Clinical nutrition最新文献

Background and aims: Butyrate is a microbiota-derived short-chain fatty acid linking colonic fermentation to host metabolism, with systemic availability limited by intestinal utilization and first-pass hepatic metabolism. Whether sodium butyrate (NaBut) supplementation might modulate its circulating levels and metabolic effects is unclear. The aim of this study is to assess whether oral NaBut supplementation improves body weight and metabolic profile in adults with overweight/obesity with or without type 2 diabetes (T2D).

Methods: In this randomized, double-blind, placebo-controlled, parallel-group trial, 46 adults (23 with T2D), aged 30-70 years and BMI 25-39.9 kg/m², were assigned (1:1) to NaBut (1875 mg/day) or placebo for 12 weeks, combined with an identical moderately hypoenergetic diet. Anthropometrics, body composition, fasting metabolic parameters, gastrointestinal symptoms, 7-day continuous glucose monitoring (CGM)-derived metrics, and serum short-chain fatty acids (GC/FID) were evaluated at baseline and week 12.

Results: In participants without diabetes, NaBut induced greater reductions in body weight compared with placebo (-7.0 ± 3.0 vs. -3.2 ± 1.6 kg; p = 0.001). In participants with T2D, weight changes did not differ between NaBut and placebo; however, NaBut significantly reduced plasma triglycerides (-0.36 ± 0.47 vs. +0.08 ± 0.30 mmol/L; p = 0.012) and increased time-in-tight-range (TITR; 70-140 mg/dL) by 9 %, independently of weight change. Serum butyrate concentrations increased with NaBut in both cohorts and were associated with weight change in obese people and CGM-derived changes in T2D..

Conclusions: NaBut supplementation supported weight loss in obesity without diabetes. In T2D, NaBut improved triglyceridemia and CGM-derived glycemic control, largely independent of weight change.

Trial registration number: NCT07252609 (https://clinicaltrials.gov/study/NCT07252609; ClinicalTrials.gov; 2025-11-17).

Background and aims: Metabolic bariatric surgery (MBS) is highly effective for weight loss, yet up to 50 % of individuals regain weight within five years. Reductions in resting metabolic rate (RMR), linked to fat-free mass (FFM) loss, have been suggested as one contributing factor. Yet, the liver and kidneys are highly metabolic organs (∼30 % of RMR); therefore, changes in their volume may contribute to a greater-than-expected decline in RMR, known as metabolic adaptation (MA), which may promote weight regain. We aim to evaluate the impact of exercise on changes in organ volume and MA following MBS.

Methods: Fifty-eight adults with severe obesity (39.6 ± 10.6y, 114.3 ± 17.5 kg, 41.4 ± 4.1 kg/m²) were enrolled in an open-label randomized controlled trial and assigned to one of three exercise intervention groups pre MBS: aerobic (n = 15), resistance (n = 13), combined training (n = 14), or to a no-exercise control group (n = 16) for 26 weeks. Training sessions were online, supervised, and progressed to 60 min, three times/week. Pre- and post-intervention RMR was measured by metabolic cart, body composition by dual-energy X-ray, and liver and kidney volume using 3-T magnetic resonance imaging (MRI).

Results: Fifty-three participants (91 %) completed the intervention, and 47 were included in the final analysis. Significant reductions were observed in body weight (-31.1 ± 8.7 kg, -27 %), RMR (-356 ± 237 kcal/day, -17 %), kidney volume (-35.1 ± 25.2 cm³, -11 %), and liver volume (-384 ± 250 cm³, -21 %) (p < 0.01 for all), similarly across all groups. Crucially, reductions in liver and kidney volume were significantly associated with lower RMR (p < 0.001). The significant (P < 0.001) MA of -289 ± 190 kcal/day was independent of exercise volume or type. Liver volume accounted for 32.1 % of MA, FFM for 29.7 %, and kidney volume for 6.2 %.

Conclusions: Our findings suggest that MA following MBS may be associated with a reduction in liver and kidney volume, potentially contributing to RMR decline. These findings highlight a potential organ-specific mechanism underlying MA and may prevent weight regain.

Clinicaltrials: gov identifier: NCT04777305.

