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Elaiophylin reduces body weight and lowers glucose levels in obese mice by activating AMPK

ABSTRACT: Elaiophylin reduces body weight and lowers glucose levels in obese mice by activating AMPK

PROVIDER: PRJNA756907 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15564857_1.fastq.gz	Fastqsanger.gz
	SRR15564857_2.fastq.gz	Fastqsanger.gz
	SRR15564858_1.fastq.gz	Fastqsanger.gz
	SRR15564858_2.fastq.gz	Fastqsanger.gz
	SRR15564859_1.fastq.gz	Fastqsanger.gz

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Elaiophylin reduces body weight and lowers glucose levels in obese mice by activating AMPK

Project description:Obesity is an epidemic affecting 13% of the global population and increasing the risk of many chronic diseases. However, only several drugs are licensed for pharmacological intervention for the treatment of obesity. As a master regulator of metabolism, the therapeutic potential of AMPK is widely recognized and aggressively pursued for the treatment of metabolic diseases. We found that elaiophylin (Ela) rapidly activates AMPK in a panel of cancer cell lines, as well as primary hepatocytes and adipocytes. Meanwhile, Ela inhibits the mTORC1 complex, turning on catabolism and turning off anabolism together with AMPK. In vitro and in vivo studies showed that Ela does not activate AMPK directly; instead, it increases cellular AMP/ATP and ADP/ATP ratios, leading to AMPK phosphorylation in a LKB1-dependent manner. AMPK activation induced by Ela caused changes in diverse metabolic genes, thereby promoting glucose consumption and fatty acid oxidation. Importantly, Ela activates AMPK in mouse liver and adipose tissue. As a consequence, it reduces body weight and blood glucose levels and improves glucose and insulin tolerance in both ob/ob and high fat diet-induced obese mouse models. Our study has identified a novel AMPK activator as a candidate drug for the treatment of obesity and its associated chronic diseases.

2021-10-27 | GSE182566 | GEO

Elaiophylin reduces body weight and lowers glucose levels in obese mice by activating AMPK.

Project description: Not available

| S-EPMC8528873 | biostudies-literature

Akkermansia muciniphila reduces lipid absorption through activating AMPK in the jejunum

Project description:Akkermansia muciniphila (Akk) associated with multiple metabolic diseases and administration of Akk can improve the metabolic disorders. However, little is known about the effect of Akk on jejunal epithelial cells which absorb lipid and interact with oral administrated Akk. We oral administrated Akk to mice and measured the lipid absorption and gene expression in small intestinal epithelial cells. The long-term effect of Akk treatment reduced lipid deposits in the liver and adipocytes with improved the glucose metabolism. This is particularly caused by reduced lipid absorption in jejunal epithelia. Akk feeding reduced the expression of those genes that regulate synthesis and cell cycles, characters of the host cell responding to energy deficiency. In fact, we detected increased AMPK-alpha phosphorylation levels in Akk-treated jejunal epithelial cells both in vivo and in vitro. Furthermore, activating AMPK inhibits lipids absorption in jejunum. Thus, we conclude that oral administration of Akk activates the AMPK pathway and represses the lipid absorption in jejunal epithelial cells, which contributes to the metabolic benefits of oral Akk administration.

2025-01-25 | GSE254234 | GEO

Inhibition of Peripheral Serotonin Activates Hepatic AMPK and Reduces Monocyte-Derived Liver Macrophages, Ameliorating Obesity-Associated Fibrosis

Project description:Monocyte-derived liver macrophages are critical in the pathogenesis of metabolic dysfunction-associated steatohepatitis (MASH) and liver fibrosis, but their recruitment mechanisms remain unclear. Serotonin (5-hydroxytryptamine, 5HT) is a conserved monoamine synthesized by tryptophan hydroxylase (Tph) 1 in peripheral tissues and Tph2 in the brain. We show that in mice housed at thermoneutrality and fed a high-fat, high-fructose diet, inhibition of peripheral serotonin (pe5HT) through genetic deletion of Tph1 prevents MASH independently of reductions in body weight. Liver flow cytometry and single-nuclei sequencing showed reduced pro-inflammatory Ly6Chigh monocytes, monocyte-derived Kupffer cells (moKCs), and lipid-associated macrophages (LAMs) in Tph1 KO mice. Tph1 deletion also decreased circulating monocytes, specifically Ly6Chigh monocytes. A single 5HT injection increased Ly6Chigh monocytes, while Tph1 KO mice had reduced monocytes without affecting bone marrow monocytes. Mechanistically, serotonin inhibition increases liver AMPK activity, and this is important for reducing CCL2 and monocyte recruitment. These findings link two ancient energy sensors, 5HT and AMPK, with obesity-associated liver fibrosis.

