Small Intestinal Microbiome Adjusts To Dietary Fats and Sugar

MedicalResearch.com Interview with:

Eugene B. Chang, MD Martin Boyer Professor of Medicine Knapp Center for Biomedical Discovery University of Chicago Chicago, IL  60637

Dr. Chang

Eugene B. Chang, MD
Martin Boyer Professor of Medicine
Knapp Center for Biomedical Discovery
University of Chicago
Chicago, IL  60637 and

Kristina Martinez-Guryn, Ph.D., R.D. Assistant Professor  Biomedical Sciences Program Midwestern University Downers Grove, IL.

Dr. Martinez-Guryn

Kristina Martinez-Guryn, Ph.D., R.D.
Assistant Professor 
Biomedical Sciences Program
Midwestern University
Downers Grove IL

MedicalResearch.com: What is the background for this study? What are the main findings?

Dr. Martinez-Guryn: The original goal of this study was to understand why mice devoid of all microorganisms (germ free mice) are protected from diet-induced obesity. We demonstrate that these mice display severely impaired lipid absorption even when fed a high fat diet.

Dr. Chang: We found that many of the processes of dietary lipid digestion and absorption are dependent on and modulated by the gut microbiome which itself responds to dietary cues to adjust the small intestine’s ability and capacity to handle dietary lipids appropriately. This interplay is important for general health, but the findings are also relevant to conditions of overnutrition (obesity, metabolic syndrome) and undernutrition (starvation, environmental enteropathy).  In conditions of overnutrition, high fat, simple sugar, low fiber foods typical of western diets promote small intestinal microbes (which have been largely neglected by the scientific community) that promote fat digestion and absorption. This increases our capacity to assimilate dietary fats which can contribute to the overnutrition problem.  In conditions of undernutrition, these types of gut microbes are lost or minimally represented.  Thus, when nutritional repletion is started, the gut’s ability to upregulate its capacity for dietary lipid digestion and absorption is compromised.

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Intestinal and Blood-Brain Barrier Alterations Linked to Autism Spectrum Disorders

MedicalResearch.com Interview with:

Maria Rosaria Fiorentino, PhD

Dr. Maria Rosaria Fiorentino

Maria Rosaria Fiorentino, PhD
Assistant Professor at Harvard Medical School
Molecular Biologist at Mucosal Immunology and Biology Research Center
Massachusetts General Hospital East
Charlestown, MA 02129-4404

MedicalResearch.com: What is the background for this study? What are the main findings?

Response: Autism Spectrum Disorders (ASD) refers to complex neurodevelopmental disorders arising from the interaction of genes and environmental factors. There are no defined mechanisms explaining how environmental triggers can lead to these conditions. One hypothesis based on the gut-brain axis connection suggests that inappropriate antigens trafficking through an impaired intestinal barrier, followed by passage of these antigens through a permissive blood-brain barrier (BBB), can be part of the chain of events leading to the disease.

Many Autism Spectrum Disorders children experience co-morbid medical conditions, including gastrointestinal (GI) dysfunctions whose underlying nature is poorly understood. Several clinical observations describe increased intestinal permeability in ASD with often conflicting findings. Permeability to neuroactive food antigens derived from the partial digestion of wheat (gliadorphins) and cow’s milk (casomorphins) has been reported in ASD. However, while evidence of a permeable gut barrier in ASD is increasingly reported, no information is available concerning a similar breach for the BBB. The BBB is a critical line of defense in the Central Nervous System, limiting the access of circulating solutes, macromolecules, and cells that could negatively impact neuronal activity. Dysfunctions of the BBB have been associated with numerous inflammatory neurologic disorders, such as stroke, epilepsy, multiple sclerosis, Parkinson’s and Alzheimer’s disease.

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Bacterial Mix Important For Intestinal Health

Dr. Sridhar Mani MD Departments of Genetics and Medicine Albert Einstein College of Medicine, Bronx, NY 10461MedicalResearch.com Interview with:
Dr. Sridhar Mani MD
Departments of Genetics and Medicine
Albert Einstein College of Medicine
Bronx, NY 10461

 

Medical Research: What are the main findings of the study?

Dr. Mani: In a series of studies using cells grown in the lab and mouse studies, the researchers found that a metabolite called indole 3-propionic acid (IPA)—produced exclusively by so-called commensal bacteria —both strengthens the intestinal epithelium’s barrier function and prevents its inflammation by activating an orphan nuclear receptor, Pregnane X Receptor (PXR). Specifically, PXR activation suppresses production of an inflammatory protein called tumor necrosis factor alpha (TNF-á) while increasing levels of a protein that strengthens the junctions between intestinal epithelial cells (makes the intestines less permeable to noxious substances). Loss of PXR protein and/or IPA results in a disrupted intestinal barrier and increased propensity towards intestinal inflammation and/or toxin induced injury to the intestines.
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