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Adiponectin improves local lipid metabolism in regenerating pancreatic islets after β-cell ablation

ABSTRACT: Pathways that stimulate β-cell regeneration remain of great clinical interest, yet effective therapeutic avenues that promote survival or reconstitution of β-cell mass remain elusive. Utilizing a mouse model with inducible β-cell apoptosis followed by adiponectin-mediated regeneration, we aimed to identify key molecules boosting β-cell viability. Within the regenerating pancreatic islets, we examined changes within the transcriptome, and observed an extensive upregulation of genes encoding proteins involved in lipid transport and metabolism. The most prominent targets were further confirmed by quantitative PCR and immunofluorescence. Among the upstream regulators predicted by pathway analysis of the transcriptome, we detected enhanced levels of two key transcription factors, HNF4α and PPARα. Enhanced leptin levels in circulation may also contribute to the anti-lipotoxic program in islets. In summary, our data suggest that improving local lipid metabolism as an important anti-lipotoxic phenomenon to boost β-cell regeneration, primarily mediated by adiponectin’s action on the β-cells directly as well as on the adipocyte.

ORGANISM(S): Mus musculus

PROVIDER: GSE64787 | GEO | 2015/01/09

SECONDARY ACCESSION(S): PRJNA271874

REPOSITORIES: GEO

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Adiponectin improves local lipid metabolism in regenerating pancreatic islets after β-cell ablation

Project description:Pathways that stimulate β-cell regeneration remain of great clinical interest, yet effective therapeutic avenues that promote survival or reconstitution of β-cell mass remain elusive. Utilizing a mouse model with inducible β-cell apoptosis followed by adiponectin-mediated regeneration, we aimed to identify key molecules boosting β-cell viability. Within the regenerating pancreatic islets, we examined changes within the transcriptome, and observed an extensive upregulation of genes encoding proteins involved in lipid transport and metabolism. The most prominent targets were further confirmed by quantitative PCR and immunofluorescence. Among the upstream regulators predicted by pathway analysis of the transcriptome, we detected enhanced levels of two key transcription factors, HNF4α and PPARα. Enhanced leptin levels in circulation may also contribute to the anti-lipotoxic program in islets. In summary, our data suggest that improving local lipid metabolism as an important anti-lipotoxic phenomenon to boost β-cell regeneration, primarily mediated by adiponectin’s action on the β-cells directly as well as on the adipocyte. RNA profiles of pancreatic islets isolated from PANIC-ATTAT mice crossed with adiponectin wild-type (P-Adn+/+) or the overexpressing transgene (P-AdnTg/+) at 5 weeks after initial dimerizer administration.

2015-01-09 | E-GEOD-64787 | biostudies-arrayexpress

Pig testis extract augments the expression and secretion of adiponectin in 3T3-L1 adipocytes

Project description:Adiponectin is known as a key molecule to ameliorate symptoms of the type 2 diabetes mellitus and disorder of lipid metabolism. In this study, we investigated whether hot water extracts of some livestock by-products induced expression of adiponectin using 3T3-L1 adipocytes. Out of 11 extracts tested, pig testis extracts (PT) enhanced adiponectin mRNA expression and secretion of adiponectin protein from 3T3-L1 cells. Furthermore, simultaneous treatment with PT and daidzein, soy phytoestrogen, enhanced synergistically adiponectin secretion. Moreover, pretreatment with an estrogen receptor β (ERβ) antagonist (PHTPP) diminished adiponectin secretion in daidzein treated cell, but not in PT treated cells. Transcriptome analyses revealed that daidzein and PT commonly regulated PPAR signaling pathway, although gene expression was differently regulated in PT-treated cells and daidzein-treated cells. The expression of 476 and 380 genes significantly up-regulated in daidzein and PT treatment, although commonly regulated genes were only 86 genes. These results suggested that PT may ameliorate lipid metabolic dysfunction via promote adipocytes differentiation and enhance adiponectin secretion through different mechanism from daidzein.

