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Microarray analyses of the effects of prenatal metformin exposure on the gene expression profile of liver, brain and subcutaneous adipose tissue of neonatal mice

ABSTRACT: The aim of the study was to characterise the effects of prenatal metformin exposure on a tissue gene expression level in mice. The data consists of two models, regular diet (study I) and high fat diet (study II) model. In both models, metformin (300 mg/kg) or control agent (water) was administered to pregnant female mice from the embryonic day E0.5 untill E17.5. In the high fat diet model, the dams had been on a high fat diet (60% of fat) for one month prior to and during the gestation. The diet was changed to regular diet from E18.5. The pups were sacrificed by decapitation at postnatal day 4 and brain (study I), liver (studies I and II) and subcutaneous adipose tissue (study II) were taken for further microarray analyses. In study I,there are 3 replicates in each group of interest: brain_male_ctrl; brain_male_met; liver_male_ctrl; liver_male_met; liver_female_ctrl; liver_female_met. In study II, there are 6 replicates in each group of interest: liver_male_ctrl; liver_male_met; wat_male_ctrl; wat_male_met.

ORGANISM(S): Mus musculus

SUBMITTER: Merja Heinäniemi

PROVIDER: E-GEOD-62612 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Microarray analyses of the effects of prenatal metformin exposure on the gene expression profile of liver, brain and subcutaneous adipose tissue of neonatal mice

Project description:The aim of the study was to characterise the effects of prenatal metformin exposure on a tissue gene expression level in mice. The data consists of two models, regular diet (study I) and high fat diet (study II) model. In both models, metformin (300 mg/kg) or control agent (water) was administered to pregnant female mice from the embryonic day E0.5 untill E17.5. In the high fat diet model, the dams had been on a high fat diet (60% of fat) for one month prior to and during the gestation. The diet was changed to regular diet from E18.5. The pups were sacrificed by decapitation at postnatal day 4 and brain (study I), liver (studies I and II) and subcutaneous adipose tissue (study II) were taken for further microarray analyses.

2014-12-11 | GSE62612 | GEO

Expression data from mouse liver treated with metformin

Project description:Optimal treatment for nonalcoholic steatohepatitis (NASH) has not yet been established, particularly for individuals without diabetes. We examined the effects of metformin, commonly used to treat patients with type 2 diabetes, on liver pathology in a non-diabetic NASH mouse model. Eight-week-old C57BL/6 mice were fed a methionine- and choline-deficient (MCD) + high fat (HF) diet with or without 0.1% metformin for 8 weeks.

2012-02-21 | E-GEOD-35961 | biostudies-arrayexpress

Nobiletin ameliorates high fat-induced disruptions in rhythmic glucagon-like peptide-1 secretion - primary L cells

Project description:RNAseq analysis of sorted primary L cells from mice fed regular chow, regular chow+nobiletin, high-fat diet or high-fat diet+nobiletin.

2022-05-06 | E-MTAB-11538 | biostudies-arrayexpress

Nobiletin ameliorates high fat-induced disruptions in rhythmic glucagon-like peptide-1 secretion - 16S

Project description:16S rRNA gene sequencing of colonic feces from mice fed regular chow, regular chow+nobiletin, high-fat diet or high-fat diet+nobiletin.

2022-05-06 | E-MTAB-11551 | biostudies-arrayexpress

Pleiotropic effects of metformin on inflammation, oxidative and dicarbonyl stress in transgenic spontaneously hypertensive rats expressing human C-reactive protein.

Project description:Inflammation, oxidative and dicarbonyl stress play important roles in the pathophysiology of type 2 diabetes. Metformin is the first-line drug of choice for the treatment of type 2 diabetes because it effectively suppresses gluconeogenesis in the liver, however, its “pleiotropic“ effects remain controversial. In the current study, we tested the effects of metformin on inflammation, oxidative and dicarbonyl stress in an animal model of inflammation and metabolic syndrome, the spontaneously hypertensive rat transgenically expressing human C-reactive protein (SHR-CRP). In the SHR-CRP transgenic strain, we found that metformin treatment decreased circulating levels of inflammatory response marker IL6 while levels of human CRP remained unchanged and metformin also significantly reduced oxidative stress (levels of conjugated dienes and TBARS) in the liver while no significant effects were observed in SHR control rats. In addition, in the presence of high human CRP, metformin reduced methylglyoxal levels in left ventricles but not in kidneys. Finally, metformin treatment reduced adipose tissue lipolysis. Possible molecular mechanisms of metformin action studied by gene expression profiling in the liver revealed deregulated genes from inflammatory, insulin signaling, AMP-activated protein kinase (AMPK) signaling and gluconeogenesis pathways. It can be concluded that in the presence of high levels of human CRP metformin protects against inflammation, oxidative and dicarbonyl stress in the heart and ameliorates insulin resistance and dyslipidemia.

