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Single-nucleus RNA-sequencing reveals singular gene signatures of human ductal cells during adaptation to insulin resistance

ABSTRACT: Single-nucleus RNA-sequencing reveals singular gene signatures of human ductal cells during adaptation to insulin resistance

PROVIDER: PRJNA855228 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19962919_1.fastq.gz	Fastqsanger.gz
	SRR19962919_2.fastq.gz	Fastqsanger.gz
	SRR19962920_1.fastq.gz	Fastqsanger.gz
	SRR19962920_2.fastq.gz	Fastqsanger.gz
	SRR19962921_1.fastq.gz	Fastqsanger.gz

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Single-nucleus RNA-sequencing reveals singular gene signatures of human ductal cells during adaptation to insulin resistance

Project description:Adaptation to increased insulin demand is mediated by β-cell proliferation and neogenesis among other mechanisms. Although it is known that pancreatic β-cells can arise from ductal progenitors, these observations have been limited mostly to the neonatal period. We have recently reported that the duct is a source of insulin secreting cells in adult insulin resistant states. To further explore the signaling pathways underlying the dynamic β-cell reserve during insulin resistance we undertook human islet and duct transplantations under the kidney capsule of immunodeficient NOD SCID gamma (NSG) mouse models that were either pregnant, insulin resistant or had insulin resistance superimposed upon pregnancy (pregnancy+insulin resistance), followed by single-nucleus RNA-sequencing (snRNA-seq) on snap-frozen graft samples. We observed an upregulation of proliferation markers (e.g., NEAT1), expression of islet endocrine cell markers (e.g., GCG and PPY) as well as mature β-cell markers (e.g., INS), in transplanted human duct grafts in response to high insulin demand. We also noted downregulation of ductal cell identity genes (e.g., KRT19 and ONECUT2) coupled with upregulation of β-cell development and insulin signaling pathways. These results indicate that subsets of ductal cells are able to gain β-cell identity and reflect a form of compensation during the adaptation to insulin resistance in both physiological and pathological states.

2022-07-19 | GSE207393 | GEO

Single-nucleus RNA-Seq reveals singular gene signatures of human ductal cells during adaptation to insulin resistance.

Project description:Adaptation to increased insulin demand is mediated by β cell proliferation and neogenesis, among other mechanisms. Although it is known that pancreatic β cells can arise from ductal progenitors, these observations have been limited mostly to the neonatal period. We have recently reported that the duct is a source of insulin-secreting cells in adult insulin-resistant states. To further explore the signaling pathways underlying the dynamic β cell reserve during insulin resistance, we undertook human islet and duct transplantations under the kidney capsule of immunodeficient NOD/SCID-γ (NSG) mouse models that were pregnant, were insulin-resistant, or had insulin resistance superimposed upon pregnancy (insulin resistance + pregnancy), followed by single-nucleus RNA-Seq (snRNA-Seq) on snap-frozen graft samples. We observed an upregulation of proliferation markers (e.g., NEAT1) and expression of islet endocrine cell markers (e.g., GCG and PPY), as well as mature β cell markers (e.g., INS), in transplanted human duct grafts in response to high insulin demand. We also noted downregulation of ductal cell identity genes (e.g., KRT19 and ONECUT2) coupled with upregulation of β cell development and insulin signaling pathways. These results indicate that subsets of ductal cells are able to gain β cell identity and reflect a form of compensation during the adaptation to insulin resistance in both physiological and pathological states.

| S-EPMC9462484 | biostudies-literature

A singular cockroach insulin-like peptide specific for a male reproductive gland

Project description:A singular cockroach insulin-like peptide specific for a male reproductive gland

| PRJNA1242779 | ENA

Choroid Plexus-Derived Insulin Inhibits Feeding via Direct Signaling through Arcuate Nucleus

Project description:The choroid plexus is an important source of trophic factors for the developing and mature brain. Recently we described the expression and production of mature insulin in epithelial cells of the choroid plexus, and how its secretion can be modulated by serotonin through Htr2c, a metabotropic receptor that signals via Gq. To understand the function of this choroid plexus-derived insulin, here we describe a way to genetically target epithelial cells of the choroid plexus using a viral vector. With this, we modulated insulin expression and evaluated behavior. Insulin overexpression in the choroid plexus of wild type mice led to an inhibition in feeding, whereas insulin knockdown in choroid plexus of Ins1-/-Ins2fl/fl mice promoted discrete increases in food intake, especially after a period of fasting. Insulin overexpression in choroid plexus induced roust transcriptomic changes in the hypothalamus, most of which related to axonal growth and synapse-related processes. Finally, activation of Gq signaling in insulin-overexpressing choroid plexuses led to acute AKT phosphorylation in neurons of the arcuate nucleus, suggesting a direct action, through the CSF, of choroid plexus-derived insulin on the hypothalamus. Taken together our findings prove that the choroid plexus is a relevant source of insulin in the central nervous system, with physiological implications in feeding behavior. We believe that choroid plexus-derived insulin has to be taken into consideration in future work pertaining insulin actions in the brain.

