Objective: The purpose of this study was to investigate the effect of high-intensity exercise training on appetite, body mass, maximal aerobic capacity (VO2max), leptin, and acylated ghrelin in overweight women.Methods: Twenty-five women aged 25-45 years (35.4 +/- 6.9 years; 74.2 +/- 7.6 kg) were randomly assigned into high-intensity exercise training (n = 15) and control (n = 10) groups. Data assessment included body mass, skinfolds, appetite questionnaire, 1-mile Rockport Walk Test, and blood sample collection. High-intensity exercise training consisted of running an intensity corresponding to 80%-85% maximal heart rate, 3 times/week for 8 weeks.Results: Estimated maximal aerobic capacity increased in high-intensity exercise training vs. controls (P = .01). Body mass, estimated fat percentage, plasma leptin, and acylated ghrelin remained stable. No difference pre-vs. post-intervention in appetite scores was detected between groups (P = .33).Conclusions: In conclusion, high-intensity exercise training was effective to improve aerobic capac-ity, but did not elicit enough negative energy balance to reduce fat mass or promoting appetite compensatory responses, nor changes in acylated ghrelin and leptin concentrations in overweight women. Further studies with longer duration and greater training volumes are warranted to ratify these findings.
Objective: Energy deprivation induces changes in various components ofthe"growth hormone"/"insul in-like growth factor-I" axis; however, it remains unclear whether Ramadan fasting could alter which ones in response to food deprivation. In this study, changes in the components of the mentioned axis during the fasting month of Ramadan are assessed. Methods: Sixty-nine healthy men were studied while fasting during Ramadan. Participants are divided into 2 groups of control (without risk of diabetes mellitus [n = 30]) and cases (with risk factors of DM [n = 39]). Serum growth hormone, insulin-like growth factor-I, and "insulin-like growth factor-binding protein-3" were assessed using the enzyme-linked immunosorbent assay (ELISA) kit. The "homeostasis model assessment to quantify insulin resistance" was also calculated. Results: Fasting increased circulating growth hormone, while decreased serum insulin and homeostasis model assessment to quantify insulin resistance index levels in both groups significantly. Plasma insulin-like growth factor-I and homeostasis model assessment to quantify insulin resistance index were found to be significantly higher in the cases group than in the controls at baseline. Fasting induced a more prominent reduction in serum insulin-like growth factor-I in the cases group than in the controls (P =.014 vs. P =.257). Although serum insulin-like growth factor-binding protein-3 level was not different between groups at baseline or 1 month after Ramadan fasting, the insulin-like growth factor-I:insulin-like growth factor-binding protein-3 ratio was decreased more in the cases group than the control group during fasting (P <.001 vs. P =.070). Conclusion: Fasting plays an effective role in regulating the studied elements of the growth hormone/insulin-like growth factor-I axis which may help improve the metabolic status induced by insulin resistance in men at risk of diabetes mellitus.
Brown tumors can be found in any bone, during the course of primary hyperparathyroidism and may be misdiagnosed as tumors of bone origin. In this case report, we emphasized the importance of considering primary hyperparathyroidism in the differential diagnosis of a patient who presented with a mass in the mandible and was thought to have a malignant mass lesion originating from the mandible on tomography. A 27-year-old male patient applied to an external center due to enlargement of the left jaw and swelling in the mouth, which started 2 months ago and increased over time. Based on the biopsy and mandibular tomography results taken from the intraoral lesion, he was referred to our hospital from the external center for excision, considering a bone orginated malignant mass in the mandible. Laboratory examinations of the patient revealed a calcium serum level of 13.6 mg/dL and the parathyroid hormone level of 508 ng/L. In parathyroid ultrasonography, hypoechoic nodular formation adjacent to the thyroid capsule on the left inferior posterior, was evaluated as a parathyroid adenoma. Histopathological diagnosis from parathyroid ademocectomy, and the the mandibular mass, revealed a parathyroid adenoma and brown tumour respectively. We have compiled 5 cases in the literature, initially thought to be malignant bone tumors but later turned out to be brown tumors due to primary hyperparathyroidism. Increasing surgeons' awareness about primary hyperparathyroidism is important as patients with brown tumors are first admitted to surgeons. Considering primary hyperparathyroidism in masses of bone origin avoids unnecessary surgeries.
