| 1. |
- Attaye, I., et al.
(författare)
-
A Crucial Role for Diet in the Relationship Between Gut Microbiota and Cardiometabolic Disease
- 2020
-
Ingår i: Annual Review of Medicine. - : Annual Reviews. - 0066-4219 .- 1545-326X. - 9780824305710 ; , s. 149-161
-
Bokkapitel (refereegranskat)abstract
- Cardiometabolic disease (CMD), such as type 2 diabetes mellitus and cardiovascular disease, contributes significantly tomorbidity and mortality on a global scale. The gut microbiota has emerged as a potential target to beneficially modulate CMD risk, possibly via dietary interventions. Dietary interventions have been shown to considerably alter gut microbiota composition and function. Moreover, several diet-derived microbial metabolites are able to modulate human metabolism and thereby alter CMD risk. Dietary interventions that affect gut microbiota composition and function are therefore a promising, novel, and cost-efficient method to reduce CMD risk. Studies suggest that fermentable carbohydrates can beneficially alter gut microbiota composition and function, whereas high animal protein and high fat intake negatively impact gut microbiota function and composition. This review focuses on the role of macronutrients (i.e., carbohydrate, protein, and fat) and dietary patterns (e.g., vegetarian/vegan and Mediterranean diet) in gut microbiota composition and function in the context of CMD.
|
|
| 2. |
- Attaye, Ilias, et al.
(författare)
-
Protein supplementation changes gut microbial diversity and derived metabolites in subjects with type 2 diabetes
- 2023
-
Ingår i: ISCIENCE. - 2589-0042. ; 26:8
-
Tidskriftsartikel (refereegranskat)abstract
- High-protein diets are promoted for individuals with type 2 diabetes (T2D). How-ever, effects of dietary protein interventions on (gut-derived) metabolites in T2D remains understudied. We therefore performed a multi-center, randomized -controlled, isocaloric protein intervention with 151 participants following either 12-week high-protein (HP; 30Energy %, N = 78) vs. low-protein (LP; 10 Energy%, N = 73) diet. Primary objectives were dietary effects on glycemic control which were determined via glycemic excursions, continuous glucose monitors and HbA1c. Secondary objectives were impact of diet on gut microbiota composition and-derived metabolites which were determined by shotgun-metagenomics and mass spectrometry. Analyses were performed using delta changes adjusting for center, baseline, and kidney function when appropriate. This study found that a short-term 12-week isocaloric protein modulation does not affect glycemic parameters or weight in metformin-treated T2D. However, the HP diet slightly worsened kidney function, increased alpha-diversity, and production of potentially harmful microbiota-dependent metabolites, which may affect host metabolism upon prolonged exposure.
|
|
| 3. |
- Aydin, Oemruem, et al.
(författare)
-
Post-Bariatric Hypoglycemia: an Impaired Metabolic Response to a Meal
- 2024
-
Ingår i: OBESITY SURGERY. - 0960-8923 .- 1708-0428.
-
Tidskriftsartikel (refereegranskat)abstract
- Aims/Hypothesis Post-bariatric hypoglycemia (PBH) is caused by postprandial hyperinsulinemia, due to anatomical alterations and changes in post-prandial metabolism after bariatric surgery. The mechanisms underlying the failing regulatory and compensatory systems are unclear. In this study, we investigated the differences in post-prandial hormones and metabolic profiles between patients with and without PBH. Methods We performed a mixed meal test (MMT) in 63 subjects before and 1 year after Roux-en-Y gastric bypass (RYGB) surgery. Blood was withdrawn at 0, 10, 20, 30, 60, and 120 min after ingestion of a standardized meal. Glucose, insulin, GLP-1, FGF-19, and FGF-21 were measured and untargeted metabolomics analysis was performed on blood plasma to analyze which hormonal and metabolic systems were altered between patients with and without PBH. Results Out of 63, a total of 21 subjects (33%) subjects developed PBH (glucose < 3.1 mmol/L) after surgery. Decreased glucose and increased insulin excursions during MMT were seen in PBH (p < 0.05). GLP-1, FGF-19, and FGF-21 were elevated after surgery (p < 0.001), but did not differ between PBH and non-PBH groups. We identified 20 metabolites possibly involved in carbohydrate metabolism which differed between the two groups, including increased carnitine and acylcholines in PBH. Conclusion Overall, 33% of the subjects developed PBH 1 year after RYGB surgery. While GLP-1, FGF-19, and FGF-21 were similar in PBH and non-PBH patients, metabolomics analysis revealed changes in carnitine and acyclcholines that are possibly involved in energy metabolism, which may play a role in the occurrence of PBH. [GRAPHICS] .
|
|
| 4. |
|
|
| 5. |
- Bakker, G. J., et al.
