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α Cell Function and Gene Expression Are Compromised in Type 1 Diabetes

ABSTRACT: α Cell Function and Gene Expression Are Compromised in Type 1 Diabetes

PROVIDER: PRJNA415746 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6216690_1.fastq.gz	Fastqsanger.gz
	SRR6216690_2.fastq.gz	Fastqsanger.gz
	SRR6216691_1.fastq.gz	Fastqsanger.gz
	SRR6216691_2.fastq.gz	Fastqsanger.gz
	SRR6216692_1.fastq.gz	Fastqsanger.gz

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α Cell Function and Gene Expression Are Compromised in Type 1 Diabetes

Project description:Many patients with type 1 diabetes (T1D) have residual beta cells producing small amounts of C-peptide long after disease onset, but develop an inadequate glucagon response to hypoglycemia following T1D diagnosis. The features of these residual beta cells and alpha cells persisting in the islet endocrine compartment are largely unknown due to difficulty of comprehensive investigation. By studying the T1D pancreas and isolated islets, we show that remnant beta cells appeared to maintain several aspects of regulated insulin secretion. However, the function of T1D alpha cells was markedly reduced and these cells had alterations in transcription factors constituting and alpha and beta cell identity. In the native pancreas and after placing the T1D islets into a non-autoimmune, normoglycemic in vivo environment, there was no evidence of alpha-to-beta cell conversion. These results suggest a new explanation for the disordered T1D counterregulatory glucagon response to hypoglycemia.

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α Cell Function and Gene Expression Are Compromised in Type 1 Diabetes.

Project description:Many patients with type 1 diabetes (T1D) have residual β cells producing small amounts of C-peptide long after disease onset but develop an inadequate glucagon response to hypoglycemia following T1D diagnosis. The features of these residual β cells and α cells in the islet endocrine compartment are largely unknown, due to the difficulty of comprehensive investigation. By studying the T1D pancreas and isolated islets, we show that remnant β cells appeared to maintain several aspects of regulated insulin secretion. However, the function of T1D α cells was markedly reduced, and these cells had alterations in transcription factors constituting α and β cell identity. In the native pancreas and after placing the T1D islets into a non-autoimmune, normoglycemic in vivo environment, there was no evidence of α-to-β cell conversion. These results suggest an explanation for the disordered T1D counterregulatory glucagon response to hypoglycemia.

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