Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA226236 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:A low meal frequency improves 24h metabolic and gene expression profiles in subjects with impaired glucose tolerance
| PRJNA226232 | ENA
Project description:A low meal frequency improves 24h metabolic and gene expression profiles in subjects with impaired glucose tolerance (PBMC)
| PRJNA226235 | ENA
Project description:Meal frequency regulates postprandial glucose and insulin responses, which may affect substrate partitioning and thus weight control. This study investigated the effects of meal frequency on the metabolic and transcriptomic profiles in subjects with impaired glucose tolerance (IGT). Eleven IGT (2h glucose; 9.0±0.3mmol/L) men stayed 2x 36 hours in a respiration chamber to measure substrate partitioning. All subjects randomly received two isoenergetic diets with a low meal frequency (3x-LFr) or a high meal frequency (14x-HFr) consisting of 15 En% prot, 30 En% fat, and 55 En% carb. Total glucose output (AUC), carbohydrate oxidation and whole body RQ significantly decreased, and FFA levels increased in the LFr diet. The HFr diet resulted in an up-regulation in expression of genes involved in immune function and inflammation after 24h in PBMCs and muscle tissue. Expression of genes involved in PPAR signalling, OXPHOS, and glutathione metabolism were up-regulated in the HFr diet in muscle tissue only. In conclusion, the LFr diet improved the metabolic and transcriptomic profiles, and appetite control compared to the HFr diet. This suggests that a LFr diet might be an effective dietary strategy with anti-inflammatory characteristics to increase metabolic flexibility and body weight control in IGT subjects.
2020-11-01 | GSE52027 | GEO
Project description:Meal frequency regulates postprandial glucose and insulin responses, which may affect substrate partitioning and thus weight control. This study investigated the effects of meal frequency on the metabolic and transcriptomic profiles in subjects with impaired glucose tolerance (IGT). Eleven IGT (2h glucose; 9.0±0.3mmol/L) men stayed 2x 36 hours in a respiration chamber to measure substrate partitioning. All subjects randomly received two isoenergetic diets with a low meal frequency (3x-LFr) or a high meal frequency (14x-HFr) consisting of 15 En% prot, 30 En% fat, and 55 En% carb. Total glucose output (AUC), carbohydrate oxidation and whole body RQ significantly decreased, and FFA levels increased in the LFr diet. The HFr diet resulted in an up-regulation in expression of genes involved in immune function and inflammation after 24h in PBMCs and muscle tissue. Expression of genes involved in PPAR signalling, OXPHOS, and glutathione metabolism were up-regulated in the HFr diet in muscle tissue only. In conclusion, the LFr diet improved the metabolic and transcriptomic profiles, and appetite control compared to the HFr diet. This suggests that a LFr diet might be an effective dietary strategy with anti-inflammatory characteristics to increase metabolic flexibility and body weight control in IGT subjects.
2020-11-01 | GSE52026 | GEO
Project description:Bezafibrate (BEZ), a pan activator of peroxisome proliferator-activated receptors (PPARs), is generally used to treat hyperlipidemia. Clinical trials on patients suffering from type 2 diabetes indicated that BEZ also has beneficial effects on glucose metabolism, but the underlying mechanisms remain elusive. Much less is known about the function of BEZ in type 1 diabetes. Here, we show that BEZ treatment markedly improves hyperglycemia, glucose and insulin tolerance in streptozotocin (STZ)-treated mice, an insulin-deficient mouse model of type 1 diabetes presenting with very high blood glucose levels. Furthermore, BEZ-treated mice also exhibited improved metabolic flexibility as well as an enhanced mitochondrial mass and function in the liver. Our data demonstrate a beneficial effect of BEZ treatment on STZ mice reducing diabetes and suggest that BEZ ameliorates impaired glucose metabolism possibly via augmented hepatic mitochondrial performance, improved insulin sensitivity and metabolic flexibility. We performed gene expression microarray analysis on liver tissue derived from streptozotocin-treated mice treated with bezafibrate in addition.
2016-06-29 | E-GEOD-79008 | biostudies-arrayexpress
Project description:Liver transcriptome profile in subjects with impaired glucose metabolism and steatosis >3 revealed differences compared with subjects with steatosis <1 and normal glucose tolerance. Several well-characterized markers of non-alcoholic fatty liver disease (NAFLD) were identified as differentially expressed between the two groups.
