effects and reduces testosterone levels; Chinese peony, which promotes the aromatization of testosterone into estrogen; green tea, which contains epigallocatechins and also inhibits 5-alpha reductase, thereby reducing the conversion of normal testosterone into the more potent DHT; black cohosh, which has been shown to kill both androgenresponsive and non-responsive human prostate cancer cells; chaste tree, which has a reduces prolactin from the anterior pituitary; and saw palmetto extract, which is used as an anti-androgen although it shown no difference in comparison to placebo in clinical trials.

Migration of cardiac neural crest cells into the pharyngeal arches and the pharyngeal and splanchnic mesoderm contributes to the development of the cardiac outflow tract. The adrenal cortex is derived from the splanchnic mesoderm. Neuroblastoma is more prevalent in patients with congenital heart disease than in the general population, because both originate from embryonal neural crest-derived cells. Similarly, and in light of recent embryological findings, abnormal development or migration of splanchnic mesoderm, possibly due to an underlying genetic defect, could contribute to the association of adrenocortical carcinoma and tetralogy of Fallot. We present the case of a cardiologically asymptomatic 49-year-old woman with total correction of tetralogy of Fallot in the first year of life.

Recently, several patients have been reported with various signs of encephalopathy and high thyroid antibody levels together with good responsiveness to glucocorticoid therapy. Despite the various clinical presentations, these cases have been termed “Hashimoto encephalopathy” (HE). Although all of the pathogenic components have not yet been clearly elucidated, it is believed that brain vasculitis and autoimmunity directed against common brain-thyroid antigens represent the most likely etiologic pathway. The most common clinical signs include unexplained or epilepsy-like seizures resistant to anticonvulsive treatment, confusion, headaches, hallucinations, stroke-like episodes, coma, impairment of cognitive function, behavioral and mood disturbance, focal neurological deficits, disturbance of consciousness, ataxia, and presenile dementia, together with the presence of high thyroid antibody levels, especially against thyroperoxidase (TPOab). In most cases, the thyroid function is normal or decreased; the thyroid function is rarely increased. The examination of the cerebrospinal fluid, EEG, MRI, SPECT, and neuropsychological examinations are primarily used as diagnostic tools. Most cases showed neural symptoms for months before the acute onset; in some cases, a dramatic acute onset was described. Once the diagnosis is made, corticosteroid treatment usually provides a dramatic recovery. The authors also present a short review of literary cases reported in last decade.