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Mice Harboring the Human SLC30A8 R138X Loss-of-Function Mutation Have Increased Insulin Secretory Capacity

ABSTRACT: Mice Harboring the Human SLC30A8 R138X Loss-of-Function Mutation Have Increased Insulin Secretory Capacity

PROVIDER: PRJNA470551 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7135450.fastq.gz	Fastqsanger.gz
	SRR7135451.fastq.gz	Fastqsanger.gz
	SRR7135452.fastq.gz	Fastqsanger.gz
	SRR7135453.fastq.gz	Fastqsanger.gz
	SRR7135454.fastq.gz	Fastqsanger.gz

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Mice Harboring the Human SLC30A8 R138X Loss-of-Function Mutation Have Increased Insulin Secretory Capacity

Project description:SLC30A8 encodes a zinc transporter that is primarily expressed in the pancreatic islets of Langerhans. In beta-cells it transports zinc into insulin-containing secretory granules. Loss-of-function (LOF) mutations in SLC30A8 protect against type 2 diabetes in humans. In this study, we generated a mouse model carrying one of the most common human LOF mutations for SLC30A8, R138X. The R138X mice had normal body weight, glucose tolerance and pancreatic beta-cell mass. Interestingly, in hyperglycemic conditions induced by the insulin receptor antagonist S961, the R138X mice showed a 50% increase in insulin secretion. This effect was not associated with enhanced beta-cell proliferation or beta-cell mass. Our data suggest that the SLC30A8 R138X LOF mutation in humans may protect from type 2 diabetes in part by increasing the capacity of beta-cells to secrete insulin.

2018-11-01 | GSE114207 | GEO

Mice harboring the human SLC30A8 R138X loss-of-function mutation have increased insulin secretory capacity.

Project description:SLC30A8 encodes a zinc transporter that is primarily expressed in the pancreatic islets of Langerhans. In ?-cells it transports zinc into insulin-containing secretory granules. Loss-of-function (LOF) mutations in SLC30A8 protect against type 2 diabetes in humans. In this study, we generated a knockin mouse model carrying one of the most common human LOF mutations for SLC30A8, R138X. The R138X mice had normal body weight, glucose tolerance, and pancreatic ?-cell mass. Interestingly, in hyperglycemic conditions induced by the insulin receptor antagonist S961, the R138X mice showed a 50% increase in insulin secretion. This effect was not associated with enhanced ?-cell proliferation or mass. Our data suggest that the SLC30A8 R138X LOF mutation may exert beneficial effects on glucose metabolism by increasing the capacity of ?-cells to secrete insulin under hyperglycemic conditions.

| S-EPMC6094147 | biostudies-literature

Cell-autonomous transcriptional mechanism for enhancement of translation capacity in secretory cells [ChIP-Seq]

Project description:Translation is a basic cellular process and its capacity is adapted to cell function. In particular, secretory cells achieve high protein synthesis levels without triggering the protein stress response. It is unknown how and when translation capacity is increased during differentiation. Here, we show that the transcription factor Creb3l2 is a scaling factor for translation capacity in pituitary secretory cells and that it directly binds ~75% of regulatory and effector genes for translation. In parallel with this cell-autonomous mechanism, implementation of the physiological UPR pathway prevents triggering the protein stress response. The pituitary differentiation factor Tpit activates Creb3l2 expression, the Creb3l2-dependent regulatory network as well as the physiological UPR pathway. Thus, Creb3l2 implements high basal translation levels through direct targeting of translation effector genes acting downstream of signaling pathways that otherwise regulate protein synthesis. Expression of Creb3l2 may be a useful means to enhance production of therapeutic proteins.

2019-07-29 | GSE132320 | GEO

Genetic mapping of multiple metabolic traits identifies novel genes for adiposity, lipids and insulin secretory capacity in outbred rats

Project description:Genetic mapping of multiple metabolic traits identifies novel genes for adiposity, lipids and insulin secretory capacity in outbred rats

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Cell-autonomous transcriptional mechanism for enhancement of translation capacity in secretory cells [RNA-Seq IL]

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Genetic mapping of multiple metabolic traits identifies novel genes for adiposity, lipids and insulin secretory capacity in outbred rats II

Project description:Genetic mapping of multiple metabolic traits identifies novel genes for adiposity, lipids and insulin secretory capacity in outbred rats II

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Cell-autonomous transcriptional mechanism for enhancement of translation capacity in secretory cells [RNA-Seq AtT-20 cells]

2019-07-29 | GSE132321 | GEO

Insulin secretory granules release exosomal miR-503 to promote insulin resistance and β-cell senescence.

Project description:Insulin secretory granules release exosomal miR-503 to promote insulin resistance and β-cell senescence.

| PRJNA655675 | ENA

Cell-autonomous transcriptional mechanism for enhancement of translation capacity in secretory cells

Project description:Cell-autonomous transcriptional mechanism for enhancement of translation capacity in secretory cells

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A circular RNA generated from an intron of the insulin gene controls insulin secretion

Project description:Fine-tuning of insulin release from pancreatic β-cells is essential to maintain blood glucose homeostasis. Here, we report that insulin secretion is regulated by a circular RNA containing the lariat sequence of the second intron of the insulin gene. Silencing of this intronic circular RNA in pancreatic islets leads to a decrease in the expression of key components of the secretory machinery of β-cells, resulting in impaired glucose- or KCl-induced insulin release and calcium signaling. The effect of the circular RNA is exerted at the transcriptional level and involves an interaction with the RNA-binding protein TAR DNA-binding protein 43 kDa (TDP-43). The level of this circularized intron is reduced in the islets of rodent diabetes models and of type 2 diabetic patients, possibly explaining their impaired secretory capacity. The study of this and other circular RNAs helps understanding β-cell dysfunction under diabetes conditions, and the etiology of this common metabolic disorder.

2020-09-21 | GSE134699 | GEO

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