Unacylated ghrelin and obestatin increase islet cell mass and prevent diabetes in streptozotocin-treated newborn rats.

No abstract is available for this paper.

• Publication year

  2010

• Venue

  Journal of Molecular Endocrinology

• Publication date

  2010-07-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1677/JME-09-0141PMID 20382773
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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  2008influential reference
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  2008influential reference
• Ghrelin is a physiological regulator of insulin release in pancreatic islets and glucose homeostasis.

  2008cited by this paper
• Heterogeneity of Ghrelin/Growth Hormone Secretagogue Receptors

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  2007influential reference
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  2004influential reference
• Endogenous ghrelin in pancreatic islets restricts insulin release by attenuating Ca2+ signaling in beta-cells: implication in the glycemic control in rodents.

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• Ghrelin cells replace insulin-producing beta cells in two mouse models of pancreas development.

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• Inflammatory mediators and islet β-cell failure: a link between type 1 and type 2 diabetes

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  2002influential reference
• Ghrelin is present in pancreatic alpha-cells of humans and rats and stimulates insulin secretion.

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• Akt/Protein Kinase B Up-regulates Bcl-2 Expression through cAMP-response Element-binding Protein*

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  1994cited by this paper
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  1988cited by this paper
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• Pancreatic Islet Cell Hormones: Secretion, Function, and Diabetes Therapy

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• Ghrelin

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• Obestatin: A new metabolic player in the pancreas and white adipose tissue

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• Chapter 173 – Obestatin

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• Chapter 132 – Ghrelin

  2013cites this paper
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• regulates function and protects

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