Home Medizin Das Fehlen von Darmmikroben nach Antibiotika und einer fettreichen Ernährung kann dafür verantwortlich sein, dass zuckerfreie Süßigkeiten und Kaugummi zu Blähungen führen

Das Fehlen von Darmmikroben nach Antibiotika und einer fettreichen Ernährung kann dafür verantwortlich sein, dass zuckerfreie Süßigkeiten und Kaugummi zu Blähungen führen

von NFI Redaktion

It has been observed that approximately 30% of the population in high-income countries suffers from carbohydrate intolerance. The exact mechanism of sorbitol intolerance is still not fully understood. A recent study published in Zelle revealed how a high-fat diet and antibiotic exposure can trigger sorbitol intolerance through the depletion of Clostridium from the gut microbiota.

Study: High-fat intake supports sorbitol intolerance after antibiotic-mediated Clostridium depletion from the gut microbiota. Image credit: liveostockimages/Shutterstock.com
Study: High-fat intake supports sorbitol intolerance after antibiotic-mediated Clostridium depletion from the gut microbiota. Image credit: liveostockimages/Shutterstock.com

Background

Sorbitol is poorly absorbed by the small intestine, resulting in reduced calorie content of foods. It is a naturally occurring polyol found in fruits such as apples, apricots, and pears, as well as in sugar-free gum. Excessive consumption of sorbitol can lead to symptoms of carbohydrate intolerance, including bloating, flatulence, and diarrhea. This is particularly true for patients with irritable bowel syndrome (IBS) or those with quiescent inflammatory bowel disease (IBD).

Antibiotic treatment can temporarily exacerbate polyol intolerance by altering the gut microbiota. This alteration may impact metabolic functions that eliminate osmotically active solutes. Since this effect is temporary, it cannot explain the sustained carbohydrate intolerance in IBD and IBS patients. Therefore, the treatment of persistent polyol intolerance focuses on dietary measures to reduce the intake of polyols and other poorly absorbed oligosaccharides.

About the Study

For this study, male C57BL6/J mice from the Jackson Laboratory were used, which were approximately six weeks old. Furthermore, through the mating of Ppargfl/fl with Villincre/- mice, the researchers were able to generate littermates Ppargfl/flVillin-/ mice and C57BL/6 Ppargfl/flVillincre/- mice. The animals were fed either a (sorbitol-free) 45% fat diet (HF) or a (sorbitol-free) 10% control diet (LF). To examine antibiotic-induced sorbitol intolerance, 20 mg of streptomycin per animal was used.

Study Results

This study developed a mouse model for sustained sorbitol intolerance and provided insights into the pathophysiology of this condition. It was found that the abundance of Clostridium was reduced by a combination of HF diet and antibiotic exposure. This observation challenges the widespread belief that malabsorption causes sustained sorbitol intolerance. HF intake and sustained antibiotic exposure are also environmental risk factors for the pathophysiology of IBD.

In this mouse model, it was demonstrated that a reduced frequency of Clostridium in the fecal microbiota and dampened butyrate production could be functionally related to sustained sorbitol intolerance. These results align well with clinical studies that demonstrate a connection between gastrointestinal symptoms in IBD patients and carbohydrate intake.

An environment that promotes the growth of Clostridium is favored by epithelial hypoxia, which reduces the diffusion of oxygen into the intestinal lumen. When the colonic microbiota is disrupted by antibiotics, there is a breakdown of short-chain fatty acids, altering epithelial metabolism and increasing the availability of oxygen from the host.

Oxidative stress is triggered in host cells by a HF diet, increasing the production of hydrogen peroxide by the mitochondria. This hinders the bioenergetic recovery of the mitochondria after antibiotic treatment, subsequently affecting microbiota recovery. The results presented here suggest that prophylaxis with 5-ASA could promote microbiota recovery and restore epithelial hypoxia following antibiotic exposure, even when the individual is on a HF diet. Thus, the intestinal epithelium could be a potential target for treating sustained sorbitol intolerance.

The results also suggest that the microbiota could be a second target for treatment. This stems from the observation that impaired microbial sorbitol catabolism could lead to prolonged sorbitol intolerance. Probiotics that consume sorbitol, such as L. plantarum or E coli Nissle 1917, could be another treatment option, but the concentration of probiotics in the feces would determine their protective effect.

The data documented here suggest that A. caccae could be a second-generation probiotic targeting both microbes and the host to guard against sorbitol intolerance. It was noted that A. caccae protects against sustained sorbitol intolerance even at a low concentration of probiotics. A. caccae was less effective once microbiota restoration was complete.

Study Limitations

The limitations of the study lie in the use of a mouse model and extrapolation to humans. It was found that antibiotic-naive mice tolerate up to 5% sorbitol. In humans, this equates to a daily intake of 20–30 g, a high dose that can potentially cause symptoms of carbohydrate intolerance in healthy control subjects. Mice tolerate a higher sorbitol intake compared to humans because the human cecum is enlarged to slow down digestion flow, supporting carbohydrate breakdown in the colonic microbiota.

The difference in morphology and function between the gastrointestinal tracts of humans and mice poses the primary constraints of rodent models. Further studies are needed to assess whether probiotics or proliferator-activated receptor-gamma (PPAR-γ) agonists might be able to treat or prevent sorbitol intolerance.

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