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36 kg. Closely satisfactory results were also achieved by an "abbreviated" model composed by the two aforementioned "lengths" and MTs (R
=0.89, limits of agreement ±2.51 kg). ALM estimates from both equations were unbiased and similar to DXA measurements (P = 0.13 and 0.09, respectively). Bootstrap analysis favorably suggested the validity of the models.
Based on two ultrasound assessments and a few anthropometric measurements, the developed equations produced accurate and unbiased ALM estimates in the sample. Hence 2 MTs+2 lengths (+ 2 circumferences)=4 limbs' muscle mass. Such models might represent promising alternatives for muscle assessment among older individuals.
Based on two ultrasound assessments and a few anthropometric measurements, the developed equations produced accurate and unbiased ALM estimates in the sample. Hence 2 MTs + 2 lengths (+ 2 circumferences) = 4 limbs' muscle mass. Such models might represent promising alternatives for muscle assessment among older individuals.
Many patients with nonalcoholic fatty liver disease (NAFLD) also have diabetes. However, the genetic factors associated with diabetes in NAFLD are unclear. In this study, we investigated the clinical course and risk factors of diabetes development.
A total of 544 patients (275 men; 50.6%) with a median age of 53 y and biopsy-confirmed NAFLD enrolled in the study. Patatin-like phospholipase 3 and voltage-gated potassium channel KQT-like subfamily member 1 (KCNQ1) single nucleotide polymorphisms were identified in 287 cases. There were 272 patients without diabetes, and 64, 141, and 67 patients with diabetes not treated with an oral hypoglycemic agent, treated with an oral hypoglycemic agent, and treated with insulin, respectively. Changes in biochemical parameters and body weight over a 1-y period were determined in patients treated with incretin agents (n=91), a sodium glucose cotransporter 2 inhibitor (n=19), or both (n=33). The prevalence and risk factors for diabetes development among patients with NAFLD were determined in nondiabetic patients.
Among patients with NAFLD, half of the patients had diabetes and the incidence was high in those with advanced fibrosis. Reduction in body weight was higher after sodium glucose cotransporter 2 inhibitor treatment (P=.050) and in KCNQ1 CC genotype patients (P < .05). Reduction in hemoglobin A1c level was significantly lower in patatin-like phospholipase 3 GG subjects (P < .05). De novo diabetes developed in 44 patients (10-y incidence 17.9%), especially in obese (P=.046) and KCNQ1 CC genotype patients (P < .01).
Patient genetic background affected treatment response and incidence of diabetes in patients with NAFLD.
Patient genetic background affected treatment response and incidence of diabetes in patients with NAFLD.
The aim of this case-control study was to investigate the relationships between carbohydrate consumption, glycemic load (GL), glycemic index (GI), and the risk of Helicobacter pylori infection among adults admitted to an Iranian hospital.
In this case-control study, we recruited 150 participants with H. pylori infection and 302 healthy participants ages 18 to 55. Dietary GI and GL were assessed using a validated 168-item quantitative food frequency questionnaire. Dietary GL was calculated as a function of GI, carbohydrate content, and the frequency of intake of certain foods.
After adjustment for potential confounders, and comparing the highest tertile with the lowest tertile, a significant direct association was observed between the consumption of carbohydrates (odds ratio [OR]=2.87; 95% confidence interval [CI], 1.18-6.96; P for trend=0.017), GI (OR=3.70; 95% CI, 2.01-6.81; P for trend < 0.001), GL (OR=3.06; 95% CI, 1.43-6.54; P for trend=0.001), the consumption of bread and refined-grain products (OR=4.24; 95% CI, 2.22-8.11; P for trend < 0.001), and the odds of H. pylori infection (OR=2.22; 95% CI, 1.30-3.79; P for trend=0.003).
Our data suggest that a high dietary GL, high GI, and high consumption of dietary carbohydrates significantly elevate the risk of H. pylori infection. Also, the amount of bread and refined-grain products consumed had a significant positive relationship with H. pylori infection.
Our data suggest that a high dietary GL, high GI, and high consumption of dietary carbohydrates significantly elevate the risk of H. pylori infection. Also, the amount of bread and refined-grain products consumed had a significant positive relationship with H. pylori infection.
The aim of this study was to examine whether paternal and maternal body mass indexes (BMIs) were independently associated with obestatin and visfatin levels in adult offspring.
This cross-sectional analysis included 124 women who participated in the Nutritionists' Health Study (NutriHS) at baseline. Early life events, anthropometry, dual-energy x-ray absorptiometry-determined body composition and blood sample were obtained. Associations of parental BMI with outcomes (obestatin and visfatin) were tested by multiple linear regression, using minimal sufficient adjustments recommended by Directed Acyclic Graph. Participants' mean BMI was 25 ± 5 kg/m
and 74% were metabolically healthy. Median obestatin and visfatin levels were 56.4 pg/mL (42-72) and 17.7 ng/mL (14-21.8), respectively. Eleven percent of mothers and 39% of fathers were overweight/obese.
