Humans ; Spinal Fractures/etiology* ; Fractures, Compression/etiology* ; Osteoporotic Fractures/complications* ; Vertebroplasty/adverse effects* ; Bone Diseases, Metabolic/complications* ; Punctures/adverse effects* ; Treatment Outcome ; Bone Cements ; Retrospective Studies

OBJECTIVE: This study aims to investigate the association of metabolic phenotypes that are jointly determined by body mass index (BMI) or fat mass percentage and metabolic health status with the ten-year risk of cardiovascular disease (CVD) among Chinese adults. METHODS: Data were obtained from a cross-sectional study. BMI and body fat mass percentage (FMP) combined with the metabolic status were used to define metabolic phenotypes. Multiple linear regression and logistic regression were used to examine the effects of metabolic phenotypes on CVD risk. RESULTS: A total of 13,239 adults aged 34-75 years were included in this study. Compared with the metabolically healthy non-obese (MHNO) phenotype, the metabolically unhealthy non-obese (MUNO) and metabolically unhealthy obese (MUO) phenotypes defined by BMI showed a higher CVD risk [odds ratio, OR (95% confidence interval, CI): 2.34 (1.89-2.89), 3.45 (2.50-4.75), respectively], after adjusting for the covariates. The MUNO and MUO phenotypes defined by FMP showed a higher CVD risk [ OR (95% CI): 2.31 (1.85-2.88), 2.63 (1.98-3.48), respectively] than the MHNO phenotype. The metabolically healthy obese phenotype, regardless of being defined by BMI or FMP, showed no CVD risk compared with the MHNO phenotype. CONCLUSION General obesity without central obesity does not increase CVD risk in metabolically healthy individuals. FMP might be a more meaningful factor for the evaluation of the association of obesity with CVD risk. Obesity and metabolic status have a synergistic effect on CVD risk.
Adipose Tissue/anatomy & histology* ; Adult ; Aged ; Body Mass Index ; Cardiovascular Diseases/etiology* ; China/epidemiology* ; Cross-Sectional Studies ; Female ; Humans ; Male ; Metabolic Diseases/etiology* ; Middle Aged ; Obesity/complications* ; Phenotype ; Regression Analysis ; Risk Factors

Excessive consumption of fructose, the sweetest of all naturally occurring carbohydrates, has been linked to worldwide epidemics of metabolic diseases in humans, and it is considered an independent risk factor for cardiovascular diseases. We provide an overview about the features of fructose metabolism, as well as potential mechanisms by which excessive fructose intake is associated with the pathogenesis of metabolic diseases both in humans and rodents. To accomplish this aim, we focus on illuminating the cellular and molecular mechanisms of fructose metabolism as well as its signaling effects on metabolic and cardiovascular homeostasis in health and disease, highlighting the role of carbohydrate-responsive element-binding protein in regulating fructose metabolism.
Fructose/adverse effects* ; Homeostasis ; Humans ; Metabolic Diseases/etiology*

OBJECTIVE: To investigate the incidence rate and risk factors for metabolic bone disease of prematurity (MBDP) in very low birth weight/extremely low birth weight (VLBW/ELBW) infants. METHODS: The medical data of 61 786 neonates from multiple centers of China between September 1, 2013 and August 31, 2016 were retrospectively investigated, including 504 VLBW/ELBW preterm infants who met the inclusion criteria. Among the 504 infants, 108 infants diagnosed with MBDP were enrolled as the MBDP group and the remaining 396 infants were enrolled as the non-MBDP group. The two groups were compared in terms of general information of mothers and preterm infants, major diseases during hospitalization, nutritional support strategies, and other treatment conditions. The multivariate logistic regression analysis was used to investigate the risk factors for MBDP. RESULTS: The incidence rate of MBDP was 19.4% (88/452) in VLBW preterm infants and 38.5% (20/52) in ELBW preterm infants. The incidence rate of MBDP was 21.7% in preterm infants with a gestational age of < 32 weeks and 45.5% in those with a gestational age of < 28 weeks. The univariate analysis showed that compared with the non-MBDP group, the MBDP group had significantly lower gestational age and birth weight, a significantly longer length of hospital stay, and a significantly higher incidence rate of extrauterine growth retardation ( CONCLUSIONS A lower gestational age, hypocalcemia, extrauterine growth retardation at discharge, and neonatal sepsis may be associated an increased risk of MBDP in VLBW/ELBW preterm infants. It is necessary to strengthen perinatal healthcare, avoid premature delivery, improve the awareness of the prevention and treatment of MBDP among neonatal pediatricians, and adopt positive and reasonable nutrition strategies and comprehensive management measures for preterm infants.
Birth Weight ; Bone Diseases, Metabolic/etiology* ; China/epidemiology* ; Female ; Humans ; Infant ; Infant, Extremely Low Birth Weight ; Infant, Newborn ; Infant, Premature ; Infant, Very Low Birth Weight ; Pregnancy ; Retrospective Studies ; Risk Factors

