Glucagon-like immunoreactivity in hypothalamic neurons of the rat

Salazar, Ianire Buceta; Vaillant, Camille

doi:10.1007/bf00318677

Cited by 16 publications

(3 citation statements)

References 22 publications

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“…However, there are data that suggest GLP‐1 may act as a modulator or regulator in the gut–brain axis at different levels. Thus, positive immunoreactivity for GLP‐1 and binding of radiolabelled GLP‐1 have been demonstrated at different levels of the brainstem, such as at the nucleus of the solitary tract (NTS), area postrema, dorsal motor nucleus of the vagus (DMVN), the thalamus or hypothalamus 33–36 . It is conceivable that in the NTS, a region where afferent information from the gut and other organs is integrated, or at the level of DMVN, locally synthesized GLP‐1 induces activation of gastric relaxatory reflex by activation of post‐synaptic neurons involved in vagal nitrergic or adrenergic inhibitory pathways.…”

Section: Discussionmentioning

confidence: 99%

“…Seven (five males and two females) diabetic patients with previously documented cardio-vagal neuropathy were studied. Median age was 65 years (IQR: 56-74) and median body mass index was 26 kg m )2 (IQR: [24][25][26][27][28][29][30][31][32][33][34][35]. Five patients had insulin-dependent diabetes mellitus (IDDM) and two non-insulin-dependent diabetes mellitus (NIDDM); five had diabetic retinopathy; five peripheral somatic neuropathy; four erectile dysfunction; and three renal impairment.…”

Section: Study Conduct and Participantsmentioning

confidence: 99%

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Effects of glucagon‐like peptide‐1 and feeding on gastric volumes in diabetes mellitus with cardio‐vagal dysfunction

Delgado-Aros

Vella

Camilleri

et al. 2003

Neurogastroenterology Motil

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Glucagon-like peptide-1 (GLP-1) increases gastric volume in humans possibly through the vagus nerve. Gastric volume response to feeding is preserved after vagal denervation in animals. We evaluated gastric volume responses to GLP-1 and placebo in seven diabetic patients with vagal neuropathy in a crossover study. We also compared gastric volume response to feeding in diabetes with that in healthy controls. We measured gastric volume using SPECT imaging. Data are median (interquartile range). In diabetic patients, GLP-1 did not increase gastric volume during fasting [5 mL (-3; 30)] relative to placebo [4 mL (-14; 50) P = 0.5], or postprandially [Delta postprandial minus fasting volume 469 mL (383; 563) with GLP-1 and 452 mL (400; 493) with placebo P = 0.3]. Change in gastric volume over fasting in diabetic patients on placebo was comparable to that of healthy controls [452 mL (400; 493)], P = 0.5. In contrast to effects in health, GLP-1 did not increase gastric volume in diabetics with vagal neuropathy, suggesting GLP-1's effects on stomach volume are vagally mediated. Normal gastric volume response to feeding in diabetics with vagal neuropathy suggests that other mechanisms compensate for vagal denervation.

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Section: Discussionmentioning

confidence: 99%

Section: Study Conduct and Participantsmentioning

confidence: 99%

Effects of glucagon‐like peptide‐1 and feeding on gastric volumes in diabetes mellitus with cardio‐vagal dysfunction

Delgado-Aros

Vella

Camilleri

et al. 2003

Neurogastroenterology Motil

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“…In the late 80ties, researchers began looking for the new glucagon-like peptides in the brain, inspired by the reports of immunoreactive glucagon in certain neurons of the brain (78), particularly in the nucleus of the solitary tract. These neurons also were immunoreactive for GLP-1 (79). In addition, binding studies suggested the presence of a large number of putative receptors for GLP-1 not only in the beta cells of the pancreatic islets but also in the brain (80).…”

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confidence: 99%

From the Incretin Concept and the Discovery of GLP-1 to Today's Diabetes Therapy

Holst

2019

Front. Endocrinol.

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Researchers have been looking for insulin-stimulating factors for more than 100 years, and in the 1960ties it was definitively proven that the gastrointestinal tract releases important insulinotropic factors upon oral glucose intake, so-called incretin hormones. The first significant factor identified was the duodenal glucose-dependent insulinotropic polypeptide, GIP, which however, turned out not to stimulate insulin secretion in patients with type 2 diabetes. But resection experiments clearly indicated the presence of an additional incretin, and in 1986, an unexpected processing fragment of the recently identified glucagon precursor, proglucagon, namely truncated glucagon-like peptide 1 (GLP-1 7–36 amide), was isolated from the gut and found to both stimulate insulin secretion and inhibit glucagon secretion. The peptide also inhibited appetite and food intake. Unlike GIP, this peptide had preserved effects in patients with type 2 diabetes and it was soon documented to have powerful antidiabetic effects in clinical studies. Its utility was limited, however, because of an extremely short half-life in humans, but this problem had two solutions, both of which gave rise to important antidiabetic drugs: (1) orally active inhibitors of the enzyme dipeptidylpeptidase 4 (DPP-4 inhibitors), which was responsible for the rapid degradation; the inhibitors protect endogenous GLP-1 from degradation and thereby unfold its antidiabetic activity, and (2) long-acting injectable analogs of GLP-1 protected against DPP-4 degradation. Particularly, the latter, the GLP-1 receptor agonists, either alone or in various combinations, are so powerful that treatment allows more than 2/3 of type 2 diabetes patients to reach glycemic targets. In addition, these agents cause a weight loss which, with the most successful compounds, may exceed 10% of body weight. Most recently they have also been shown to be renoprotective and reduce cardiovascular risk and mortality.

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Glucagon and Glucagon‐like Peptide Production and Degradation

Kieffer

Hussain

Habener

2001

Comprehensive Physiology

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The sections in this article are: History Glucagon Glucagon‐like Peptides The Glucagon Superfamily of Peptide Hormones Tissue Distribution of Proglucagon Expression Pancreas Intestine Brain Proglucagon Biosynthesis Organization and Structure of the Proglucagon Gene Regulation of Glucagon Gene Expression Posttranslational Processing of Proglucagon Chemistry and Structure Regulation of Glucagon Secretion Overview Intracellular Signals Nutrients Endocrine/Paracrine Neural Pulsatility Regulation of Glucagon‐like Peptide‐1 Secretion Overview Intracellular Signals Nutrients Endocrine Neural Metabolism and Degradation Overview Renal Clearance Hepatic Clearance Degradation in the Circulation Biologically Active Fragments Physiological Actions Glucagon Glucagon‐like Peptide‐1 Glucagon‐like Peptide‐2 Mechanisms of Action Glucagon Glucagon‐like Peptide‐1 Glucagon‐like Peptide‐2 Human Disease Glucagon Glucagon‐like Peptide‐1 Glucagon‐like Peptide‐2

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Glucagon-like immunoreactivity in hypothalamic neurons of the rat

Cited by 16 publications

References 22 publications

Effects of glucagon‐like peptide‐1 and feeding on gastric volumes in diabetes mellitus with cardio‐vagal dysfunction

Effects of glucagon‐like peptide‐1 and feeding on gastric volumes in diabetes mellitus with cardio‐vagal dysfunction

From the Incretin Concept and the Discovery of GLP-1 to Today's Diabetes Therapy

Glucagon and Glucagon‐like Peptide Production and Degradation

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