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Time-dependent network analysis reveals molecular targets underying the development of diet-induced obesity and non-alcoholic steatohepatitis.

ABSTRACT: Core diet-induced obesity networks were constructed using Ingenuity pathway analysis (IPA) based on 332 high-fat diet responsive genes identified in liver by time-course microarray analysis (8 time-points over 24 weeks) of high-fat diet fed mice compared to normal diet fed mice. IPA identified five core diet-induced obesity networks with time-dependent gene expression changes in liver. When we merged core diet-induced obesity networks, Tlr2, Cd14 and Ccnd1 emerged as hub genes associated with both liver steatosis and inflammation and were altered in a time-dependent manner. Further protein-protein interaction network analysis revealed Tlr2, Cd14 and Ccnd1 were inter-related through the ErbB/insulin signaling pathway. Dynamic changes occur in molecular networks underlying diet-induced obesity. Tlr2, Cd14 and Ccnd1 appear to be hub genes integrating molecular interactions associated with the development of NASH. Therapeutics targeting hub genes and core diet-induced obesity networks may help ameliorate diet-induced obesity and NASH.

ORGANISM(S): Mus musculus

PROVIDER: GSE40481 | GEO | 2014/03/01

SECONDARY ACCESSION(S): PRJNA174123

REPOSITORIES: GEO

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Time-dependent network analysis reveals molecular targets underying the development of diet-induced obesity and non-alcoholic steatohepatitis.

Project description:Core diet-induced obesity networks were constructed using Ingenuity pathway analysis (IPA) based on 332 high-fat diet responsive genes identified in liver by time-course microarray analysis (8 time-points over 24 weeks) of high-fat diet fed mice compared to normal diet fed mice. IPA identified five core diet-induced obesity networks with time-dependent gene expression changes in liver. When we merged core diet-induced obesity networks, Tlr2, Cd14 and Ccnd1 emerged as hub genes associated with both liver steatosis and inflammation and were altered in a time-dependent manner. Further protein-protein interaction network analysis revealed Tlr2, Cd14 and Ccnd1 were inter-related through the ErbB/insulin signaling pathway. Dynamic changes occur in molecular networks underlying diet-induced obesity. Tlr2, Cd14 and Ccnd1 appear to be hub genes integrating molecular interactions associated with the development of NASH. Therapeutics targeting hub genes and core diet-induced obesity networks may help ameliorate diet-induced obesity and NASH. Total RNA obtained from isolated liver of C57BL/6J mice fed normal diet or high fat diet for 0, 2, 4, 6, 8, 12, 16, 20 and 24 weeks.

2014-03-01 | E-GEOD-40481 | biostudies-arrayexpress

Toll-like receptors 2 and 4 control adaptive β-cell expansion in diet-induced obesity

Project description:Adult pancreatic β cells are refractory to proliferation, a roadblock for the treatment of insulin-deficient diabetes. Consumption of energy-dense Western or high-fat diet (HFD) triggers mild adaptive β cell mass expansion to compensate for peripheral insulin resistance; however, the underlying molecular mechanism remains unclear. Here we show that Toll-like receptors (TLR) 2/TLR4 act as molecular “brakes” for diet-induced β cell replication in both mice and humans. The combined loss of TLR2/TLR4, but not individually, dramatically increases facultative β, not α, cell replication, leading to progressively enlarged islet mass and hyperinsulinemia in diet-induced obesity. Mechanistically, loss of TLR2/TLR4 increases β cell proliferation and nuclear abundance of Cyclin D2 and CDK4 in an extracellular signal-regulated kinase (ERK)-dependent manner. These data reveal a novel mechanism governing adaptive β cell mass expansion in diet-induced obesity and suggest that selective targeting of TLR2/TLR4 pathways may hold promise for reversing β cell failure in diabetic patients.