2017-06-30 | GSE92630 | GEO

Endogenous renal adiponectin drives gluconeogenesis through enhancing pyruvate and fatty acid utilization

Project description:Adiponectin is an important secretory protein, primarily produced in adipose tissue. However, low but detectable expression of adiponectin can be observed in cell types beyond adipocytes, particularly in kidney tubular cells, but its local renal role is unknown. We assessed the role of renal adiponectin by utilizing male doxycycline inducible kidney tubular cell-specific adiponectin overexpression or knockout mice. Kidney-specific adiponectin overexpression induces a doubling of phosphoenolpyruvate carboxylase expression and enhanced pyruvate-mediated glucose production, tricarboxylic acid cycle intermediates and an upregulation of fatty acid oxidation (FAO). The inhibition of FAO reduces the adiponectin-induced enhancement of glucose production, highlighting the role of FAO in the induction of renal gluconeogenesis. In contrast, kidney-specific adiponectin deleted mice exhibit enhanced glucose tolerance as well as a lower utilization and greater accumulation of lipid species. In summary, renal adiponectin is a potent inducer of gluconeogenesis by driving enhanced FAO in the kidney and underline the important systemic role of renal gluconeogenesis.

2023-09-20 | GSE242095 | GEO

Adiponectin regulates expression of hepatic genes critical for glucose and lipid metabolism.

2012-09-04 | GSE38144 | GEO

Mus musculus

Project description:Adiponectin improves local lipid metabolism in regenerating pancreatic islets after β-cell ablation

| PRJNA271874 | ENA

Adiponectin regulates expression of hepatic genes critical for glucose and lipid metabolism.

Project description:The effects of adiponectin on hepatic glucose and lipid metabolism at transcriptional level are largely unknown. We profiled hepatic gene expression in adiponectin knockout (KO) and wild-type (WT) mice by RNA-Seq. Comparing to WT mice, adiponectin KO mice exhibited decreased mRNA expression of rate-limiting enzymes in several important glucose and lipid metabolic pathways including glycolysis, TCA cycle, fatty-acid activation and synthesis, triglyceride synthesis and cholesterol synthesis. In addition, binding of the transcription factor Hnf4a to DNAs encoding several key metabolic enzymes was reduced in KO mice, suggesting that adiponectin might regulate hepatic gene expression via Hnf4a. Phenotypically, adiponectin KO mice possessed smaller epididymal fat pads and showed reduced body weights comparing to WT mice. When fed a high fat diet, adiponectin KO mice showed significantly reduced lipid accumulation in the livers. These lipogenic defects are consistent with the downregulation of lipogenic genes in the KO mice. Mice were fasted overnight before euthanization. Liver tissues from WT or adiponectin KO male mice (n = 9-10) at 12 weeks of age were harvested and subjected to total RNA extraction using an RNeasy Plus Mini Kit (Qiagen, Valencia, CA). Total RNA from nine to ten mice of the same strain was pooled together as one biological sample. The mRNA sequencing samples were prepared using the Illumina sample preparation protocol (RS-930-1001, Illumina, Inc. San Diego, CA). The cDNA fragments of 200–250 bp were purified on an agarose gel and then enriched by PCR with Phusion polymerase. The cDNA libraries were sequenced by an Illumina Genome analyzer II at the Whitehead Genome Technology Core.

