A Diet Enriched with Lacticaseibacillus rhamnosus HN001 and Milk Fat Globule Membrane Alters the Gut Microbiota and Decreases Amygdala GABA a Receptor Expression in Stress-Sensitive Rats.

Brain signalling pathways involved in subclinical anxiety and depressed mood can be modulated via the gut brain axis (GBA), providing the potential for diet and dietary components to affect mood. We investigated behavioural, physiological and gut microbiome responses to the Lacticaseibacillus rhamnosus strain HN001 (LactoB HN001™), which has been shown to reduce postpartum anxiety and depression, and a milk fat globule membrane-enriched product, Lipid 70 (SurestartTM MFGM Lipid 70), which has been implicated in memory in stress-susceptible Wistar Kyoto rats. We examined behaviour in the open field, elevated plus maze and novel object recognition tests in conjunction with the expression of host genes in neuro-signalling pathways, and we also assessed brain lipidomics. Treatment-induced alterations in the caecal microbiome and short-chain fatty acid (SCFA) profiles were also assessed. Neither ingredient induced behavioural changes or altered the brain lipidome (separately or when combined). However, with regard to brain gene expression, the L. rhamnosus HN001 + Lipid 70 combination produced a synergistic effect, reducing GABAA subunit expression in the amygdala (Gabre, Gat3, Gabrg1) and hippocampus (Gabrd). Treatment with L. rhamnosus HN001 alone altered expression of the metabotropic glutamate receptor (Grm4) in the amygdala but produced only minor changes in gut microbiota composition. In contrast, Lipid 70 alone did not alter brain gene expression but produced a significant shift in the gut microbiota profile. Under the conditions used, there was no observed effect on rat behaviour for the ingredient combination. However, the enhancement of brain gene expression by L. rhamnosus HN001 + Lipid 70 implicates synergistic actions on region-specific neural pathways associated with fear, anxiety, depression and memory. A significant shift in the gut microbiota profile also occurred that was mainly attributable to Lipid 70.

Actinidin from kiwifruit (Actinidia deliciosa cv. Hayward) increases the digestion and rate of gastric emptying of meat proteins in the growing pig.

The present study aimed to investigate the effect of dietary actinidin on the kinetics of gastric digestion of beef muscle proteins and on the rate of stomach emptying in growing pigs. For this purpose, 120 pigs (mean body weight 28 (sd 2·9) kg) were fed beef muscle protein-based diets containing either actinidin (fresh green kiwifruit pulp or gold kiwifruit pulp supplemented with purified actinidin) or no actinidin (fresh gold kiwifruit pulp or green kiwifruit pulp with inactivated actinidin). Additionally, fifteen pigs were fed with a protein-free diet to determine the endogenous protein flow. Pigs were euthanised at exactly 0·5, 1, 3, 5 and 7 h postprandially (n 6 per time point for each kiwifruit diet and n 3 for protein-free diet). Stomach chyme was collected for measuring gastric retention, actinidin activity, individual beef muscle protein digestion based on SDS-PAGE and the degree of hydrolysis based on the appearance of free amino groups. The stomach emptying of DM and N was faster when actinidin was present in the diet (P< 0·05): the half gastric emptying time of DM was 137 v. 172 min ( ± 7·4 min pooled standard error) for the diets with and without actinidin, respectively. The presence of dietary actinidin in the stomach chyme increased the digestion of beef muscle protein (P< 0·05) and, more specifically, those proteins with a high molecular weight (>34 kDa; P< 0·05). In conclusion, dietary actinidin fed in the form of fresh green kiwifruit increased the rate of gastric emptying and the digestion of several beef muscle proteins.

Novel insights into mechanisms of inhibition of colonic motility by loperamide.

Background: It is well known that opiates slow gastrointestinal (GI) transit, via suppression of enteric cholinergic neurotransmission throughout the GI tract, particularly the large intestine where constipation is commonly induced. It is not clear whether there is uniform suppression of enteric neurotransmission and colonic motility across the full length of the colon. Here, we investigated whether regional changes in colonic motility occur using the peripherally-restricted mu opioid agonist, loperamide to inhibit colonic motor complexes (CMCs) in isolated mouse colon. Methods: High-resolution video imaging was performed to monitor colonic wall diameter on isolated whole mouse colon. Regional changes in the effects of loperamide on the pattern generator underlying cyclical CMCs and their propagation across the full length of large intestine were determined. Results: The sensitivity of CMCs to loperamide across the length of colon varied significantly. Although there was a dose-dependent inhibition of CMCs with increasing concentrations of loperamide (10 nM - 1 µM), a major observation was that in the mid and distal colon, CMCs were abolished at low doses of loperamide (100 nM), while in the proximal colon, CMCs persisted at the same low concentration, albeit at a significantly slower frequency. Propagation velocity of CMCs was significantly reduced by 46%. The inhibitory effects of loperamide on CMCs were reversed by naloxone (1 µM). Naloxone alone did not change ongoing CMC characteristics. Discussion: The results show pronounced differences in the inhibitory action of loperamide across the length of large intestine. The most potent effect of loperamide to retard colonic transit occurred between the proximal colon and mid/distal regions of colon. One of the possibilities as to why this occurs is because the greatest density of mu opioid receptors are located on interneurons responsible for neuro-neuronal transmission underlying CMCs propagation between the proximal and mid/distal colon. The absence of effect of naloxone alone on CMC characteristics suggest that the mu opioid receptor has little ongoing constitutive activity under our recording conditions.

In vivo digestion of bovine milk fat globules: effect of processing and interfacial structural changes. I. Gastric digestion.

The aim was to study the in vivo gastric digestion of fat globules in bovine cream from raw, pasteurised or pasteurised and homogenised milk. Fasted rats were gavaged once and chyme samples were collected after 30, 120 and 180 min post-gavage. Proteins from raw (RC) and pasteurised (PC) creams appeared to be digested faster and to a greater extent. Free fatty acids (FAs) increased throughout the 3h postprandial period. Short and medium chain FAs were released more rapidly than long chain FAs which were hydrolysed to a greater degree from PC. The size of the fat globules of all creams increased in the stomach. Protein aggregates were observed in pasteurised and homogenised cream chyme. Protrusions, probably caused by the accumulation of insoluble lipolytic products, appeared at the surface of the globules in RC and PC chyme. Overall, PC proteins and lipids appeared to be digested to a greater extent.