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Kdm6 inhibitor as leptin sensitizer in the hypothalamus of high fat diet induced obesity mice

ABSTRACT: Kdm6 inhibitor as leptin sensitizer in the hypothalamus of high fat diet induced obesity mice

PROVIDER: PRJNA473819 | ENA |

REPOSITORIES: ENA

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Kdm6 inhibitor as leptin sensitizer in the hypothalamus of high fat diet induced obesity mice

Project description:To further identify the mostly influenced signal pathways under Kdm6 inhibitor treatment, the microarray analysis was performed to screen the gene expression profile in the hypothalamus of DIO mice. The DIO mice were administrated with vehicle or 30 mg/kg GSK-J4 i.p. for 4 days. Totally, 205 genes were up regulated over 2 fold and 845 genes were down regulated over 2 fold.

2021-05-01 | GSE115113 | GEO

The response of the hypothalamus to leptin and a high-fat diet in mice

Project description:Energy homeostasis is regulated by the hypothalamus but fails when animals are fed a high-fat diet (HFD), and leptin insensitivity and obesity develops. We have used a microarray-based transcriptomics approach to identify novel genes regulated by HFD and leptin in the hypothalamus using mouse global arrays.

2018-09-30 | GSE113943 | GEO

Leptin responsive neurons

Project description:Genome wide association studies (GWAS) in obesity have identified a large number of noncoding loci located near genes expressed in the central nervous system. However, due to the difficulties in isolating and characterizing specific neuronal subpopulations, very few obesity-associated SNPs have been functionally characterized. Leptin responsive neurons in the hypothalamus are essential in controlling energy homeostasis and body weight. Here, we show that by combining FACS-sorting of leptin-responsive hypothalamic neuron nuclei with genomic approaches (RNA-seq, ChIP-seq, ATAC-seq), we can provide a comprehensive map of leptin-response specific regulatory elements, several of which overlap obesity-associated GWAS variants. Further demonstrating the robustness of our leptin-response neuron regulome, we functionally characterize a novel enhancer near Socs3, a leptin response-associated transcription factor. Combined, our results provide a comprehensive map of active genomic regions in leptin-responsive neurons and present a blueprint for functionally characterizing obesity-associated SNPs in the hypothalamus.

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Project description:Leptin resistance is a driving force for obesity and metabolic syndrome. Slug (Snai2 or Snail2) is an epignetic factor that may play a critical role in the development of leptin resistance in obesity. We conducted a microarray to detect molecular targets of Slug in the hypothalamus.

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Central Inhibition of HDAC6 Re-Sensitizes Leptin Signaling During Obesity to Induce Profound Weight Loss

Project description:Leptin resistance during excess weigh gain significantly contributes to the recidivism of obesity to leptin-based pharmacological therapies. The mechanisms underlying the inhibition of Leptin receptor b (LepR) signaling during obesity is still elusive. Here we report that histone deactylase 6 (HDAC6) interacts with LepR, reducing the latter’s activity, and that pharmacological inhibition of HDAC6 activity disrupts this interaction and augments leptin signaling. Treatment of obese mice with blood brain barrier (BBB)-permeable HDAC6 inhibitors profoundly reduces food intake and leads to a potent weight loss without affecting the muscle mass. Genetic depletion of Hdac6 in AgRP-expressing neurons or administration with BBB-impermeable HDAC6 inhibitors result in a lack of such anti-obesity effect. Together, these findings represent the first report describing a mechanistically validated and pharmaceutically tractable therapeutic approach to directly increase LepR activity as well as identifying centrally-, but not peripherally-acting HDAC6 inhibitors as potent leptin-sensitizers and anti-obesity agents.

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Hypothalamus proteomics from mouse models with obesity and anorexia reveals novel therapeutic targets of appetite regulation

Project description:This study examined the proteomic profile of hypothalamus in mouse models of obesity and anorexia

2016-03-11 | PXD003475 | Pride

Fat BodFat Body, Hungry Brain: Nutriproteomics in the Hypothalamus from a Mouse Model with Obesity and Anorexiay, Hungry Brain: Nutriproteomics in the Hypothalamus from a Mouse Model with Obesity and Anorexia

Project description:Systemic acute inflammatory signals can cause profound anorexia by disrupting the physiological appetite regulation in the hypothalamic milieu. Conversely, obesity related chronic inflammation of the hypothalamus can disturb anorexigenic signals and promote abnormal body weight control. The aim of the present study was to compare the global hypothalamic endophenotype in C57/Bl6 mice exposed to a high-fat diet or with acute illness mediated by LPS. Ten-week old male C57/Bl6 mice (n=18) were randomly divided into four groups; the control 1 group (n =3) was fed a normal diet whereas the high-fat diet (HFD) group (n =6) was fed a high-fat diet for eight weeks. The control 2 group (n=3) received an intraperitoneal injection of saline whereas the LPS group (n=6) received an intraperitoneal injection of LPS. Mice were sacrificed 18-hr post-injection. Both control 2 and LPS groups were fed a normal diet for eight weeks before the injection. The hypothalamic regions were removed and analysed using a 2D LC-MS methodology. The proteomic analysis profiled 9,235 proteins (q<0.05) across all biological states, of which 522 proteins were found modulated in the HFD group and another 579 in the LPS group. The proteomic profiles demonstrated that the systemic acute inflammation linked with anorexia induced a negative feedback loop of appetite control in the hypothalamus, suggesting an effort to re-establish homeostasis. By contrast, the chronic inflammation associated with obesity initiated a “perpetual cycle” of positive feedback enhancement of appetite regulation further exacerbating positive energy balance.

2018-01-29 | PXD002119 | Pride

Skeletal glucocorticoid signaling determines aging-related leptin resistance and obesity

Project description:Aging contributes to many chronic conditions, including central obesity, insulin resistance and osteoporosis, which are also critical features of glucocorticoid excess. To investigate tissue-specific sites of glucocorticoid (GC) action during aging, we disrupted GC signalling in mouse osteoblasts via transgenic overexpression of the GC-inactivating enzyme, 11β-hydroxysteroid-dehydrogenase type 2 (11β-HSD2). Wild-type mice with intact osteoblastic GC signalling developed leptin resistance, obesity and insulin resistance with aging. In contrast, transgenic (HSD2OB-tg) mice remained lean and leptin-sensitive, and were protected against aging-related hyperinsulinaemia, blunted sympathetic responses and loss of thermogenic adipose tissue. These salutary effects were independent of the osteoblast-derived factors osteocalcin and lipocalin-2. Gene expression analysis of bones from HSD2OB-tg mice indicated an early induction of pro-osteogenic and anti-adipogenic factors, and activation of a local pro-inflammatory TLR4-ZBTB16-NR1H3 network in osteoblastic cells. These findings reveal a critical role for skeletal glucocorticoid signaling in central leptin action, and in impaired metabolic function with aging

2020-11-09 | GSE141448 | GEO

Gene expression in the hypothalamus that responds to STZ-induced type 1 diabetes and can be reversed by central leptin action

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