BackgroundDiet-induced obesity (DIO) is a significant health concern which has been linked to structural and functional changes in the gut microbiota. Exercise (Ex) is effective in preventing obesity, but whether Ex alters the gut microbiota during development with high fat (HF) feeding is unknown.ObjectiveDetermine the effects of voluntary Ex on the gastrointestinal microbiota in LF-fed mice and in HF-DIO.MethodsMale C57BL/6 littermates (5 weeks) were distributed equally into 4 groups: low fat (LF) sedentary (Sed) LF/Sed, LF/Ex, HF/Sed and HF/Ex. Mice were individually housed and LF/Ex and HF/Ex cages were equipped with a wheel and odometer to record Ex. Fecal samples were collected at baseline, 6 weeks and 12 weeks and used for bacterial DNA isolation. DNA was subjected both to quantitative PCR using primers specific to the 16S rRNA encoding genes for Bacteroidetes and Firmicutes and to sequencing for lower taxonomic identification using the Illumina MiSeq platform. Data were analyzed using a one or two-way ANOVA or Pearson correlation.ResultsHF diet resulted in significantly greater body weight and adiposity as well as decreased glucose tolerance that were prevented by voluntary Ex (p<0.05). Visualization of Unifrac distance data with principal coordinates analysis indicated clustering by both diet and Ex at week 12. Sequencing demonstrated Ex-induced changes in the percentage of major bacterial phyla at 12 weeks. A correlation between total Ex distance and the ΔCt Bacteroidetes: ΔCt Firmicutes ratio from qPCR demonstrated a significant inverse correlation (r2 = 0.35, p = 0.043).ConclusionEx induces a unique shift in the gut microbiota that is different from dietary effects. Microbiota changes may play a role in Ex prevention of HF-DIO.

No abstract

No abstract

Most fast excitatory postsynaptic potentials (fEPSPs) recorded from guinea pig ileum myenteric plexus are mediated by acetylcholine acting at nicotinic receptors and ATP acting at P2X receptors. These studies examine length and polarity of projection of neurons releasing mediators of fEPSPs. Under ketamine-xylazine anesthesia, animals were sham treated or myenteric pathways were interrupted. After severed axons degenerated, fEPSPs were recorded at the operated site using conventional, intracellular electrophysiological methods and were classified as nicotinic or mixed on the basis of sensitivity to hexamethonium. Cholinergic and noncholinergic fEPSPs were recorded from small, operated segments, suggesting that some neurons have projections between adjacent ganglia. The mean amplitudes of nicotinic and mixed fEPSPs were reduced after circumferential and descending pathways degenerated. The proportion of nicotinic vs. mixed fEPSPs recorded from tissues lacking descending projections was greater than that recorded from sham-treated tissues, suggesting that fibers releasing noncholinergic mediators project aborally. Descending projections communicate with neurons in ganglia at least three rows aboral to their origin. The data suggest that fast noncholinergic neurotransmission could contribute to hexamethonium-resistant descending inhibition during the peristaltic reflex.

No abstract