2012-09-04 | E-GEOD-38144 | biostudies-arrayexpress

Decreases in adiponectin mediate inhibition of regenerative lung growth in obese mice

Project description:Obesity is associated with impairments of wound healing and tissue regeneration. Angiogenesis, the formation of new blood capillaries, plays a key role in organ regeneration and repair. Inhibition of lung angiogenesis impairs regenerative lung growth after unilateral pneumonectomy (PNX). However, the effects of obesity on post-PNX lung vascular and alveolar morphogenesis remain unclear. In this report, we have demonstrated that regenerative lung growth and angiogenic factor VEGFA expression induced by PNX are inhibited in Lepob/ob obese mice compared to Lepob/- mice. The levels of adiponectin, one of the adipokines that exhibits pro-angiogenic and vascular protective properties, increase in endothelial cells (ECs) isolated from remaining mouse lungs after unilateral PNX, while these effects are attenuated in Lepob/ob obese mice. Post-PNX lung growth, vascular and alveolar morphogenesis, and VEGFA levels in the lungs are inhibited in adiponectin knockout mice. Adiponectin agonist, AdipoRon stimulates post-PNX lung growth and vascular and alveolar morphogenesis in Lepob/ob obese mice. These findings suggest that obesity impairs lung vascular and alveolar regeneration and adiponectin may be one of the key molecules to improve lung regeneration in obese people.

2024-11-06 | GSE179227 | GEO

Uncoupling effects of ERalfa on LKB1/AMPK interaction upon adiponectin exposure in breast cancer

Project description:Adipose tissue is a metabolic and endocrine organ that secretes numerous bioactive molecules called adipocytokines. Among these, adiponectin has been argued to have a crucial role in obesity-associated breast cancer. The key molecule of adiponectin signaling is AMP-activated protein kinase (AMPK), mainly activated by Liver Kinase B1 (LKB1). Here, we demonstrated how the ERalfa/LKB1 interaction may negatively interfere with the capability of LKB1 to phosphorylate AMPK and then inhibit its downstream signaling TSC2/mTOR/p70S6k. In MCF-7 cells upon adiponectin AMPK signaling was not working, keeping its downstream protein Acetyl-CoA Carboxylase (ACC) still active. In contrast, in MDA-MB-231 cells the phosphorylation of AMPK and ACC was enhanced with consequent inhibition of both lipogenesis and cell growth. Thus, upon adiponectin, ERalfa signaling switched the energy balance of breast cancer cells towards a lipogenic phenotype. In other words, adiponectin in all the concentrations tested played an inhibitory role on ERalpha-negative breast cancer cell growth and progression either in vitro or in vivo. In contrast, low adiponectin levels, similar to those circulating in obese patients, worked on ERalfa-positive cells as a growth factor, stimulating their growth and progression. The latter effect seems to be blunted in vivo only in the presence of high adiponectin concentration. Based on the present results, it can be concluded that if we prospectively address adiponectin as a pharmacological tool, a separate therapeutic treatment should be carefully assessed in ERalfa-positive and negative breast-cancer patients.

2020-02-27 | E-MTAB-6120 | biostudies-arrayexpress

Gene regulation by full length human adiponectin

Project description:Transcriptionnal profiling of 4 human cell lines treated during 3 hours with human adiponectin Keywords: transcriptionnal analysis Four human cell lines (Hela, HepG2, Panc-1, Hek293) were grown until confluence. These cell lines were serum depleted during 2 hours and then treated with human adiponectin (2,5 µg/ml) during 3 hours. Each adiponectin stimulated cell line was compared to depleted cell line. Depleted cell line was considered as control.

2010-12-09 | E-GEOD-14070 | biostudies-arrayexpress

The transcriptomic profile of porcine anterior pituitary cells is influenced by adiponectin

Project description:Adiponectin is thought to be involved in the regulation of metabolic homeostasis and reproductive processes. Adiponectin controls carbohydrate and lipid metabolism by regulating the fatty acid oxidation process, increasing insulin sensitivity and decreasing plasma triglyceride levels. Adiponectin also plays an important role in the modulation of female reproductive functions, both directly and by influencing the secretory functions of the higher branches of the hypothalamic-pituitary-gonadal axis. The main aim of this study was to determine the effect of adiponectin on global gene expression and on differentially expressed genes (DE-genes) under the influence of the studied hormone in porcine anterior pituitary (AP) cells.

2018-11-09 | GSE122311 | GEO

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