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1.
BMC Nephrol ; 19(1): 172, 2018 07 11.
Artículo en Inglés | MEDLINE | ID: mdl-29996796

RESUMEN

BACKGROUND: Nephrolithiasis is a risk factor for Osteopenia and osteoporosis. Receptor activator of nuclear factor kappaB ligand (RANKL) and osteoprotegerin (OPG) regulate bone remodeling and osteoclastogenesis. This study aimed to evaluate the relation between serum OPG, RANKL concentration, and bone mineral density (BMD) in patients with kidney stone disease. METHODS: Forty-four nephrolithiasis patients with either low bone mass or normal BMD (considered control group) were enrolled in this study. BMD was measured at lumbar spine (L1-L4) and femoral neck by dual-energy X-ray absorptiometry (DEXA). The serum OPG and RANKL were determined using the ELISA method. RESULTS: The median levels of serum OPG were significantly higher in nephrolithiasis patients with low bone mass compared to the nephrolithiasis patients with normal BMD (3.9 pmol/l versus 3.1 pmol/l; P = 0.03), respectively. Negative correlation was detected between bone densities of femoral neck and OPG in patients with nephrolithiasis (r = -.0344, P = 0.02). CONCLUSION: The present study showed that high serum fasting OPG levels may be indicative of femoral neck BMD in patients with nephrolithiasis.


Asunto(s)
Densidad Ósea/fisiología , Cuello Femoral/diagnóstico por imagen , Nefrolitiasis/sangre , Nefrolitiasis/diagnóstico por imagen , Osteoprotegerina/sangre , Ligando RANK/sangre , Absorciometría de Fotón/métodos , Adulto , Biomarcadores/sangre , Remodelación Ósea/fisiología , Femenino , Cuello Femoral/metabolismo , Humanos , Masculino , Persona de Mediana Edad
2.
Arch Iran Med ; 21(2): 56-60, 2018 02 01.
Artículo en Inglés | MEDLINE | ID: mdl-29664655

RESUMEN

BACKGROUND: Beta thalassemia major (BTM) and its treatment by hematopoietic stem cell transplantation (HSCT) may have deleterious effects on the endocrine systems. We assessed endocrine complications of HSCT in pediatric patients for 3 months. METHODS: In 20 (6 female) pediatric major thalassemic patients (mean age of 10.8 ± 3.9 years old), prolactin, luteinizing hormone (LH), follicle-stimulating hormone (FSH), T4, T3, thyroid-stimulating hormone (TSH), IGF-1, testosterone (in males) or estradiol (in females) were measured as a batch at the Endocrinology and Metabolism Research Center (EMRC) of Tehran University of Medical Sciences (TUMS) laboratories before HSCT and 1 and 3 months afterwards. The cosyntropin test for all and the clonidine test for short stature patients was conducted before HSCT. RESULTS: Before HSCT, delayed puberty and hypogonadotropic hypogonadism was found in 10% and 20% of patients, respectively. GH deficiency, low IGF1 and short stature was found in 25%, 55% and 40% of patients, respectively. Hypocortisolism, hypothyroidism and panhypopituitarism was found in 15%, 10% and 15% of patients, respectively. Prevalence of hypogonadotropic hypogonadism, low IGF1, hypothyroidism and panhypopituitarism was found in 20%, 40%, 10% and 10% of patients after 3 months, respectively (delayed puberty and short stature prevalence do not change after 3 months). HSCT caused lower T3 and estradiol and higher TSH. Corticosteroid users (15) had higher GH and lower T3 and testosterone or estradiol. Ferritin had a significant (negative) correlation with (before) prolactin and a significant correlation with T3 and T4 after HSCT. Age and acute graft-versus-host disease (GVHD) had no significant effect. CONCLUSION: Considering the small sample size and short duration of the study, it is difficult to reach any conclusion however it seems HSCT does not appear to have an overall positive or negative effect on prevalence of pituitary- hypothalamus axis disorders in pediatric thalassemic patients in 3 months.


Asunto(s)
Enfermedades del Sistema Endocrino/etiología , Trasplante de Células Madre Hematopoyéticas/efectos adversos , Sistema Hipotálamo-Hipofisario/fisiología , Sistema Hipófiso-Suprarrenal/fisiología , Talasemia beta/cirugía , Adolescente , Niño , Preescolar , Enfermedades del Sistema Endocrino/epidemiología , Femenino , Humanos , Hipogonadismo/epidemiología , Hipogonadismo/etiología , Hipopituitarismo/epidemiología , Hipopituitarismo/etiología , Hipotiroidismo/epidemiología , Hipotiroidismo/etiología , Irán/epidemiología , Masculino
3.
Nutrition ; 29(6): 813-20, 2013 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-23415393

RESUMEN

The hormone glucagon-like peptide (GLP-1) is secreted from gut endocrine L cells in response to ingested nutrients. The activities of GLP-1 include stimulating insulin gene expression and biosynthesis, improving ß-cell proliferation, exogenesis, and survival. Additionally, it prevents ß-cell apoptosis induced by a variety of cytotoxic agents. In extrapancreatic tissues, GLP-1 suppresses hunger, delays gastric emptying, acts as an ileal brake, and increases glucose uptake. The pleiotropic actions of GLP-1, especially its glucose-lowering effect, gave rise to the suggestion that it is a novel approach to insulin resistance treatment. Hormones secreted from the gut including GLP-1, which are involved in the regulation of insulin sensitivity and secretions, have been found to be affected by nutrient intake. In recent years, there has been a growing interest in the effect nutrients may have on GLP-1 secretion; some frequently studied dietary constituents include monounsaturated fatty acids, fructooligosaccharides, and glutamine. This review focuses on the influence that the carbohydrate, fat, and protein components of a meal may have on the GLP-1 postprandial responses.


Asunto(s)
Péptido 1 Similar al Glucagón/metabolismo , Péptido 1 Similar al Glucagón/fisiología , Animales , Proliferación Celular , Diabetes Mellitus Tipo 2/metabolismo , Grasas de la Dieta/administración & dosificación , Fibras de la Dieta/administración & dosificación , Proteínas en la Dieta/administración & dosificación , Vaciamiento Gástrico , Glutamina/administración & dosificación , Humanos , Insulina/sangre , Resistencia a la Insulina , Edulcorantes no Nutritivos/administración & dosificación , Periodo Posprandial
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