Urolithin Metabotypes can Anticipate the Different Restoration of the Gut Microbiota and Anthropometric Profiles during the First Year Postpartum.

Adrián Cortés-Martín,María Carmen Collado,María Victoria Selma,Juan Carlos Espín,Izaskun García-Mantrana,María Romo-Vaquero,Ana Rodríguez-Varela

doi:10.3390/nu11092079

Abstract

The metabolism of dietary polyphenols ellagitannins by the gut-microbiota allows the human stratification in urolithin metabotypes depending on the final urolithins produced. Metabotype-A only produces urolithin-A, metabotype-B yields urolithin-B and isourolithin-A in addition to urolithin-A, and metabotype 0 does not produce urolithins. Metabotype-A has been suggested to be ‘protective’, and metabotype-B dysbiotic-prone to cardiometabolic impairments. We analyzed the gut-microbiome of 40 healthy women and determined their metabotypes and enterotypes, and their associations with anthropometric and gut-microbial changes after 3 weeks, 4, 6, and 12 months postpartum. Metabotype-A was predominant in mothers who lost weight (≥2 kg) (75%) versus metabotype-B (54%). After delivery, the microbiota of metabotype-A mothers changed, unlike metabotype-B, which barely changed over 1 year. The metabotype-A discriminating bacteria correlated to the decrease of the women’s waist while some metabotype-B bacteria were inversely associated with a reduction of body mass index (BMI), waist, and waist-to-hip ratio. Metabotype-B was associated with a more robust and less modulating microbial and anthropometric profiles versus metabotype-A, in which these profiles were normalized through the 1-year follow-up postpartum. Consequently, urolithin metabotypes assessment could be a tool to anticipate the predisposition of women to normalize their anthropometric values and gut-microbiota, significantly altered during pregnancy and after childbirth.

Highlights

During a healthy pregnancy, body fat increases followed by a reduction of insulin sensitivity and the elevation of circulating cytokines that are thought to drive obesity-associated metabolic inflammation [1]
Most of the mothers were grouped into the enterotype 3 (Ruminococcus-type, 88%) at early lactation (T1) and remained invariable throughout the study (Table 1)
Urolithin Metabotypes (UMs) distribution for UM-0, UM-B, and UM-A was maintained through T1 to T2, and slightly changed at T3 (0%, 53%, 47%, respectively) but especially at T4, after lactation (0%, 60%, 40%, respectively) (Table 1)

Summary

Introduction

Body fat increases followed by a reduction of insulin sensitivity and the elevation of circulating cytokines that are thought to drive obesity-associated metabolic inflammation [1]. The gut microbiota of pregnant women is profoundly altered with a vast expansion of alpha-diversity and a general increase of different bacterial groups, which persists at least 1 month after delivery [2,3]. This change induces higher adiposity and insulin insensitivity, which resembles obesity-associated metabolic syndrome traits. PPWR has been associated with an increased risk of many adverse outcomes in a subsequent pregnancy, independently of the woman’s initial body mass index (BMI) [4]. A clear understanding of the PPWR risk factors is needed to face the problem, and the microbiota seems to play an important role [4,5]

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