2022-03-09 | GSE177050 | GEO
Project description:Insulin resistance represents a hallmark during the development of type 2 diabetes mellitus (T2D) and in the pathogenesis of obesity-associated disturbances of glucose and lipid metabolism 1,2,3. MicroRNA (miR)-dependent posttranscriptional gene silencing has recently been recognized to control gene expression in disease development and progression including that of insulin-resistant T2D. MiRs, whose deregulation alters hepatic insulin sensitivity include miR-143, miR-181 and miR-103/107. Here we report that expression of miR-802 is increased in liver of two obese mouse models and of obese human subjects. Inducible transgenic overexpression of miR-802 in mice causes impaired glucose tolerance and attenuates insulin sensitivity, while reduction of miR-802 expression improves glucose tolerance and insulin action. We identify Hnf1b as a target of miR-802-dependent silencing and shRNA-mediated reduction of Hnf1b in liver causes glucose intolerance, impairs insulin signaling and promotes hepatic gluconeogenesis. In turn, hepatic overexpression of Hnf1b improves insulin sensitivity in db/db mice. Thus, the present study defines a critical role for deregulated expression of miR-802 in the development of obesity-associated impairment of glucose metabolism via targeting Hnf1b and assigns Hnf1b an unexpected role in the control of hepatic insulin sensitivity.
2012-11-10 | GSE42188 | GEO
Project description:First version (1.0) of the Eindhoven Diabetes Simulator (EDES) model, describing postprandial glucose and insulin dynamics for a healthy human. Model can also be used to simulate insulin resistance (pre-diabetes, Metabolic Syndrome) and Type 2 Diabetes Mellitus (T2DM). Next to simulating a meal, the model can simulate oral glucose tolerance tests (OGTT's).
2024-07-11 | MODEL2403070001 | BioModels
Project description:Bezafibrate (BEZ), a pan activator of peroxisome proliferator-activated receptors (PPARs), is generally used to treat hyperlipidemia. Clinical trials on patients suffering from type 2 diabetes indicated that BEZ also has beneficial effects on glucose metabolism, but the underlying mechanisms remain elusive. Much less is known about the function of BEZ in type 1 diabetes. Here, we show that BEZ treatment markedly improves hyperglycemia, glucose and insulin tolerance in streptozotocin (STZ)-treated mice, an insulin-deficient mouse model of type 1 diabetes presenting with very high blood glucose levels. Furthermore, BEZ-treated mice also exhibited improved metabolic flexibility as well as an enhanced mitochondrial mass and function in the liver. Our data demonstrate a beneficial effect of BEZ treatment on STZ mice reducing diabetes and suggest that BEZ ameliorates impaired glucose metabolism possibly via augmented hepatic mitochondrial performance, improved insulin sensitivity and metabolic flexibility.
2016-06-29 | GSE79008 | GEO
Project description:Insulin resistance represents a hallmark during the development of type 2 diabetes mellitus (T2D) and in the pathogenesis of obesity-associated disturbances of glucose and lipid metabolism 1,2,3. MicroRNA (miR)-dependent posttranscriptional gene silencing has recently been recognized to control gene expression in disease development and progression including that of insulin-resistant T2D. MiRs, whose deregulation alters hepatic insulin sensitivity include miR-143, miR-181 and miR-103/107. Here we report that expression of miR-802 is increased in liver of two obese mouse models and of obese human subjects. Inducible transgenic overexpression of miR-802 in mice causes impaired glucose tolerance and attenuates insulin sensitivity, while reduction of miR-802 expression improves glucose tolerance and insulin action. We identify Tcf2 as a target of miR-802-dependent silencing and shRNA-mediated reduction of Tcf2 in liver causes glucose intolerance, impairs insulin signaling and promotes hepatic gluconeogenesis. In turn, hepatic overexpression of Tcf2 improves insulin sensitivity in db/db mice. Thus, the present study defines a critical role for deregulated expression of miR-802 in the development of obesity-associated impairment of glucose metabolism via targeting Tcf2 and assigns Tcf2 an unexpected role in the control of hepatic insulin sensitivity. Adenoviruses (Ad5) encoding either GFP (Ad-Ctrl 1-3) or shTcf2 (Ad-shTcf2 1-4) were injected into the tail vein of C57BL/6 mice at 1x10E10 viral particles (VP) per gram bodyweight. Biotin-labeled cDNA was synthesized using GeneChip Whole Transcript Sense Labeling Assay (Affymetrix) according to vendorM-bM-^@M-^Ys instructions. After fragmentation, cDNAs were hybridized for 17h at 45M-BM-0C on Affymetrix Mouse Gene 1.0 ST Arrays. The Arrays were washed and stained in the GeneChip Fluidics Station 450 and scanned on a GeneChip Scanner 3000 7G (Affymetrix). Data intensities were log transformed and normalized with a quantile normalization method using Affymetrix Power Tools. Differentially expressed genes were identified according to statistical evidence indicated by Student's t-test and fold change statistics
2012-11-10 | E-GEOD-42188 | biostudies-arrayexpress