(författare)
-
Fecal microbiota transplantation does not alter bacterial translocation and visceral adipose tissue inflammation in individuals with obesity
- 2022
-
Ingår i: Obesity Science & Practice. - : Wiley. - 2055-2238. ; 8:1, s. 56-65
-
Tidskriftsartikel (refereegranskat)abstract
- Aims: Visceral adipose tissue inflammation is a fundamental mechanism of insulin resistance in obesity and type 2 diabetes. Translocation of intestinal bacteria has been suggested as a driving factor for the inflammation. However, although bacterial DNA was detected in visceral adipose tissue of humans with obesity, it is unclear to what extent this is contamination or whether the gut microbiota is causally involved. Effects of fecal microbiota transplantation (FMT) on bacterial translocation and visceral adipose tissue inflammation in individuals with obesity and insulin resistance were assessed. Material and Methods: Eight individuals with clinically severe obesity (body mass index [BMI] >35 kg/m(2)) and metabolic syndrome received lean donor FMT 4 weeks prior to elective bariatric surgery. The participants were age-, sex-, and BMI-matched to 16 controls that underwent no fecal transplantation. Visceral adipose tissue was collected during surgery. Bacterial translocation was assessed by 16S rRNA gene sequencing of adipose tissue and feces. Pro-inflammatory cytokine expression and histopathological analyses of visceral adipose tissue were performed to assess inflammation. Results: Fecal microbiota transplantation significantly altered gut microbiota composition. Visceral adipose tissue contained a very low quantity of bacterial DNA in both groups. No difference in visceral bacterial DNA content between groups was observed. Also, visceral expression of pro-inflammatory cytokines and macrophage infiltration did not differ between groups. No correlation between inflammatory tone and bacterial translocation was observed. Conclusions: Visceral bacterial DNA content and level of inflammation were not altered upon FMT. Thus, bacterial translocation may not be the main driver of visceral adipose tissue inflammation in obesity.
|
|
| 6. |
- Bakker, G. J., et al.
(författare)
-
Fecal Microbiota Transplantation: Therapeutic Potential for a Multitude of Diseases beyond Clostridium difficile
- 2017
-
Ingår i: Microbiology Spectrum. - 2165-0497. ; 5:4
-
Tidskriftsartikel (refereegranskat)abstract
- The human intestinal tract contains trillions of bacteria, collectively called the gut microbiota. Recent insights have linked the gut microbiota to a plethora of diseases, including Clostridium difficile infection (CDI), inflammatory bowel disease (IBD), and metabolic diseases such as obesity, type 2 diabetes (T2D), and nonalcoholic steatohepatitis (NASH). Fecal microbiota transplantation (FMT) is currently tested as a therapeutic option in various diseases and can also help to dissect association from causality with respect to gut microbiota and disease. In CDI, FMT has been shown to be superior to antibiotic treatment. For IBD, T2D, and NASH, several placebo-controlled randomized controlled trials are under way. Moreover, techniques and standardization are developing. With the extension of FMT as a treatment modality in diseases other than CDI, a whole new treatment option may be emerging. Moreover, correlating alterations in specific strains to disease outcome may prove pivotal in finding new bacterial targets. Thus, although causality of the gut microbiota in various diseases still needs to be proven, FMT may prove to be a powerful tool providing us with diagnostic and therapeutic leads.
|
|
| 7. |
- Bakker, G. J., et al.