Background and aims: Wholegrain rye foods have shown promising effects on metabolic regulation and weight-loss, which may be mediated via gut microbiota and derived metabolites. This study aimed to investigate effects of hypocaloric diets with wholegrain rye versus commonly consumed refined wheat on body weight, fat mass, metabolic risk markers and gut microbiota. The study also explored determinants of diet-induced weight loss..

Methods: Participants with overweight or obesity were randomized (1:1) to 12-week hypocaloric diets, substituting habitual cereals with wholegrain rye or refined wheat foods. Body weight and composition were measured and fecal- and blood samples were collected at baseline, after 6 weeks and 12 weeks.

Results: Of 255 participants, 229 completed the study. Weight loss was 3.2 kg in the rye-group and 2.9 kg in the wheat-group, with no significant difference between groups (p = 0.32). Plasma acetate and butyrate were higher after 12 weeks in the rye-group versus wheat-group (p = 0.003) and microbial taxa, previously associated with negative health outcomes were reduced in the rye-group. Reductions in CRP by 17 % (p = 0.03) were observed in the rye-group, while both CRP (r = 0.17, p = 0.001) and HOMA-IR (r = 0.13, p = 0.02) at baseline were associated with fat mass change in the wheat-group. Additionally, acetate at baseline was inversely associated with body weight change across groups (r = -0.25, p < 0.001). Baseline gut microbiota was not associated with weight loss after 12 weeks.

Conclusions: Wholegrain rye versus refined wheat foods as part of a hypocaloric diet did not result in larger weight loss. However, wholegrain rye reduced CRP and induced changes in gut microbiota and short-chain fatty acids which may have positive implications for cardiometabolic health. Notably, baseline HOMA-IR and CRP correlated with weight and fat mass reductions, suggesting that individuals with elevated inflammation and insulin resistance may benefit more from wholegrain rye foods. Gut microbiota at baseline was not associated with intervention-induced weight loss.

Trial registration: ClinicalTrials.gov ID: NCT04203758. https://classic.

Clinicaltrials: gov/ct2/show/NCT04203758?term=Rye&cond=Overweight+and+Obesity&cntry=SE&city=Gothenburg&draw=2&rank=3.

Background and aims: Psoriasis is a chronic inflammatory skin condition that adversely affects quality of life. Given limited evidence to inform dietary recommendations for psoriasis prevention, this study used data from the UK Biobank to examine associations between diet quality and incident psoriasis, and whether genetic susceptibility moderates this relationship.

Methods: Participants without psoriasis at baseline who completed ≥2 Oxford WebQ 24-h dietary recalls were included. Psoriasis incidence was identified through self-report, primary care, and hospital records. Ten diet quality indices (DQIs) were computed: Low Carbohydrate Diet Score (LCDS), Alternative Mediterranean Diet (aMed) Score, Eatwell Score (EWS), Alternative Binary Eatwell Score (BEWS), Alternative Graded Eatwell Score (GEWS), Healthy Diet Index (HDI), Alternative Healthy Eating Index (aHEI), Dietary Approaches to Stop Hypertension Score (DASH), Dietary Inflammatory Index (DII), and Plant-Based Diet Index (PDI). A multivariable Cox proportional hazards regression model adjusted for sociodemographic, lifestyle, and clinical, estimated association between each DQI and psoriasis incidence.

Results: Among 121,299 participants followed up for a mean 11.4 years, 822 developed psoriasis (incidence 0.68 %). In fully adjusted models, higher PDI scores (Q4: 56-77) were associated with a 19 % lower risk of psoriasis (HR: 0.806, [95 % CI: 0.651-0.997]) compared to lower PDI scores (Q1: 26-47). This was driven by lower intake of unhealthy plants (HR: 1.036, [95 % CI: 1.015-1.057], P_FDR-trend = 0.021) and meat components (HR: 1.027, [95 % CI: 1.002-1.052]). While there was no strong evidence of interaction between PDI and genetic risk, the protective effect of PDI was stronger among individuals with low genetic risk (HR: 0.965, [95 % CI: 0.939-0.991], P = 0.009). Mediation analyses suggested partial effects via lower adiposity.