Adult ; Asymptomatic Diseases/epidemiology* ; Autoimmune Diseases/etiology* ; China/epidemiology* ; Female ; Humans ; Hypothyroidism/etiology* ; Male ; Metabolic Syndrome/epidemiology* ; Middle Aged ; Obesity/epidemiology* ; Risk Factors ; Thyroid Diseases/etiology* ; Young Adult

OBJECTIVE: To verify the association between sleep duration and television time with cardiometabolic risk and the moderating role of age, gender, and skin color/ethnicity in this relationship among adolescents. METHODS: Cross-sectional study with 1411 adolescents (800 girls) aged 10 to 17 years. Television time, sleep duration, age, gender, and skin color/ethnicity were obtained by self-reported questionnaire. Cardiometabolic risk was evaluated using the continuous metabolic risk score, by the sum of the standard z-score values for each risk factor: high-density lipoprotein cholesterol, triglycerides, glycemia, cardiorespiratory fitness, systolic blood pressure, and waist circumference. Generalized linear regression models were used. RESULTS: There was an association between television time and cardiometabolic risk (β, 0.002; 95% CI, 0.001; 0.003). Short sleep duration (β, 0.422; 95% CI, 0.012; 0.833) was positively associated with cardiometabolic risk. Additionally, age moderated the relationship between television time and cardiometabolic risk (β, - 0.009; 95% CI, - 0.002; - 0.001), suggesting that this relationship was stronger at ages 11 and 13 years (β, 0.004; 95% CI, 0.001; 0.006) compared to 13 to 15 years (β, 0.002; 95% CI, 0.001; 0.004). No association was found in older adolescents (β, 0.001; 95% CI, - 0.002; 0.002). CONCLUSIONS Television time and sleep duration are associated with cardiometabolic risk; adolescents with short sleep have higher cardiometabolic risk. In addition, age plays a moderating role in the relationship between TV time and cardiometabolic risk, indicating that in younger adolescents the relationship is stronger compared to older ones.
Age Factors ; Brazil ; epidemiology ; Cardiovascular Diseases ; epidemiology ; ethnology ; etiology ; Cross-Sectional Studies ; Metabolic Syndrome ; epidemiology ; ethnology ; etiology ; Prevalence ; Risk Factors ; Sedentary Behavior ; ethnology ; Sex Factors ; Sleep ; Television ; statistics & numerical data

Breastfeeding is well-known for its benefits of preventing communicable and non-communicable diseases. Human breastmilk consists not only of nutrients, but also of bioactive substances. What's more, the epigenetic effects of human breast milk may also play an important role. Alterations in the epigenetic regulation of genes may lead to profound changes in phenotype. Clarifying the role of human breast milk on genetic expression can potentially benefit the infant's health and his later life. This review article makes a brief summary of the epigenetic mechanism of breast milk, and its epigenetic effects on neonatal necrotizing enterocolitis, infectious diseases, metabolism syndrome, cognitive function and anaphylactic diseases.
Breast Feeding ; Cognition ; Communicable Diseases ; etiology ; genetics ; Enterocolitis, Necrotizing ; etiology ; genetics ; Epigenesis, Genetic ; Female ; Humans ; Hypersensitivity ; etiology ; genetics ; Infant, Newborn ; Metabolic Syndrome ; etiology ; genetics

