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Oral vancomycin treatment does not alter markers of postprandial inflammation in lean and obese subjects.

ABSTRACT: Intake of a high-fat meal induces a systemic inflammatory response in the postprandial which is augmented in obese subjects. However, the underlying mechanisms of this response have not been fully elucidated. We aimed to assess the effect of gut microbiota modulation on postprandial inflammatory response in lean and obese subjects. Ten lean and ten obese subjects with metabolic syndrome received oral vancomycin 500 mg four times per day for 7 days. Oral high-fat meal tests (50 g fat/m² body surface area) were performed before and after vancomycin intervention. Gut microbiota composition, leukocyte counts, plasma lipopolysaccharides (LPS), LPS-binding protein (LBP), IL-6 and MCP-1 concentrations and monocyte CCR2 and cytokine expression were determined before and after the high-fat meal. Oral vancomycin treatment resulted in profound changes in gut microbiota composition and significantly decreased bacterial diversity in both groups (phylogenetic diversity pre- versus post-intervention: lean, 56.9 ± 7.8 vs. 21.4 ± 6.6, P < 0.001; obese, 53.9 ± 7.8 vs. 21.0 ± 5.9, P < 0.001). After intervention, fasting plasma LPS significantly increased (lean, median [IQR] 0.81 [0.63-1.45] EU/mL vs. 2.23 [1.33-3.83] EU/mL, P = 0.017; obese, median [IQR] 0.76 [0.45-1.03] EU/mL vs. 1.44 [1.11-4.24], P = 0.014). However, postprandial increases in leukocytes and plasma LPS were unaffected by vancomycin in both groups. Moreover, we found no changes in plasma LBP, IL-6 and MCP-1 or in monocyte CCR2 expression. Despite major vancomycin-induced disruption of the gut microbiota and increased fasting plasma LPS, the postprandial inflammatory phenotype in lean and obese subjects was unaffected in this study.

SUBMITTER: Bakker GJ

PROVIDER: S-EPMC6698488 | biostudies-literature | 2019 Aug

REPOSITORIES: biostudies-literature

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Oral vancomycin treatment does not alter markers of postprandial inflammation in lean and obese subjects.

Bakker Guido J GJ Schnitzler Johan G JG Bekkering Siroon S de Clercq Nicolien C NC Koopen Annefleur M AM Hartstra Annick V AV Meessen Emma C E ECE Scheithauer Torsten P TP Winkelmeijer Maaike M Dallinga-Thie Geesje M GM Cani Patrice D PD Kemper Elles Marleen EM Soeters Maarten R MR Kroon Jeffrey J Groen Albert K AK van Raalte Daniël H DH Herrema Hilde H Nieuwdorp Max M

Physiological reports 20190801 16

Intake of a high-fat meal induces a systemic inflammatory response in the postprandial which is augmented in obese subjects. However, the underlying mechanisms of this response have not been fully elucidated. We aimed to assess the effect of gut microbiota modulation on postprandial inflammatory response in lean and obese subjects. Ten lean and ten obese subjects with metabolic syndrome received oral vancomycin 500 mg four times per day for 7 days. Oral high-fat meal tests (50 g fat/m<sup>2</sup ...[more]

PMID: 31423751

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Project description:BackgroundObesity is characterized by low grade inflammation and an altered secretion of inflammatory cytokines from the adipose tissue. Weight loss has shown to reduce inflammation; however, changes in cytokine profiles during massive weight loss are not well described. The present study explored the hypothesis that Roux-en-Y gastric bypass (RYGB) reduces circulating levels of pro-inflammatory cytokines, while increasing anti-inflammatory cytokines in obese subjects with type 2 diabetes (T2D) and in obese normal glucose tolerant (NGT) subjects.MethodsThirteen obese subjects with T2D [weight; 129 ± 14 kg, glycated hemoglobin (HbA1c); 7.0 ± 0.9%, body mass index (BMI); 43.2 ± 5.3 kg/m(2), mean ± SD] and twelve matched obese NGT subjects [weight; 127 ± 15 kg, HbA1c; 5.5 ± 0.4%, BMI; 41.5 ± 4.8 kg/m(2), mean ± SD] were examined before, one week, three months, and one year after surgery. Interleukin (IL)-6, leptin, adiponectin, IL-8, transforming growth factor beta (TGF-β), and the incretin hormone glucagon-like peptide-1 (GLP-1) were measured in the fasting state and during a liquid meal. Insulin resistance was evaluated by HOMA-IR.ResultsWeight loss did not differ between the two groups. Before surgery, HbA1c was higher and HOMA-IR lower in T2D patients, however, converged to the values of NGT subjects one year after surgery. Circulating cytokine concentrations did not differ between the two groups at any time point. One week after surgery, circulating IL-6 and IL-8 were increased, while adiponectin and leptin were reduced compared with pre-surgical concentrations. Three months after surgery, IL-8 was increased, leptin was reduced, and no change was observed for IL-6, TGF-β, and adiponectin. One year after surgery, concentrations of IL-6, TGF-β, and leptin were significantly reduced compared to before surgery, while adiponectin was significantly increased.ConclusionsOne year after RYGB, fasting concentrations of IL-6 and leptin were reduced, while no changes were observed in IL-8. TGF-β was decreased and adiponectin increased in both T2D and NGT obese subjects. This study is the first to examine IL-8 and TGF-β in obese subject after RYGB. Resolution of inflammation could offer a potential explanation for the health improvement associated with major weight loss after bariatric surgery.Trial registrationhttp://www.clinicaltrials.gov (NCT01579981).

Project description:ObjectiveHypercortisolism is a risk factor for obesity. Cortisol increases in response to food intake in lean subjects. In obese subjects, disturbances of the food-induced cortisol peak were reported, but data from sufficiently powered and well-controlled trials are lacking. Understanding the cortisol response to food is essential as amplified or recurrent cortisol surges could lead to hypercortisolism and contribute to obesity. Therefore, we investigate the cortisol response to food in lean and obese subjects.DesignThis is a non-randomized, open-label study.MethodsWe assessed serum cortisol values after a high-calorie meal in lean and obese male subjects. Cortisol levels were frequently assessed before and for 3 h after food intake.ResultsA total of 36 subjects (18 lean and 18 obese) were included. There was no difference in overall cortisol levels between both groups during the study (area under the curve (AUC) obese: 55,409 ± 16,994, lean: 60,334 ± 18,001, P = 0.4). Total cortisol levels reached peak concentrations 20 min after food intake in both groups; the maximum cortisol increase was similar in both groups (cortisol increase obese: 69.6 ± 135.5 nmol/L, lean: 134.7 ± 99.7 nmol/L; P = 0.1). There was no correlation between body mass index and baseline cortisol values (R2 = 0.001, P = 0.83), cortisol increase (R2 = 0.05, P = 0.17), or cortisol AUC (R2 = 0.03, P = 0.28).ConclusionsThis study demonstrates that high-calorie food intake causes an immediate and substantial cortisol response in lean and obese subjects and is independent of body weight.Significance statementThis study demonstrates that high-calorie food intake causes an immediate and substantial cortisol response in lean and obese subjects, independent of body weight. In contrast to the current literature, our findings show that the physiological cortisol response to food is intact in obesity. The substantial and prolonged increase further supports the hypothesis that frequent high-calorie meals cause hypercortisolism and aggravate weight gain.

Dataset Information

Oral vancomycin treatment does not alter markers of postprandial inflammation in lean and obese subjects.

Publications

Oral vancomycin treatment does not alter markers of postprandial inflammation in lean and obese subjects.

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