2016-07-03 | E-MTAB-3791 | biostudies-arrayexpress

Gene expression changes in Ahnak knockout mice

Project description:Transcriptional profiling of WAT comparing wild-type control with Ahnak Knockout mice fed regular chow and high fat diet We obtained white adipose tissue from mice fed regular chow and high fat diet for Affymetrix microarrays

2012-04-12 | E-GEOD-37218 | biostudies-arrayexpress

Gene expression changes in aortas of mice on high fat versus regular chow diet.

Project description:To determine effects of hyperglycemia and insulin resistance on arterial wall biology, gene expression profiles were generated using aortas from mice on high fat (35% fat) diet and their respective non diabetic regular chow fed controls. Keywords: Chip Experiment was done in triplicate with three independent pools from test mice on high fat diet and control mice on regular chow diet. For RNA isolation aortas were striped of adventitia and periaortic fat. RNA from three aortas was pooled for the synthesis of probe for affymetrix array analysis.

2011-12-23 | E-GEOD-6735 | biostudies-arrayexpress

Gene Expression in the Human Mammary Epithelium in response to consumption of high fat (H-FAT) and high carbohdyrate (H-CHO) diets.

Project description:Mammary gland (MG) de novo lipogenesis contributes significantly to milk fat in animals but little is known in humans. We hypothesized that de novo lipogenesis, as reflected by incorporation of 13C carbons from [U-13C]glucose into fatty acids (FAs) and glycerol in triglycerides (TG), will be greater: a. in milk than plasma TG, b. during a high carbohydrate (H-CHO) diet than high fat (H-FAT) diet and c. during feeding than fasting. Healthy lactating women were studied on two isocaloric, isonitrogenous diets. On one occasion subjects received diets containing H-FAT or H-CHO diet for 1 week. Incorporation of 13C from infused [U-13C]glucose into FAs and glycerol was measured using GC/MS methodology and gene expression using RNA isolated from breast milk fat globule (MFG). Incorporation of 13C2 into milk FAs, increased with increased chain length of the FAs from C2:0 to C12:0 but progressively declined in C14:0 and C16:0 and was not detected in FAs >C16. During feeding, regardless of diets, enrichment of 13C2 in milk FA and 13C3 in milk glycerol were ~3 and ~7 fold higher compared to plasma FA and glycerol, respectively. Following an overnight fast during H-CHO and H-FAT diets study periods, 25% and 6%, respectively, of medium chain FAs (MCFAs, C6-C12) were derived from glucose but increased to 75% and 25% with feeding. The expression of genes involved in FA or glycerol synthesis pathways was unchanged regardless of diet or fast-fed conditions. Conclusions: The human MG is capable of de novo lipogenesis, of primarily MCFAs and glycerol, which is influenced by the macro-nutrient composition of the maternal diet. On day 7 of consumption of each of the two diets milk samples collected from 7 healthy, lean, exclusively breastfeeding women following an overnight fast and feeding conditions [7 x 2 x 2 = 28 samples] were processed for isotope enrichments and RNA isolation from the milk fat globules. The total RNA was utilized for microarray analyses.

2014-05-19 | E-GEOD-51874 | biostudies-arrayexpress

Whole transcriptome analysis of white adipose tissue in high fat diet induced insulin resistance mice

Project description:To determine the effect of resveratrol or metformin on high fat diet induced insulin resistance mice and elucidate their underlying mechanisms, we conducted a high-throughput sequencing analysis on epididymal fat tissue. LncRNAs and mRNAs were quantified and differentially expressed genes were identified, providing a potential gene signature for pharmacological mechanism of resveratrol and metformin.

2024-09-13 | GSE184366 | GEO

Metformin Targets Intestinal Immune System Signaling Pathways in High-Fat Diet-Induced Type 2 Diabetes Mouse Model

Project description:Research findings of the past decade have highlighted the gut as the main site of action of the oral antihyperglycemic agent metformin despite its pharmacological role in the liver. Extensive evidence supports metformin’s modulatory effect on the composition and function of gut microbiota, nevertheless, the underlying mechanisms of the host responses remain elusive. Our study aimed to evaluate metformin-induced alterations in the intestinal transcriptome profiles at different metabolic states. The high-fat diet-induced type 2 diabetes mouse model of both sexes was developed in a randomized block experiment and bulk RNA-Seq of the ileum tissue was the method of choice for comparative transcriptional profiling after metformin intervention for ten weeks. We found a prominent transcriptional effect of the diet itself with comparatively fewer genes responding to metformin intervention. The overrepresentation of immune-related genes was observed, including pronounced metformin-induced upregulation of immunoglobulin heavy-chain variable regioncoding Ighv1-7 gene in both high-fat diet and control diet-fed animals, supporting the contribution of intestinal immunoglobulin responses. Finally, we provide evidence of the downregulation NF-kappa B signaling pathway in the small intestine of both hyperglycemic and normoglycemic animals after metformin treatment. Moreover, our data pinpoint the gut microbiota as a crucial component in the metformin-mediated downregulation of NF-kappaB signaling evidenced by a positive correlation between the Rel and Rela gene expression levels and abundances of Parabacteroides distasonis, Bacteroides spp., and Lactobacillus spp. in the gut microbiota of the same animals.

2023-08-12 | GSE240206 | GEO

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