Gene expression in human subcutaneous adipose tissue after administration of Gastric Insulinotropic Peptide (GIP)
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE40589 | GEO | 2012/09/05
SECONDARY ACCESSION(S): PRJNA174352
REPOSITORIES: GEO
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Project description:The intention of this clinical study was to investigate the effect of GIP administration for 240 min on gene expression in human subcutaneous adipose tissue. Three conditions have been tersted: 1. Sole infusion of GIP or NaCl as control; 2. GIP or NaCl administration under euglycemic-hyperinsulinemic clamp conditions; 3. GIP or NaCl administration under hyperglycemic-hyperinsulinemic clamp conditions to mimic the postprandial state. In each participant a complete physical examination and evaluation of medical history was performed, including an oral glucose tolerance test (oGTT) with 75 g glucose after overnight fast to ensure the metabolic state. Standard fasting laboratory and clinical chemistry evaluations were done. Synthetic human GIP (1-42) was dissolved in saline (0.9% NaCl-solution) under sterile conditions. All studies were done in the morning in the overnight fasted state (>10h since last meal). The effect of GIP administration on gene expression in subcutaneous adipose tissue was studied under 3 different conditions in a single blind design. Either the participants received only a GIP- or a saline- infusion (0.9% NaCl-isotonic solution, Fresenius, Germany) for 240 min. At different investigation days participants underwent euglycemic (EU)- and hyperglycemic (HC), hyperinsulinemic clamps combined with GIP- or placebo-infusions for 240 min at different examination days in a randomized, single-blind, crossover design. The capillary glucose concentration was 80mg/dl during EU-clamp and 140mg/dl during HC-clamp. The following numbers of treatments were performed: EU with GIP-infusion (N=9); EU with NaCl-infusion (N=9); HC with GIP-infusion (N=8), HC with NaCl-infusion (N=8); sole GIP-infusion (N=11) and sole placebo-infusion (N=11). Between examination days an intermission time of at least 7 days was maintained.
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Project description:Cellular and tissue defects associated with insulin resistance are coincident with transcriptional abnormalities and are improved after insulin sensitization with thiazolidinedione (TZD) PPAR? ligands. We transcriptionally profiled 364 biopsies gathered from 72 human subjects harvested before and after hyperinsulinemic-euglycemic clamp, at baseline and after three-month TZD treatment. Subjects range from insulin-sensitive to insulin-resistant. Insulin resistant subjects responded to TZD treatment with varied improvements in insulin sensitivity, thus they were ranked by their degree of TZD response to define responder and non-responder subgroups. Skeletal muscle biopsies were obtained from vastus lateralis before and after hyperinsulinemic-euglycemic clamp, at baseline and after three-month TZD treatment. Adipose tissue biopsies were obtained from abdominal subcutaneous before clamp, at baseline and after three-month TZD treatment. *** CEL files not provided for 40 Samples. ***
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Project description:The goal of this study was to analyse the effect of a 12 weeks treatment with rosiglitazone on insulin sensitivity in the muscle of type 2 diabetic patients. Ten diabetic patients were submitted to a 3 hours euglycemic-hyperinsulinemic clamp. Skeletal muscle biopsies were taken before and after the clamp. Samples from the same patients (obtained before and after the clamp) were hybridized on the same microarray. Biopsie taken before the clamp was considered as the control. Then, the patients were treated with rosiglitazone, agonist of PPAR gamma, during 12 weeks. After the treatment, all the patients were submitted to a second 3 hours euglycemic-hyperinsulinemic clamp. Skeletal muscle biopsies for 7 patients were taken before and after the clamp. Samples from the same patients (obtained before and after the clamp) were hybridized on the same microarray. Biopsie taken before the clamp was considered as the control. Set of arrays that are part of repeated experiments Compound Based Treatment: patient biopsies taken before (no) and after (yes) rosiglitazone (TZD) treatment`
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Project description:To identify insulin responsive genes in humans, in the first protocol, skeletal muscle biopsies from six non-diabetic subjects were obtained before and after a two-hour of hyperinsulinaemic (infusion rate 40 mU/m2/min) euglycemic clamp. A variable infusion of glucose (180 g/l) enriched with tritiated glucose (100 μCi/500 ml) maintained euglycemia during insulin infusion, with monitoring of plasma glucose concentration every 5 to 10 min during the basal and clamp periods using an automated glucose oxidation method (Glucose Analyzer 2, Beckman Instruments, Fullerton, CA). In the second protocol, skeletal muscle biopsies from six non-diabetic subjects were obtained before and after a 3-hour hyperinsulinemic (infusion rate 40 mU/m2/min) euglycemic clamp in order to increase the effects of insulin on gene expression. A variable infusion of glucose (180 g/l) was used to maintain euglycemia during insulin infusion with monitoring of plasma glucose concentration every 5 to 10 min using an automated glucose oxidation method (Glucose Analyzer 2, Beckman Instruments, Fullerton, CA). Keywords: dose response The muscle biopsies were obtained from the vastus lateralis muscle under local anesthesia before and after hyperinsulinaemic (infusion rate 40 mU/m2/min) euglycemic clamp
