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Review
. 2008 Aug;25(8):889-94.
doi: 10.1111/j.1464-5491.2008.02514.x.

RD Lawrence Lecture 2008: Targeting GLP-1 release as a potential strategy for the therapy of Type 2 diabetes

F M Gribble  1
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Free PMC article
Review

"VSports最新版本" RD Lawrence Lecture 2008: Targeting GLP-1 release as a potential strategy for the therapy of Type 2 diabetes

F M Gribble. Diabet Med. 2008 Aug.
Free PMC article

V体育2025版 - Abstract

Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are gastrointestinal hormones that play an important role in stimulating postprandial insulin release from pancreatic beta-cells VSports手机版. Agents that either mimic GLP-1 or prevent its degradation are now available for the treatment of Type 2 diabetes, and strategies to enhance endogenous GLP-1 release are under assessment. As intestinal peptides have a range of actions, including appetite regulation and coordination of fat metabolism, harnessing the enteric endocrine system is a promising new field for drug development. .

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"V体育官网" Figures

FIGURE 1
FIGURE 1
Glucose-dependent stimulation of insulin release by glucagon-like peptide-1 (GLP-1). At low glucose concentrations (left), intracellular [Ca2+] is low, and although stimulation by GLP-1 causes an increase in cyclic adenosine monophosphate (cAMP), this causes only small increases in [Ca2+] and minimal enhancement of insulin release (dashed arrows). The amount of insulin released is not enough to induce hypoglycaemia. At high glucose concentrations or in the presence of sulphonylureas (right), [Ca2+] is elevated, and the elevation of cAMP by GLP-1 can then potently enhance the rate of insulin release, as well as further increasing [Ca2+].
FIGURE 2
FIGURE 2
A working model of glucagon-like peptide-1 (GLP-1) release from the intestinal L-cell. Dietary nutrients stimulate GLP-1 release from intestinal L-cells, as a consequence of their Na+-coupled uptake and subsequent metabolism, which cause membrane depolarization (ΔΨ) and Ca2+ entry. Indirect signals from hormones and neurotransmitters can stimulate release by a variety of mechanisms, including elevation of cyclic adenosine monophosphate (cAMP) (which acts as both an initiator and an amplifier of GLP-1 release), and Ca2+ release from stores. GLP-1 released at the basolateral membrane stimulates insulin release from pancreatic β-cells and reduces appetite.
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References

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