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DOI: 10.1055/s-0033-1336673
Endocrine and metabolic effects of dietary intake of probiotics in glucose tolerant humans
Ingestion of probiotics can modify gut microbiota composition, insulin resistance and diabetes development in rodents. In humans, faecal transfer from lean into obese subjects can improve insulin sensitivity. We hypothesized that daily intake of Lactobacillus (L.) reuteri increases insulin sensitivity and secretion in humans by modulating gut hormone secretion.
A prospective, double-blind, randomized, parallel-group trial was performed in 21 glucose tolerant humans (10 obese; age 51 ± 7 years, BMI 35.5 ± 4.9 kg/m2; 11 lean; 49 ± 7 years, 23.6 ± 1.7 kg/m2). Participants ingested 1010 L. reuteri (Nutraceutix, WA, USA) or placebo b.i.d. over 4 weeks. Oral glucose tolerance and matching "isoglycemic” glucose infusion tests were used to assess incretin and insulin secretion, euglycemic-hyperinsulinemic clamps combined with isotopic dilution (6,6[2H2]glucose) to measure peripheral insulin sensitivity (M) and endogenous glucose production (EGP). Muscle and hepatic lipid content were assessed by 1H magnetic resonance spectroscopy. Systemic cytokines, C-reactive protein and lipopolysaccharide (LPS) was measured.
Participants' compliance was confirmed by detection of L. reuteri in stool samples, only from persons ingesting L. reuteri. Glucose-stimulated insulin, C-peptide, and GLP-2 levels increased in L. reuteri-treated subjects (p < 0.05). Subgroup analysis showed that insulin and C-peptide increased in obese (p < 0.05), whereas GLP-2 increased in lean subjects of the L. reuteri group (p < 0.05). Ingestion of L. reuteri did not affect body mass, ectopic lipid content, and immune mediators. M was 37% lower (p < 0.01) in obese than in lean volunteers and remained unchanged. EGP was comparable between groups at baseline and during suppression by insulin, L. reuteri treatment did not affect EGP.
In conclusion, enrichment of gut microbiota with L. reuteri specifically increased insulin and GLP-2 release, but did not affect tissue-specific insulin resistance in humans.