Maturity-onset diabetes of the young is the most common monogenic diabetes form affecting between 1% and 5% of all diabetes cases. Clinical characteristics include young onset (usually before 45 years), autosomal dominant inheritance, absence of autoantibodies and metabolic syndrome, and impaired glucose-dependent insulin secretion. To date, at least 14 maturity-onset diabetes of the young subtypes have been identified, harboring numerous mutations that contribute to highly heterogeneous clinical phenotypes. While much is known about the common subtypes of maturityonset diabetes of the young linked to mutations in HNF4A, GCK, HNF1A, and HNF1B; little is known about relatively rare mutations in IPF1/PDX1, NEUROD1, KLF11, PAX4, INS, BLK, ABCC8, KCNJ11, and APPL1 genes. However, with the advent of next-generation sequencing, rare maturity-onset diabetes of the young subtypes are being increasingly reported worldwide. Although nearly 6 decades have passed since the first cases were identified, maturity-onset diabetes of the young is often misdiagnosed as type 1 or type 2 diabetes mellitus due to overlapping clinical features, limited use of genetic testing, and lack of awareness of this type of diabetes. Although there are many clinical characteristics suggesting the diagnosis of maturity-onset diabetes of the young, there is no single criterion. Identifying clinical features of different maturity-onset diabetes of the young subtypes can reduce the number and cost of genetic testing; On the other hand, early diagnosis will reduce the risks of inappropriate treatment and related side effects. The aim of this review is to highlight the role of clinical features, demonstrate the effectiveness of clinical biomarkers in the differential diagnosis of maturity-onset diabetes of the young subtypes, and identify the most suitable candidates for genetic testing.
Objective: This study aims to evaluate the presence of multiple endocrine neoplasia-1 mutations in patients with primary hyperparathyroidism detected on clinical and sonographical suspicion. Methods: We scanned the medical records of 361 patients with primary hyperparathyroidism between January 2010 and December 2017. Results: Fourteen of 361 patients (i.e., 2 males and 12 females) with primary hyperparathyroidism were evaluated genetically upon clinical and sonographical suspicion. Menin gene mutations were found in 3 of 14 patients (21.4%) patients. The frequency of multiple endocrine neoplasia-1 (n = 3) was estimated to be 0.83% in all patients with primary hyperparathyroidism (n = 361). Data of 4 patients with menin mutation analyses were as follows: case 1: A 37-year-old man presented with a 14-year history of recurring nephrolithiasis. He was diagnosed with primary hyperparathyroidism. Genetic analysis was reported as multiple endocrine neoplasia-1: c.643_646delACAG (p.Thr215Serfs*13) heterozygote; case 2: A 35-year-old man with primary hyperparathyroidism and prolactinoma was diagnosed. Genetic analysis was reported as multiple endocrine neoplasia-1: c.654+1G>A heterozygote; case 3: A 26-year- old woman with hyperammonemia, partial empty sella, and hyperprolactinemia was evaluated. Genetic testing revealed heterozygote genomic changes in c984c>a in the multiple endocrine neoplasia-1 gene on the seventh exon; case 4: A 27-year-old man was diagnosed with nephrolithiasis when he was 19 years old. He had both primary hyperparathyroidism and prolactinoma. Multiple endocrine neoplasia-1 and CDKN1B genetic mutation analyses were negative. Because mutation-negative syndromes could not be ruled out, a neck exploration was performed, and a parathyroid adenoma was excised. Conclusions: Patients with primary hyperparathyroidism should be evaluated for multiple endocrine neoplasia-1 mutations upon clinical and sonographical suspicion. It should be noted that an individual with the multiple endocrine neoplasia-1 gene mutation has a 100% penetrance up to the age of 40-50 years. Additionally, 2 novel multiple endocrine neoplasia-1 mutations were identified.
