Effect of supplementation with select human milk oligosaccharides on artificially reared newborn rats

2021 ◽  
pp. 1-26
Author(s):  
W. Wang ◽  
C. Mu ◽  
N.A. Cho ◽  
E.W. Noye Tuplin ◽  
D.E. Lowry ◽  
...  

Abstract Early life nutrition fundamentally influences neonatal development and health. Human milk oligosaccharides (HMOs) are key components of breast milk, but not standard infant formula that support establishment of the newborn gut microbiota. Using an artificial rearing system, our objective was to test the effect of two HMOs on whole body and organ growth, adiposity, glucose tolerance, and fecal microbiota in young rat pups. From postnatal day 4 to 21, Sprague Dawley rats were randomized to receive one of: 1) CTR (rat milk substitute); 2) 2’FL (CTR +1.2 g/L 2’-fucosyllactose); 3) 3’SL (CTR+1.2 g/L 3’-sialyllactose); 4) 2’FL+3’SL (CTR+0.6 g/L 2’-FL+0.6 g/L 3’-SL). Body weight, bowel movements and food intake were monitored daily, fecal samples collected each week, and oral glucose tolerance, body composition, and organ weight measured at weaning. No significant differences were observed between groups in growth performance, body composition, organ weight and abundance of dominant fecal microbes. A decreased relative abundance of genus Proteus in week1 fecal samples and Terrisporobacter in week3 fecal samples (P<0.05) was suggestive of a potential pathogen inhibitory effect of 3’SL. Longitudinal changes in the fecal microbiota of artificially reared suckling rats were primarily governed by age (P =0.001) and not affected by the presence of 2’-FL and/or 3’-SL in rat milk substitutes (P =0.479). Considering the known protective effects of HMOs, further investigation of supplementation with these and other HMOs in models of premature birth, extremely low body weight, or malnutrition may show more pronounced outcomes.

2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Cilius Esmann Fonvig ◽  
Ingvild Dybdrodt Amundsen ◽  
Louise Kristine Vigsnæs ◽  
Nikolaj Sørensen ◽  
Christine Frithioff-Bøjsøe ◽  
...  

2022 ◽  
Vol 9 ◽  
Author(s):  
Sarah Bajorek ◽  
Rebbeca M. Duar ◽  
Maxwell Corrigan ◽  
Christa Matrone ◽  
Kathryn A. Winn ◽  
...  

Not all infants carry specialized gut microbes, meaning they cannot digest human milk oligosaccharides and therefore do not receive complete benefits from human milk. B. infantis EVC001 is equipped to convert the full array of complex oligosaccharides into compounds usable by the infant, making it an ideal candidate to stabilize gut function and improve nutrition in preterm infants. A prospective, open-label study design was used to evaluate the tolerability of B. infantis EVC001 and its effects on the fecal microbiota in preterm infants in a Neonatal Intensive Care Unit. Thirty preterm infants &lt;1,500 g and/or &lt;33 weeks gestation at birth were divided into two matched groups, and control infants were enrolled and discharged prior to enrolling EVC001 infants to prevent cross-colonization of B. infantis: (1) fifteen control infants received no EVC001, and (2) fifteen infants received once-daily feedings of B. infantis EVC001 (8.0 x 109 CFU) in MCT oil. Clinical information regarding medications, growth, nutrition, gastrointestinal events, diagnoses, and procedures was collected throughout admission. Infant stool samples were collected at baseline, Study Days 14 and 28, and 34-, 36-, and 38-weeks of gestation. Taxonomic composition of the fecal microbiota, functional microbiota analysis, B. infantis, and human milk oligosaccharides (HMOs) in the stool were determined or quantified using 16S rRNA gene sequencing, metagenomic sequencing, qPCR, and mass spectrometry, respectively. No adverse events or tolerability issues related to EVC001 were reported. Control infants had no detectable levels of B. infantis. EVC001 infants achieved high levels of B. infantis (mean = 9.7 Log10 CFU/μg fecal DNA) by Study Day 14, correlating with less fecal HMOs (ρ = −0.83, P &lt; 0.0001), indicating better HMO utilization in the gut. In this study, B. infantis EVC001 was shown to be safe, well-tolerated, and efficient in colonizing the preterm infant gut and able to increase the abundance of bifidobacteria capable of metabolizing HMOs, resulting in significantly improved utilization of human milk.Clinical Trial Registration:https://clinicaltrials.gov/ct2/show/NCT03939546, identifier: NCT03939546.


2019 ◽  
Vol 156 (6) ◽  
pp. S-235 ◽  
Author(s):  
Cristina Iribarren ◽  
Maria K. Magnusson ◽  
Hans Törnblom ◽  
Imran Aziz ◽  
Ingvild Dybdrodt Amundsen ◽  
...  