2022-12-15 | GSE218188 | GEO

A singular cockroach insulin-like peptide specific for a male reproductive gland

Project description:The insulin-IGF-signalling (IIS) pathway plays crucial roles in animal physiology. In insects, this pathway works using multiple ligands, insulin-like peptides (ILPs), and a lower number of insulin receptors (InRs). Consequently, much of the regulation of IIS pathway activity is driven by the expression of ILPs, its timing, tissue, and mode of action: endocrine, paracrine, or autocrine. In the adult male of the cockroach Blattella germanica, tissue expression and the regulation in relation to food restriction of the BgILP1-7 genes is similar to that observed in females. However, we identified the expression of BgILP8, an ILP absent in females, in the conglobate gland of males, and only in this organ. BgILP8 expression in the conglobate gland is high during the initial days of adulthood and is reduced under starvation. The conglobate gland is a male sexual accessory gland specific to cockroaches, involved in spermatophore formation. It is composed of twisted tubules that ramify into different branches and converge in a general collecting tubule that opens into the ejaculatory duct. The tubules are lined with a single layer of secretory cells, each of the cells crossed by a small ductule formed by cuticle and actin fibres through which the secretory products will be released. Decreasing BgILP8 levels through RNAi (dsILP8) resulted in a reduction in the size of secretory cells, although the total protein extracted remained unaffected. A comparison of the transcriptomes of control and dsILP8 glands revealed only small differences. Further, comparing genes expressed in the conglobate gland to those expressed in adult females provided a list of putative conglobate gland-specific genes. Our results suggest that BgILP8 plays a role in the development of the conglobate gland. However, a potential function in other male organs or its possible transfer to the female in the copulation cannot be ruled out.

2025-06-17 | GSE293087 | GEO

Insulin/IGF signaling and vitellogenin provisioning mediate intergenerational adaptation to nutrient stress

Project description:Insulin/IGF signaling and vitellogenin provisioning mediate intergenerational adaptation to nutrient stress

| PRJNA531474 | ENA

Nucleus Type-Specific DNA Methylomics Reveals Epigenetic "Memory" of Prior Adaptation in Skeletal Muscle

Project description:Using a mouse model of conditional and inducible in vivo fluorescent myonuclear labeling (HSA-GFP), sorting purification of nuclei, low-input reduced representation bisulfite sequencing (RRBS), and a translatable and reversible model of exercise (progressive weighted wheel running, PoWeR), we provide the first nucleus type-specific epigenetic information on skeletal muscle adaptation and detraining.

2021-12-08 | GSE180433 | GEO

Choroid Plexus-Derived Insulin Inhibits Feeding via Direct Signaling through Arcuate Nucleus

Project description:Choroid Plexus-Derived Insulin Inhibits Feeding via Direct Signaling through Arcuate Nucleus

| PRJNA902709 | ENA

Nucleus Type-Specific DNA Methylomics Reveals Epigenetic “Memory” of Prior Adaptation in Skeletal Muscle

2021-12-08 | GSE180877 | GEO

Nutrient regulation of the islet epigenome controls adaptive insulin secretion

Project description:Adaptation of the islet β-cell insulin secretory response to changing insulin demand is critical for blood glucose homeostasis, yet the mechanisms underlying this adaptation are unknown. Here, we show that nutrient cues adapt insulin secretion by modulating chromatin state and transcription of genes regulating β-cell nutrient sensing and metabolism. Feeding stimulates histone acetylation at sites occupied by the chromatin-modifying enzyme Lsd1 in islets. We demonstrate that β-cell-specific deletion of Lsd1 leads to insulin hypersecretion, aberrant expression of nutrient response genes, and histone hyperacetylation, features we also observed in the db/db model of chronically increased insulin demand. Moreover, genetic variants associated with fasting glucose levels and type 2 diabetes risk are enriched at LSD1-bound sites in human islets, suggesting interindividual variation in β-cell functional adaptation in humans. These findings reveal nutrient state-dependent modulation of the islet epigenome and identify Lsd1 as a regulator of feeding-stimulated chromatin modification and adaptive insulin secretion.

2023-02-24 | GSE134901 | GEO

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