2025-10-30 | E-MTAB-15760 | biostudies-arrayexpress

A Novel Selective Inhibitor of Delta-5 Desaturase Lowers Insulin Resistance and Reduces Body Weight in Diet-Induced Obese C57BL/6J Mice.

Project description: Not available

| S-EPMC5104425 | biostudies-literature

Bariatric surgery mediated weight loss reduces breast cancer risk by reducing estrogen receptor alpha activity

Project description:Bariatric surgery mediated weight loss has been shown to significantly reduce breast cancer incidence in women. We hypothesize that loss of excessive adiposity, reduces net Estrogen Receptor Alpha activation which in turn lowers breast cancer risk. A differential gene expression analysis and subsequent pathway enrichment analysis would reveal the relevant molecular mechanism behind the preventive effect of weight loss. We will correlate our RNASeq data findings with serum and breast tissue concentration of hormones as well as expression of proteins regulating hormone synthesis in breast. For this study, we recruited 30 patients who were prescribed baritaric surgery and met our selection criteria (no familial or personal history of breast cancer and free of other confounding conditions). Breast tissue and blood was collected at the day of surgery and at follow up after the patient lost 25% excess body weight. The breast core biopsy was preserved in RNALater till rna isolation and library preparation.

2022-02-20 | GSE126803 | GEO

Long-acting CCK analogue NN9056 lowers food intake and body weight in obese Gottingen Minipigs.

Project description: Not available

| S-EPMC6997118 | biostudies-literature

Chronic Activation of γ2 AMPK Induces Obesity and Reduces Beta Cell Function

Project description:Despite significant advances in our understanding of the biology determining systemic energy homeostasis, the treatment of obesity remains a medical challenge. Activation of AMP-activated protein kinase (AMPK) has been proposed as an attractive strategy for the treatment of obesity and its complications. AMPK is a conserved, ubiquitously expressed, heterotrimeric serine/threonine kinase whose short-term activation has multiple beneficial metabolic effects. Whether these translate into long-term benefits for obesity and its complications is unknown. Here, we observe that mice with chronic AMPK activation, resulting from mutation of the AMPK γ2 subunit, exhibit ghrelin signalling-dependent hyperphagia, obesity and impaired pancreatic islet insulin secretion. Humans bearing the homologous mutation manifest a congruent phenotype. Our studies highlight that long-term AMPK activation can have adverse metabolic consequences with implications for pharmacological strategies seeking to chronically activate AMPK systemically to treat metabolic disease.

2016-05-03 | GSE73436 | GEO

Conjugated linoleic acid activates AMPK and reduces adiposity more effectively when used with metformin

Project description:Trans-10, cis-12 conjugated linoleic acid (t10c12 CLA) causes dramatic reductions in white adipose tissue in mice but has had limited effectiveness in humans. Determination of the signaling pathways involved may lead to better regulation of adiposity. T10c12 CLA was found to activate AMP-activating protein kinase (AMPK), a central regulator of cell metabolism. Compound C, a potent inhibitor of AMPK, prevents many of the typical responses to treatments with t10c12 CLA including the integrated stress response (ISR), the inflammatory response, the reduction in key lipogenic transcription factors, and delipidation. Treatment of adipocytes or mice with t10c12 CLA in conjunction with AMPK activator metformin results in more delipidation than treatment with the individual chemicals. Additionally, the combination showed a reduced inflammatory response relative to a t10c12 CLA treatment alone. The combination of t10c12 CLA and metformin, widely used to treat insulin resistance and Type II diabetes, has potential as a treatment for reducing adiposity in humans. Keywords: control/treatment Mouse 3T3-L1 RNA for was isolated from control linoleic acid (LA) and treatment (CLA, CLA+metformin, metformin) samples for analysis on microarrays with three biological reps.

2009-11-01 | E-GEOD-14888 | biostudies-arrayexpress

Akkermansia muciniphila reduces lipid absorption through activating AMPK in the jejunum

Project description:Akkermansia muciniphila reduces lipid absorption through activating AMPK in the jejunum

| PRJNA1069053 | ENA