A one-year-old girl visited the hospital due to limb torsion and developmental regression for one month after hand, foot and mouth disease. At the age of 11 months, she visited a local hospital due to fever for 5 days and skin rash with frequent convulsions for 2 days and was diagnosed with severe hand, foot and mouth disease, viral encephalitis, and status epilepticus. Brain MRI revealed symmetric abnormal signals in the bilateral basal ganglia, bilateral thalamus, cerebral peduncle, bilateral cortex, and hippocampus. She was given immunoglobulin, antiviral drugs, and anticonvulsant drugs for 2 weeks, and the effect was poor. Blood and urine screening for inherited metabolic diseases were performed to clarify the etiology. The analysis of urine organic acids showed significant increases in glutaric acid and 3-hydroxyglutaric acid, which suggested glutaric aciduria type 1, but her blood glutarylcarnitine was normal, and free carnitine significantly decreased. After the treatment with low-lysine diets, L-carnitine, and baclofen for 1 month, the patient showed a significant improvement in symptoms. Hand, foot and mouth disease is a common viral infectious disease in children, and children with underlying diseases such as inherited metabolic diseases and immunodeficiency may experience serious complications. For children with hand, foot and mouth disease and unexplained encephalopathy, inherited metabolic diseases should be considered.
Amino Acid Metabolism, Inborn Errors ; etiology ; Brain Diseases, Metabolic ; etiology ; Developmental Disabilities ; etiology ; Female ; Glutaryl-CoA Dehydrogenase ; deficiency ; Hand, Foot and Mouth Disease ; complications ; Humans ; Infant ; Torsion Abnormality ; etiology

Sleep deprivation (SD) has been associated with an increased morbidity and mortality of coronary heart disease (CHD). SD could induce autonomic nervous dysfunction, hypertension, arrhythmia, hormonal dysregulation, oxidative stress, endothelial dysfunction, inflammation and metabolic disorder in CHD patients. This paper reviewed the study results of SD in clinical trials and animal experiments and concluded that SD was associated with cardiovascular risk factors, which aggravated CHD in pathogenesis and outcomes.
Autonomic Nervous System Diseases ; etiology ; Coronary Artery Disease ; etiology ; Humans ; Hypertension ; etiology ; Metabolic Diseases ; etiology ; Oxidative Stress ; Sleep Deprivation ; complications

OBJECTIVETo investigate the clinical, biochemical and genetic profiles of 28 Chinese patients with glutaric aciduria type 1.

METHODTwenty-eight patients with glutaric aciduria type 1 seen in the Department of Pediatrics, Peking University First Hospital from July 2003 to October 2013 were studied. The data of clinical course, laboratory examinations, cranial MRI and GCDH gene mutations of the patients were analyzed.

RESULT(1) Three cases were detected by newborn screening, and the other patients were diagnosed at the age of 2 months to 17 years. (2) 22 patients (79%) were infant onset cases with psychomotor retardation, dystonia, seizures, athetosis, recurrent vomiting, drowsiness or feeding difficulty. Only two of the 22 patients with infant onset got normal intelligence and movement after treatment. Twenty of them were improved slowly with delayed development, dystonia and other neurological problems. Three patients (11%) had late onset. They had motor regression, headache and seizure at the age of 8, 9 and 17 years, respectively. Rapid improvement was observed after treatment. (3) Cranial MRI has been checked in 23 patients; 22 of them showed characteristic widening of the Sylvian fissure, abnormalities of the basal ganglia, leukoencephalopathy and brain atrophy. Thirty-five mutations in GCDH gene of the patients were identified; c.148T>C (p.W50R) was the most common mutation with the frequency of 7.7%; 6 mutations (c.628A>G, c.700C>T, c.731G>T, c.963G>C, c.1031C>T and c.1109T>C) were novel.

CONCLUSIONGlutaric aciduria type 1 usually induced neurological deterioration resulting in severe psychomotor retardation and dystonia. Most of our patients were clinically diagnosed. Patients with early onset usually remained having neurological damage. Phenotype and genotype correlation has not been found in the patients. Neonatal screening for organic acidurias should be expanded in China.

Age of Onset ; Amino Acid Metabolism, Inborn Errors ; diagnosis ; genetics ; metabolism ; Brain Diseases, Metabolic ; diagnosis ; genetics ; metabolism ; DNA Mutational Analysis ; Follow-Up Studies ; Gas Chromatography-Mass Spectrometry ; Glutarates ; urine ; Glutaryl-CoA Dehydrogenase ; deficiency ; genetics ; metabolism ; Humans ; Infant, Newborn ; Intellectual Disability ; etiology ; pathology ; Magnetic Resonance Imaging ; Movement Disorders ; etiology ; pathology ; Mutation ; Neonatal Screening ; methods ; Retrospective Studies