Human milk (HM) incorporates butyrate, a short-chain fatty acid (SCFA). This four-carbon fatty acid is present in HM at a varied concentration of 0.1–0.75 mg/100 mL. Butyrate has many biological functions, akin to anti-inflammatory properties, and prevents insulin resistance and obesity. A recent study within the journal Nutrients provided evidence on the origin of HM butyrate based on HM microbiota composition. This study also elucidated the maternal and antenatal aspects linked with HM butyrate concentration.

Study: Butyrate in Human Milk: Associations with Milk Microbiota, Milk Intake Volume, and Infant Growth. Image Credit: evso / Shutterstock

Background

Previous studies have revealed that gut anaerobic bacteria synthesize butyrate via fermentation of non-digestible carbohydrates. Amongst many SCFAs (e.g., acetate and propionate), butyrate is a major energy source utilized by colonic epithelial cells. 

Although much research related to intestinal butyrate is accessible, not many studies have elucidated the origins of HM butyrate. It has been hypothesized that maternal gut microbiota synthesizes butyrate, which could reach HM through maternal circulation. So far, no evidence has been documented that indicates local butyrate production through in situ HM microbiota. As well as, it’s imperative to know whether maternal and pregnancy-related aspects influence HM butyrate concentration.

Infants are introduced to this fatty acid through oral intake of HM or solid food. One other way through which infants receive butyrate is bacterial fermentation of dietary compounds, particularly human milk oligosaccharides (HMOs), within the colon. Hence, HM butyrate doesn’t represent the actual butyrate concentration consumed by infants. The advantages of HM butyrate for infants have been indicated in lots of studies. As an illustration, HM butyrate prevents unnecessary weight and adiposity gain, which substantially decreases later obesity risk. Subsequently, it can be crucial to measure absolutely the butyrate intake via HM to raised understand the mechanistic links with weight and adiposity gains.

In regards to the Study

This current longitudinal prospective cohort is a component of the Cambridge Baby Growth and Breastfeeding Study which goals to elucidate the aspects in HM that influence infants’ growth rate and discover parameters that enhance the chance of obesity in later life. The authors measured the overall HM consumed by a baby using a deuterium-labeled water technique. The HM composition, i.e., its macronutrients, butyrate, HMOs, HM microbiota, and infant’s gut microbiome, was also evaluated.

On this study, mother-infant pairs were recruited at birth on the Rosie Maternity Hospital in England. Healthy moms with healthy body mass index (BMI) before pregnancy and who had the intention of breastfeeding as much as no less than six weeks of the infants’ age were included on this study.

Birth weights were obtained at different time points, i.e., at birth, 2 and 6 weeks, after which 3, 6, and 12 months. A Holtain Tanner/Whitehouse Skinfold Caliper was used to measure relative subcutaneous body fat and skinfold thickness (SFT). HM samples were collected to find out composition.

Study Findings

A complete of 71 healthy singletons were included on this longitudinal study to investigate how HM butyrate influences infant growth. Overall, negative associations were found between HM butyrate concentrations and measures of infant weight and adiposity. This finding was consistent with a previous study that reported butyrate to stop excessive weight gain and obesity during childhood.

Since HM butyrate concentration was found to be inversely correlated with HM intake volume, it was presumed that top butyrate concentration in HM may very well be the rationale for low HM intake in some infants. The authors speculated that butyrate odor and/or taste in HM and its ability to manage appetite can potentially decrease infant HM intake. This may also cause early attenuation from HM intake, leading to early infant weight gain.

Notably, the present study reported a relative abundance of Oscillospira in HM, a standard butyrate producer. Nonetheless, other butyrate producers, akin to Faecalibacterium prausnitzii, Roseburia intestinalis, or Eubacterium rectale, weren’t detected. The authors didn’t expect the presence of butyrate-producing bacteria of the gut microbial community, typically anaerobes, in HM. Subsequently, increased bacterial metabolism may very well be attributed to the increased HM butyrate levels and never to changes in bacterial community composition.

Interestingly, a positive correlation between butyrate concentrations and non-butyrate-producing bacterial taxa in HM (e.g., Acinetobacter sp.) was observed. The abundance of Acinetobacter in HM microbiota was related to food allergy in infants. As well as, butyrate exhibited an antimonial effect on certain strains of Acinetobacter; due to this fact, the abundance of this species was not related to butyrate synthesis.

Conclusions

HM butyrate was found to be negatively related to infants’ growth. Nonetheless, this association was found to weaken with age, potentially due to the child’s introduction to other types of nutrition. Notably, a weak relationship between HM butyrate and HM microbiota composition was observed on this study.