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Project description:High intakes of carbohydrates, particularly sucrose, in Western societies are associated with the development of non-alcoholic fatty liver (NAFL) and diabetes mellitus. It is unclear whether this is related to the carbohydrate quantity or the hormonal responses, particularly Glucose-dependent Insulinotropic Polypeptide (GIP) which is released in the proximal intestine. We, therefore, used the glucose-fructose dimer as proximally resorbed, 1,4-linked sucrose or distally resorbed 1,6-linked palatinose. Palatinose compared to sucrose, indeed, resulted in slower glucose absorption and reduced postprandial insulin and GIP levels. After 22 weeks of isocaloric diets, palatinose feeding prevented hepatic steatosis (48.5%) compared to sucrose and improved glucose tolerance, without differences in body composition and food intake. Ablation of GIP receptor (GIPR) signaling in Gipr-/- mice completely prevented the deleterious metabolic effects of sucrose feeding. Furthermore, our microarray analysis indicated that sucrose increased the hepatic expression of Suppressor of Cytokine Signaling 2 (SOCS2), which is involved in the growth hormone signaling pathway and participates in the development of NAFL. Our results suggest that the site of glucose absorption and the GIP response determine liver fat accumulation and insulin resistance. GIP may play a role in sucrose induced fatty liver by regulating the expression of SOCS2. Expression data from liver tissue of mice fed with isocaloric diets containing either sucrose or palatinose
2014-12-05 | E-GEOD-54723 | biostudies-arrayexpress
Project description:High intakes of carbohydrates, particularly sucrose, in Western societies are associated with the development of non-alcoholic fatty liver (NAFL) and diabetes mellitus. It is unclear whether this is related to the carbohydrate quantity or the hormonal responses, particularly Glucose-dependent Insulinotropic Polypeptide (GIP) which is released in the proximal intestine. We, therefore, used the glucose-fructose dimer as proximally resorbed, 1,4-linked sucrose or distally resorbed 1,6-linked palatinose. Palatinose compared to sucrose, indeed, resulted in slower glucose absorption and reduced postprandial insulin and GIP levels. After 22 weeks of isocaloric diets, palatinose feeding prevented hepatic steatosis (48.5%) compared to sucrose and improved glucose tolerance, without differences in body composition and food intake. Ablation of GIP receptor (GIPR) signaling in Gipr-/- mice completely prevented the deleterious metabolic effects of sucrose feeding. Furthermore, our microarray analysis indicated that sucrose increased the hepatic expression of Suppressor of Cytokine Signaling 2 (SOCS2), which is involved in the growth hormone signaling pathway and participates in the development of NAFL. Our results suggest that the site of glucose absorption and the GIP response determine liver fat accumulation and insulin resistance. GIP may play a role in sucrose induced fatty liver by regulating the expression of SOCS2.
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Project description:This study was undertaken to test the hypothesis that short term exposure (4 hours) to physiologic hyperinsulinemia in normal, healthy subjects without a family history of diabetes would induce a low grade inflammatory response, independently of glycemic status. We performed euglycemic hyperinsulinemic (80 mU/m2/min) clamps in 12 healthy, insulin sensitive subjects with no family history of diabetes followed by biopsies of the vastus lateralis muscle taken basally and after 30 and 240 minutes of insulin infusion. Gene expression profiles were generated using Affymetrix HG-U133A arrays. No probe sets had significantly altered expression at 30 minutes of the insulin clamp, but 121 probe sets (117 upregulated and 4 downregulated) were significantly altered after 240 minutes. Hyperinsulinemia in normal, healthy human subjects increased the mRNAs for a number of inflammatory genes and transcription factors. Microarray and quantitative RT-PCR revealed the upregulation of chemokine, cc motif, ligand 2 (CCL2), CCL8, thrombomodulin (THBD), ras-related associated with diabetes (RRAD), metallothionein (MT), and serum/glucocorticoid regulated kinase (SGK), and downregulation of CITED2 (a CREB-binding protein-interacting transactivator), a known coactivator of PPAR-alpha. Interestingly, SGK and CITED2 are located at chromosome 6q23, where we previously detected strong linkage to hyperinsulinemia. A control saline infusion performed on 3 normal, healthy subjects without a family history of diabetes demonstrated that the genes altered following the euglycemic-hyperinsulinemic clamp were due to insulin and independent of biopsy removal. This study demonstrates that insulin acutely regulates the expression of genes involved in inflammation and transcription, and identifies several candidate genes/pathways for further investigation. Experiment Overall Design: Twelve subjects received a vastus lateralis muscle biopsy followed by a 180-min euglycemic, hyperinsulinemic (80 mU/m2.min) clamp. Muscle biopsies from each subject were homogenized in RNAStat solution (Tel-Test Inc., Friendswood, TX), using a Polytron homogenizer (Brinkmann Instruments Westbury, NY). Total RNA was purified with RNeasy and DNase I treatment (Qiagen, Chatsworth, CA). RNA was prepared for hybridization to Affymetrix (Santa Clara, CA) HG-U133A arrays according to the manufacturerâs instructions.
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