Daughters born from overweight/obese mothers had higher BMI than those born from normal weight women (P=0.003). In adjusted regression model, offspring obestatin levels were associated with maternal BMI (β=-0.03; P=0.045) and paternal BMI (β=-0.02; P=0.048) independently of maternal and paternal education, maternal age, and maternal use of tobacco, alcohol, and/or drugs. No association was detected with visfatin levels.
Inverse associations of maternal and paternal BMIs with offspring obestatin concentrations in women could suggest a utility of this biomarker of energy regulation determined in early adulthood. Whether obestatin could be an indicator of protection against obesity-related disorders in the life course requires investigation in studies designed to test such hypothesis.
Inverse associations of maternal and paternal BMIs with offspring obestatin concentrations in women could suggest a utility of this biomarker of energy regulation determined in early adulthood. Whether obestatin could be an indicator of protection against obesity-related disorders in the life course requires investigation in studies designed to test such hypothesis.
The intestinal microbiota plays an important role in the nutritional status and energy metabolism of the host. Liver cirrhosis is accompanied by muscle wasting or sarcopenia. The aim of this study was to to explore the changes in intestinal microbiota in patients with liver cirrhosis and muscle wasting by using metagenomics.
This was a cross-sectional study of patients with (n=30) and without (n=30) muscle wasting and age- and sex-matched healthy controls (n=30) to evaluate changes in intestinal microbiota by metagenomic gene sequencing. Eribulin mouse Muscle wasting was determined by the third lumbar vertebrae skeletal muscle index (L3 SMI).
The Shannon index, which represents species diversity, of patients in the muscle-wasting group (2.11 ± 0.88) was lower than in the non-muscle-wasting group (2.64 ± 0.68; P = 0.039), which was significantly lower than in the healthy control group (2.70 ± 0.53; P = 0.023). There were 17 microbial species with significant differences in relative abundance between the two groups (linear discriminant analysis score >2; P < 0.05). The relative abundance of Escherichia coli, Peptostreptococcus stomatis, and Bacteroides uniformis showed the most significant association with L3 SMI.
There were compositional alterations in intestinal microbiota in patients with liver cirrhosis and muscle wasting. L3 SMI is closely related to E. coli, P. stomatis, and B. uniformis in liver cirrhosis. Further interventional studies are needed to confirm whether improving intestinal microbiota can improve the nutritional status of patients with liver cirrhosis.
There were compositional alterations in intestinal microbiota in patients with liver cirrhosis and muscle wasting. L3 SMI is closely related to E. coli, P. stomatis, and B. uniformis in liver cirrhosis. Further interventional studies are needed to confirm whether improving intestinal microbiota can improve the nutritional status of patients with liver cirrhosis.
Neuronal Ceroid Lipofuscinosis type 2 (CLN2) is a neurodegenerative lysosomal disease which leads to early dementia and death without treatment. The recently available therapy consists of intracerebroventricular enzyme substitution cerliponase alfa. In this report, we describe the evolution of the first French children treated with cerliponase alfa.
CLN2 Clinical Rating Scale Motor-Language (CLN2 ML) assesses the motor and language evolution of CLN2 patients. We retrospectively studied patients' medical records clinical symptoms, MRI conclusions, gene mutation, side effects of infusions, patient's age and CLN2 ML scores at diagnosis, at the beginning of enzyme replacement therapy (ERT) and at the last evaluation. Seven patients were included.
Average age at diagnosis was 50 months ( ±10) with CLN2 ML score equal to 3.6 [1.5-5]. link2 Average age at the beginning of ERT was 56 months ( ±13) with CLN2 ML score equal to 3.1 [1-5]. link3 At the last available evaluation, average age was 82 months ( ±20) with CLN2 ML score equal to 2.8 [0-5]. Thus, in 26 months, the mean CLN2 ML score only decreased by 0.3 points. However, patients with a CLN2 ML score greater than three at the onset of ERT experienced a stabilisation or improvement of clinical signs, whereas patients with a CLN2 ML score less than three at baseline continue to deteriorate.
For patients starting ERT at an early stage of the disease, cerliponase alfa changes the natural history of the disease with a halt in disease progression or even a slight improvement in clinical symptoms.
For patients starting ERT at an early stage of the disease, cerliponase alfa changes the natural history of the disease with a halt in disease progression or even a slight improvement in clinical symptoms.The insulin-like growth factor (IGF) system is a critical regulator of growth, especially during fetal development, while also playing a central role in metabolic homeostasis. Endocrine disruptors (EDs) are ubiquitous compounds able to interfere with hormone action and impact human health. For example, exposure to EDs is associated with decreased birthweight and increased incidence of metabolic disorders. Therefore, the IGF system is a potential target for endocrine disruption. This review summarises the state of the science regarding effects of exposure to major classes of endocrine disruptors (dioxins and dioxin-like compounds, polycyclic aromatic hydrocarbons, polybrominated diphenyl ethers, phthalates, perfluoroalkyl substances and bisphenol A) on the IGF system. Evidence from both experimental models (in vitro and in vivo) and epidemiological studies is presented. In addition, possible molecular mechanisms of action and effects on methylation are discussed. There is a large body of evidence supporting the link between dioxins and dioxin-like compounds and IGF disruption, but mixed findings have been reported in human studies.