2007 ◽  
Vol 293 (3) ◽  
pp. R1102-R1109 ◽  
Author(s):  
Stefany D. Primeaux ◽  
Melissa Tong ◽  
Gregory M. Holmes

The inability to maintain body weight within prescribed ranges occurs in a significant portion of the human spinal cord injury (SCI) population. Using a rodent model of long-term high thoracic (spinal level T3) spinal cord transection (TX), we aimed to identify derangements in body weight, body composition, plasma insulin, glucose tolerance, and metabolic function, as measured by uncoupling protein 1 (UCP1) expression in interscapular brown adipose tissue (IBAT). Sixteen weeks after SCI, body weights of injured female rats stabilized and were significantly lower than surgical control animals. At the same time point, SCI rats had a significantly lower whole body fat:lean tissue mass ratio than controls, as measured indirectly by NMR. Despite lower body weight and fat mass, the cumulative consumption of standard laboratory chow (4.0 kcal/g) and mean energy intake (kcal·day−1·100 g body wt−1) of chronic SCI rats was significantly more than controls. Glucose tolerance tests indicated a significant enhancement in glucose handling in 16-wk SCI rats, which were coupled with lower serum insulin levels. The post mortem weight of gonadal and retroperitoneal fat pads was significantly reduced after SCI and IBAT displayed significantly lower real-time PCR expression of UCP1 mRNA. The reduced fat mass and IBAT UCP1 mRNA expression are contraindicative of the cumulative caloric intake by the SCI rats. The prolonged postinjury loss of body weight, including fat mass, is not due to hypophagia but possibly to permanent changes in gastrointestinal transit and absorption, as well as whole body homeostatic mechanisms.


2019 ◽  
Vol 316 (3) ◽  
pp. E347-E357 ◽  
Author(s):  
Evelyn Jantscher-Krenn ◽  
Johanna Aigner ◽  
Birgit Reiter ◽  
Harald Köfeler ◽  
Bence Csapo ◽  
...  

Human milk oligosaccharides (HMOs) are bioactive glycans linked with health benefits to both the breast-fed infant and lactating mother. We hypothesized that HMOs are present before lactation, already during pregnancy, and are influenced by maternal body composition. In a pilot study, we investigated individual and temporal variations in HMO composition and concentration in maternal serum at gestational weeks 10–14 ( visit 1), 20–24 ( visit 2), and 30–35 (visit 3) (V1, V2, and V3, respectively) and associations with maternal body composition. HMOs were quantified by HPLC and confirmed by enzymatic digest and mass spectrometry. Associations of maternal prepregnancy body mass index (BMI), subcutaneous adipose tissue (SAT) thickness, and adipokines with absolute and relative HMO concentrations were analyzed by Spearman correlation. We identified 16 HMOs and 2 oligosaccharides not common to human milk. HMO concentration and composition varied with gestational age and secretor status. HMO concentration increased with gestational age and changed from a predominantly sialylated profile at V1 to a more balanced fucosylated-to-sialylated ratio at V3, mostly due to a profound increase in 2′-fucosyllactose (2′-FL), reflecting secretor phenotype. In secretor-positive women, BMI was negatively correlated with 2′-FL at V2. SAT at V1 and V2 were strongly negatively correlated with 2′-FL concentrations. This pilot study shows that prenatal HMOs are present in maternal serum, suggesting roles for HMOs already during pregnancy. Our result that maternal body composition is associated with prenatal HMOs might indicate that maternal metabolism modulates HMO composition with unknown implications for maternal and fetal health already during pregnancy.


2015 ◽  
Vol 102 (6) ◽  
pp. 1381-1388 ◽  
Author(s):  
Tanya L Alderete ◽  
Chloe Autran ◽  
Benjamin E Brekke ◽  
Rob Knight ◽  
Lars Bode ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Brittany B. Rice ◽  
Sara Y. Ngo Tenlep ◽  
Obadah Tolaymat ◽  
Attaas T. Alvi ◽  
Fallon R. Slone ◽  
...  

Human environmental exposures to toxicants, such as polychlorinated biphenyls (PCBs), increase oxidative stress and disease susceptibility. Such exposures during pregnancy and/or nursing have been demonstrated to adversely affect offspring health outcomes. Nuclear factor erythroid-2-related factor 2 (Nrf2) regulates the antioxidant response and is involved in the detoxification of coplanar PCBs, like PCB126. The purpose of this study was to investigate glucose tolerance and body composition in PCB-exposed offspring expressing or lacking Nrf2. We hypothesized that offspring lacking Nrf2 expression would be more susceptible to the long-term health detriments associated with perinatal PCB exposure. During gestation, whole-body Nrf2 heterozygous (Het) and whole-body Nrf2 knockout (KO) mice were exposed to vehicle or PCB126. Shortly after birth, litters were cross-fostered to unexposed dams to prevent PCB exposure during nursing. Offspring were weaned, and their body weight, body composition, and glucose tolerance were recorded. At two months of age, PCB exposure resulted in a significant reduction in the average body weight of offspring born to Nrf2 Het dams (p &lt; 0.001) that primarily arose from the decrease in average lean body mass in offspring (p &lt; 0.001). There were no differences in average body weight of PCB-exposed offspring born to Nrf2 KO dams (p &gt; 0.05), and this was because offspring of Nrf2 KO dams exposed to PCB126 during pregnancy experienced a significant elevation in fat mass (p = 0.002) that offset the significant reduction in average lean mass (p &lt; 0.001). Regardless, the lack of Nrf2 expression in the offspring themselves did not enhance the differences observed. After an oral glucose challenge, PCB-exposed offspring exhibited significant impairments in glucose disposal and uptake (p &lt; 0.05). Offspring born to Nrf2 Het dams exhibited these impairments at 30 min and 120 min, while offspring born to Nrf2 KO dams exhibited these impairments at zero, 15, 30, 60 and 120 min after the glucose challenge. Again, the interactions between offspring genotype and PCB exposure were not significant. These findings were largely consistent as the offspring reached four months of age and demonstrate that the lack of offspring Nrf2 expression does not worsen the metabolic derangements caused by in utero PCB exposure as we expected. Future directions will focus on understanding how the observed maternal Nrf2 genotypic differences can influence offspring metabolic responses to in utero PCB exposure.


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