摄入 NAD + 前体补充剂后葡萄糖代谢、C 反应蛋白和肝酶的变化：系统综述和元回归分析。

IF 3.9 2区医学 Q2 NUTRITION & DIETETICS

Nutrition & Metabolism Pub Date : 2024-06-24 DOI:10.1186/s12986-024-00812-0

Mohammad Hassan Sohouli, Sogand Tavakoli, Marcela Gomes Reis, Azita Hekmatdoost, Nathalia Sernizon Guimarães

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引用次数: 0

摘要

背景：关于NAD+前体对糖代谢和肝酶的影响，存在着相互矛盾的影响。为了从中获得更好的观点，本研究旨在全面探讨补充 NAD + 前体对糖代谢、C 反应蛋白（CRP）和肝酶的影响：方法：使用标准关键词检索 PubMed/MEDLINE、Web of Science、SCOPUS 和 Embase 数据库，以确定所有研究 NAD + 前体对糖代谢、CRP 和肝酶影响的对照试验。通过随机效应模型分析，得出汇总加权平均差（WMD）和95%置信区间（95% CI），以获得对结果的最佳估计：本文共收录了45篇文章，9256名参与者。汇总结果显示，补充 NAD + 前体可显著提高血糖（WMD：2.17 mg/dL，95% CI：0.68, 3.66，P = 0.004）和 HbA1c（WMD：0.11，95% CI：0.06, 0.16，P 结论：NAD + 前体可显著降低血糖和 HbA1c：总之，这些研究结果表明，补充 NAD + 前体可能会增加葡萄糖代谢的效果，并降低 CRP。

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Changes in glucose metabolism, C-reactive protein, and liver enzymes following intake of NAD + precursor supplementation: a systematic review and meta-regression analysis.

Background: There are contradictory effects regarding the effect of NAD + precursor on glucose metabolism and liver enzymes. In order to obtain a better viewpoint from them, this study aimed to comprehensively investigate the effects of NAD + precursor supplementation on glucose metabolism, C-reactive protein (CRP), and liver enzymes.

Methods: PubMed/MEDLINE, Web of Science, SCOPUS, and Embase databases were searched using standard keywords to identify all controlled trials investigating the glucose metabolism, CRP, and liver enzymes effects of NAD + precursor. Pooled weighted mean difference (WMD) and 95% confidence intervals (95% CI) were achieved by random-effects model analysis for the best estimation of outcomes.

Results: Forty-five articles with 9256 participants' were included in this article. The pooled findings showed that NAD + precursor supplementation had a significant increase in glucose (WMD: 2.17 mg/dL, 95% CI: 0.68, 3.66, P = 0.004) and HbA1c (WMD: 0.11, 95% CI: 0.06, 0.16, P < 0.001) as well as a significant decrease in CRP (WMD: -0.93 mg/l, 95% CI -1.47 to -0.40, P < 0.001) compared with control group, and was not statistically significant with respect to insulin and homeostasis model assessment of insulin resistance (HOMA-IR). However, we found no systemic changes in aspartate transaminase (AST), alanine transaminase (ALT), or alkaline phosphatase (ALP) levels after NAD + precursor supplementation. The results of the subgroup analysis showed that the intake of NAD + precursor during the intervention of more than 12 weeks caused a greater increase in the glucose level. Furthermore, Nicotinic acid supplementation (NA) causes a greater increase in glucose and HbA1c levels than nicotinamide (NE) supplementation.

Conclusions: Overall, these findings suggest that NAD + precursor supplementation might have an increase effect on glucose metabolism as well as a decrease in CRP.

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来源期刊

Nutrition & Metabolism 医学-营养学

CiteScore

8.40

自引率

0.00%

发文量

审稿时长

4-8 weeks

期刊介绍： Nutrition & Metabolism publishes studies with a clear focus on nutrition and metabolism with applications ranging from nutrition needs, exercise physiology, clinical and population studies, as well as the underlying mechanisms in these aspects. The areas of interest for Nutrition & Metabolism encompass studies in molecular nutrition in the context of obesity, diabetes, lipedemias, metabolic syndrome and exercise physiology. Manuscripts related to molecular, cellular and human metabolism, nutrient sensing and nutrient–gene interactions are also in interest, as are submissions that have employed new and innovative strategies like metabolomics/lipidomics or other omic-based biomarkers to predict nutritional status and metabolic diseases. Key areas we wish to encourage submissions from include: -how diet and specific nutrients interact with genes, proteins or metabolites to influence metabolic phenotypes and disease outcomes; -the role of epigenetic factors and the microbiome in the pathogenesis of metabolic diseases and their influence on metabolic responses to diet and food components; -how diet and other environmental factors affect epigenetics and microbiota; the extent to which genetic and nongenetic factors modify personal metabolic responses to diet and food compositions and the mechanisms involved; -how specific biologic networks and nutrient sensing mechanisms attribute to metabolic variability.