(författare)
-
Gut microbiota and energy expenditure in health and obesity
- 2015
-
Ingår i: Journal of Clinical Gastroenterology. - 0192-0790 .- 1539-2031. ; 49
-
Tidskriftsartikel (refereegranskat)abstract
- The contribution of intestinal bacterial strains (gut microbiota) to the development of obesity and obesity-related disorders is increasingly recognized as a potential diagnostic and pharmacologic target. Alterations in the intestinal bacterial composition have been associated with presence of chronic low-grade inflammation, a known feature of insulin resistance and type 2 diabetes mellitus. However, causality still needs to be proven. Fecal transplantation studies in germ-free mice have provided crucial insight into the causality of gut microbiota in development of obesity and obesity-related disorders. Moreover, fecal transplantation studies in conjunction with fecal sampling in prospectively followed cohorts will help identify causally involved intestinal bacterial strains in human obesity. Results from these studies will lead to characterization of novel diagnostic markers as well as therapeutic strategies that aim to treat obesity and obesityrelated disorders Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
|
|
| 8. |
- Bakker, G. J., et al.
(författare)
-
Oral vancomycin treatment does not alter markers of postprandial inflammation in lean and obese subjects
- 2019
-
Ingår i: Physiological Reports. - : Wiley. - 2051-817X. ; 7:16
-
Tidskriftsartikel (refereegranskat)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/m(2) 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.
|
|
| 9. |
- Bakker, G. J., et al.
(författare)
-
Pancreatic 18 F-FDG uptake is increased in type 2 diabetes patients compared to non-diabetic controls
- 2019
-
Ingår i: Plos One. - : Public Library of Science (PLoS). - 1932-6203. ; 14:3
-
Tidskriftsartikel (refereegranskat)abstract
- Introduction Increasing evidence indicates that the development of type 2 diabetes is driven by chronic low grade beta-cell inflammation. However, it is unclear whether pancreatic inflammation can be noninvasively visualized in type 2 diabetes patients. We aimed to assess pancreatic 18 F-FDG uptake in type 2 diabetes patients and controls using 18 F-fluorodeoxylglucose positron emission tomography/computed tomography ( 18 F-FDG PET/CT). Material and methods In this retrospective cross-sectional study, we enrolled 20 type 2 diabetes patients and 65 controls who had undergone a diagnostic 18 F-FDG PET/CT scan and obtained standardized uptake values (SUVs) of pancreas and muscle. Pancreatic SUV was adjusted for background uptake in muscle and for fasting blood glucose concentrations. Results The maximum pancreatic SUVs adjusted for background muscle uptake (SUV max.m ) and fasting blood glucose concentration (SUV glucose ) were significantly higher in diabetes patients compared to controls (median 2.86 [IQR 2.24–4.36] compared to 2.15 [IQR 1.51–2.83], p = 0.006 and median 2.76 [IQR 1.18–4.34] compared to 1.91 [IQR 1.27–2.55], p<0.001, respectively). In linear regression adjusting for age and body mass index, diabetes remained the main predictor of SUV max.m and SUV glucose . Conclusion Pancreatic 18 F-FDG uptake adjusted for background muscle uptake and fasting blood glucose concentration was significantly increased in type 2 diabetes patients. © 2019 Bakker et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
|
|
| 10. |
- Bakker, G. J., et al.
(författare)
-
Relationship Between Gut Microbiota, Energy Metabolism, and Obesity
- 2016
-
Ingår i: The Microbiota in Gastrointestinal Pathophysiology Implications for Human Health, Prebiotics, Probiotics, and Dysbiosis. - 9780128040621 ; , s. 255-258
-
Bokkapitel (övrigt vetenskapligt/konstnärligt)abstract
- The gut microbiota is increasingly recognized as an important regulator of energy metabolism. Alterations in gut microbiota composition have been associated with the presence of obesity, which is accompanied by a low-grade inflammatory state and increases the risk of several diseases, including type 2 diabetes mellitus. Although causality still needs to be proven, there is a large body of evidence supporting a role for the gut microbiota in the development of obesity and the associated diseases. In this regard, prospective human trials targeting the gut microbiota, using, for example, probiotics or fecal transplantation, are needed. This approach may yield exciting novel diagnostic markers as well as therapeutic targets. In this chapter, we will describe several mechanisms, which may contribute to the influence of the gut microbiota on metabolism, including direct energy extraction from the diet, production of short-chain fatty acids, and bacterial translocation. © 2017 Elsevier Inc. All rights reserved.
|
|