Conclusion: Individuals with the highest adherence to a plant-based dietary pattern were at lower risk of incident psoriasis in this large UK cohort, with no evidence that this association differed by genetic risk.

Background: Obesity is a growing global health concern. Some evidence suggests that exposure to polychlorinated biphenyls (PCBs) and dioxins, may play a role in weight gain, but human prospective data are limited and have shown inconsistent results. Therefore, this study investigate the association between dietary exposure to dioxins and PCBs and changes in weight and in waist circumference after 5 years of follow-up in a large prospective cohort.

Method: We included 215,556 participants recruited between 1992 and 2000; of whom 99,046 provided data on waist circumference. Body weight or waist circumference were measured at recruitment and self-reported at follow-up. Intakes of dioxins and PCBs were estimated using country-specific dietary questionnaires collected at baseline, and food contamination concentrations based on a European Food Safety Authority database. Associations were estimated using multilevel mixed linear regression models.

Results: Higher intake of both dioxins and dioxin-like PCBs (dioxins + DL-PCBs) (Q4vsQ1 = 0.07kg/5-years (95%CI 0.01, 0.13)), and non-dioxin like PCBs (NDL-PCBs) (Q4vsQ1 = 0.27kg/5-years (95%CI 0.20, 0.35), p-trend<0.001)) were associated with weight gain. Inverse associations were observed between dietary intake of dioxins + DL-PCBs and NDL-PCBs and waist circumference change (Q4vsQ1 = -0.44cm/5-years (95%CI -0.56, -0.31), p-trend<0.001 and Q4vsQ1 = -0.21cm/5-years (95%CI -0.34, -0.07), p-trend<0.001, respectively). These inverse associations were primarily caused by a subset of participants from one country who provided most of the waist circumference data. Results were consistent across stratified and sensitivity analyses.

Conclusion: Results obtained in this large prospective study show a positive association between dietary intake of both dioxins + DL-PCBs and NDL- PCBs and weight gain. Although the observed associations were small and there may be measurement errors, the consistency of these associations across multiple stratified analyses and sensitivity analyses strengthens the validity of the findings. The findings suggest that the effect of dioxins and PCBs are still present in the food chain despite regulatory bans. Efforts should be strengthened to reduce the exposure levels in the general population not only to lower the risk of obesity, but also to prevent various chronic conditions.

Background and AimEmerging evidence suggests that weight loss associated with glucagon-like peptide-1 receptor agonists (GLP-1 RAs) may be in part attributable to changes in lean mass, which has potential clinical implications. This study evaluates the disproportionate reporting of muscle atrophy in association with GLP-1 RA therapy using real-world global data.. MethodsWe analyzed reports of muscle atrophy submitted to the FDA Adverse Event Reporting System (FAERS) database from October 2003 to March 2024 using the validated pharmacovigilance tool OpenVigil 2.1. Disproportionality was assessed using reporting odds ratios (RORs) with 95 % confidence intervals (CIs), the standard metric for pharmacovigilance signal detection worldwide. To contextualize associations, disproportionality estimates were calculated using niacin, simvastatin, and the complete FAERS database (all other drugs) as comparators. ResultsA total of 142 cases of muscle atrophy were identified with GLP-1 RA therapy, the majority occurring in adults aged 18-64 years (43 % female, 57 % male). Disproportionality analysis showed pharmacovigilance signals for semaglutide (ROR = 2.39, 95 % CI = 1.63-3.52) and tirzepatide (ROR = 1.69, 95 % CI = 1.14-2.50), indicating increased reporting of muscle atrophy relative to all other drugs in FAERS. In contrast, exenatide (ROR = 0.26, 95 % CI = 0.12-0.55) and liraglutide (ROR = 0.27, 95 % CI = 0.09-0.83) were associated with significantly lower reporting odds. All significant signals satisfied thresholds of p < 0.05 and IC₀₂₅ > 0.. ConclusionsCertain GLP-1 receptor agonists demonstrate a pharmacovigilance signal of disproportionate reporting of muscle atrophy. These findings should be interpreted as signal detection rather than evidence of causality and highlight the need for future studies incorporating objective measures of muscle mass and function..