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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. Selleck XL177A 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. 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.
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