Of Microbes and Meals

Abstract

The human intestinal tract is comprised of a rich and complex microbial ecosystem. This intestinal microbota provides a large reservoir of potentially toxic molecules, including bacterial endotoxin (i.e., lipopolysaccharide). This potent inflammatory molecule is detectable in the circulation of healthy individuals and levels transiently increase following ingestion of energy rich meals. Chronic exposure to circulating endotoxin has been associated with obesity, diabetes, and cardiovascular disease. Western-style meals augment LPS translocation and by this mechanism may contribute to the pathogenesis of these diseases. By contrast, the gut and other organs have evolved mechanisms to detoxify endotoxin and to neutralize the potentially inflammatory qualities of circulating endotoxin. Of specific interest to clinicians is evidence that acute postprandial elevation of circulating endotoxin is dependent on meal composition. In this review we present an overview of the biochemical and cellular mechanisms that lead to endotoxemia, with emphasis on the interplay between microbial and nutritional determinants of this condition. The link between endotoxemia, diet, and changes in the intestinal microbiota raise the possibility that dietary interventions can, at least in part, ameliorate the detrimental outcomes of endotoxemia.

Ingestion of bacterial lipopolysaccharide inhibits peripheral taste responses to sucrose in mice

“…Second, pure LPS does not cross the healthy, rat intestinal barrier (Benoit et al, 1998). The intestine is likely healthy in SPF, barrier-housed mice on a standard lab diet, as we used here (Kelly et al, 2012). Ingested L PS is non-toxic even at doses 50X higher than fatal doses of systemic endotoxin (Inagawa et al, 2011), and several mechanisms inactivate or detoxify LPS at the gut mucosa (Kelly et al, 2012).…”

“…The intestine is likely healthy in SPF, barrier-housed mice on a standard lab diet, as we used here (Kelly et al, 2012). Ingested L PS is non-toxic even at doses 50X higher than fatal doses of systemic endotoxin (Inagawa et al, 2011), and several mechanisms inactivate or detoxify LPS at the gut mucosa (Kelly et al, 2012). Mice that ingested LPS in the current work also appear to be in good general health, indicated by the absence of sickness behavior and the maintenance of control-like body temperature and weight, though we cannot rule out more subtle effects on systemic immune responses.…”

Association of Lipopolysaccharide-Binding Protein With Aging-Related Adiposity Change and Prediabetes Among African Ancestry Men

“…In recent years, the gut microbiota have come to be recognized as a contributor to this inflammation (2,3). Gram-negative bacteria contain lipopolysaccharide (LPS) in their outer membranes (4), and through their life cycles the bacteria can shed LPS into the circulation (5).…”

The Immunomodulatory Role of Bile Acids

“…Western-style meals (high-fat diet) invoke an acute postprandial elevation of endotoxin contributing to the pathogenesis of these diseases [43]. Some gut microbiota increase the intestinal permeability, resulting in elevated systemic levels of bacterial LPS, thereby inducing a low-grade systemic inflammation with increased insulin resistance [44,45].…”