2019-03-21 | GSE101392 | GEO

Mus musculus

Project description:Diet-induced obesity Kozak1_ABI_ING

| PRJNA96737 | ENA

Protection from obesity and diabetes by blockade of TGF-beta/Smad3 signaling

Project description:Imbalances in glucose and energy homeostasis are at the core of the worldwide epidemic of obesity and diabetes. Here, we illustrate an important role of the TGF-beta/Smad3 signaling pathway in regulating glucose and energy homeostasis. Smad3 deficient mice are protected from diet-induced obesity and diabetes. Interestingly, the metabolic protection is accompanied by Smad3-/- white adipose tissue acquiring the bioenergetic and gene expression profile of brown fat/skeletal muscle. Smad3-/- adipocytes demonstrate a marked increase in mitochondrial biogenesis, with a corresponding increase in basal respiration, and Smad3 acts as a repressor of PGC-alpha1 expression. We observe significant correlation between TGF-beta1 levels and adiposity in rodents and humans. Further, systemic blockade of TGF-beta1 signaling protects mice from obesity, diabetes and hepatic steatosis. Together, these results demonstrate that TGF-beta signaling regulates glucose tolerance and energy homeostasis and suggest that modulation of TGF-beta1 activity might be an effective treatment strategy for obesity and diabetes. Smad3-/- and WT mice were fed with regular diet (RD) and high fat diet (HFD), and diet induced obese (DIO) mice were treated with IgG and anti-TGF-b1 antibody

2011-07-12 | E-GEOD-28598 | biostudies-arrayexpress

Expression data from mouse liver tumor-initiating cells.

2014-09-16 | GSE61435 | GEO

Expression data from mouse liver tumor-initiating cells.

Project description:We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process. Goal and objectives: To study the requirement of HCV viral proteins and/or environmental factors (such as alcohol or obesity) in synergistic liver caner development in HCV Core or NS5A Tg mice given alcohol or high-cholesterol high-fat diet, mice were fed alcohol or high-cholesterol high-fat diet and liver tissues from these mice were examined for gene profiles. Alcohol or obesity contributes to synergistic tumor incidence and HCV Core or Ns5a-induced effects. Thus, analysis of gene profiling of these transgenic mice will identify the critical pathways to induce synergistic tumor formation caused by alcohol or obesity. Liver samples for RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain gene profiling data in order to increase understanding the pathways. To perform gene array and proteomic analyses, mice were fed alcohol or high-cholesterol high-fat for 12 months and euthanized after 12 months feeding. Livers were collected at the time of euthanasia.

2014-09-16 | E-GEOD-61435 | biostudies-arrayexpress

Project description:High-fat diet induced obesity mice

| PRJNA543567 | ENA

Luteolin protects against obese sarcopenia in mice with high-fat diet-induced obesity by ameliorating inflammation and protein degradation in muscle

Project description:Although there are studies on obesity and sarcopenia, our understanding of obesity-mediated sarcopenia is insufficient. Additionally, no studies have investigated the application of luteolin in sarcopenia. We attempted to determine the effect of luteolin on obese sarcopenia in mice with high-fat diet (HFD)-induced obesity. Luteolin exerted suppressive effects on obesity, inflammation, and protein degradation in HFD-fed obese mice. Luteolin inhibited lipid infiltration into the muscle and decreased p38 and JNK activity and mRNA expression of inflammatory factors, such as TNFα, Tlr2, Tlr4, MCP1, and MMP2, in the muscle. Suppression of muscle inflammation by luteolin led to the inhibition of myostatin, FoxO, atrogin, and MuRF expression, which reduced protein degradation and improved muscle function. This is the first study to demonstrate that luteolin exerts a protective effect against obese sarcopenia, as its anti-obesity and anti-inflammatory activities inhibited protein degradation. Therefore, luteolin may be a useful supplement for prevention of obese sarcopenia.

2022-07-27 | GSE209778 | GEO

microRNA expression profiles in myocardium of diet-induced obesity rat

Project description:Diet induced obesity in rat was associated with myocardial dysfunction, hypertension and fibrosis. This study aimed to explore microRNA expression profiles in diet obesity-induced rat myocardium. Wistar rats were feed normal chow or high-fat diet for 20 weeks. After that, cardiac function was evaluated by echocardiography. Left ventricular myocardium was harvest to assess the extent of hypertension and fibrosis, meanwile, the left ventricular microRNA expression was analyzed using Agilent Rat miRNA microarray. Significant cardiac dysfunction, hypertension and fibrosis were found in diet-induced obesity rats as compared with normal diet rats. rno-miR-141-3p and rno-miR-144-3p were also significantly increased in myocardium of diet-induced obesity rat. These findings suggest that specific miRNA differences may contribute to the alteration in cardiac function, hypertension and fibrosis which responses to diet-induced obesity.

2020-01-07 | GSE143168 | GEO

Diet Induced Obesity Signature in Mouse Liver Tissue

Project description:The purpose of this experiment was to determine the murine liver expression traits that were changed in response to diet induced obesity. Keywords: diet induced obesity signature

2007-02-17 | GSE7028 | GEO

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