Disease relevance of GCG

• Glucagon prevented ocular elongation and myopia and induced choroidal thickening in form-deprived eyes [1].
• RESULTS: The Phe(6)-antagonist at 10(-5) M (in the syringe) inhibited changes in both refractive error and axial length compensation induced by +7-D lens wear; however, des-Phe(6)-antagonist (10(-5) M) had weak, inconsistent effects and did not antagonize the action of exogenous glucagon [1].
• Glucose tolerance, plasma insulin and immunoreactive glucagon in chickens selected for high and low body weight [2].
• Intracerebroventricular administration of glucagon in chicks significantly suppressed food intake and significantly induced hyperglycemia [3].
• The glucagon antagonist inhibited hyperopia development, albeit only in a narrow concentration range, and at most by 50%, but not myopia development [4].

Psychiatry related information on GCG

• The present findings support the idea that endogenous GLP-1 is involved in feeding behavior of chicks [5].
• Central administration of norepinephrine (NE) suppressed food intake with narcolepsy as GLP-1 in chicks [6].

High impact information on GCG

• Fos synthesis was enhanced by termination of visual deprivation, but not by defocus and not in glucagon-containing amacrine cells [7].
• Insulin, glucagon, and calcitonin (1 microgram/ml) did not compete for PTH binding sites [8].
• Mechanism for acute control of fatty acid synthesis by glucagon and 3':5'-cyclic AMP in the liver cell [9].
• Thus, it appears that glucagon, acting via cyclic AMP, inhibits fatty acid synthesis by blocking the formation of citrate, an essential activator of acetyl-CoA carboxylase [9].
• However, the cytoplasmic concentration of citrate, a required allosteric activator of acetyl-CoA carboxylase, is depressed more than 90% by glucagon or dibutyrl cyclic AMP [9].

Chemical compound and disease context of GCG

• Abdominal adipose tissue from broiler chickens selected for body weight or for food efficiency differ in in vitro lipolytic sensitivity to glucagon and to chicken growth hormone, but not to dibutyryl cAMP [10].
• The role of endogenous glucagon and insulin on the hepatic glycogen and triglyceride storage syndrome in propylthiouracil (PTU)-induced hypothyroidism was investigated in the chick [11].
• However, in spite of that dopamine (DA) did not affect food intake, coadministration of inhibitor of dopamine-beta-hydroxylase (DBH), fusaric acid (FA), attenuated the suppressive effect of GLP-1 on feeding behavior [6].
• Further studies on the biochemical characterization of the MC-29 virus derived transplantable hepatoma (VTH). II. Modification of cyclic adenosine-3',5'-monophosphate levels by catecholamines, glucagon and Vinca alkaloids in normal chicken liver and VTH [12].
• 2. NaF stimulated the enzyme activity in both liver and hepatoma plasma membranes, while only liver adenylate cyclase was activated by glucagon and epinephrine [13].

Biological context of GCG

• Insulin and glucagon increased after hatch, which may be due to increased feed consumption and increased utilization of carbohydrates as the key energy source, compared with nutrients obtained through lipolysis and proteolysis in the embryos [14].
• Plasma glucagon levels remained low until 17E, and then significantly increased approximately 3-fold at hatch, which corresponded with increasing plasma glucose levels during late embryo development [14].
• Chicken glucagon. Isolation and amino acid sequence studies [15].
• These results show that proglucagon gene expression is regulated at the level of mRNA splicing and serve to reemphasize the potential biological importance of GLP 2 [16].
• Trout and chicken proglucagon: alternative splicing generates mRNA transcripts encoding glucagon-like peptide 2 [16].

Anatomical context of GCG

• Developmental Changes of Plasma Insulin, Glucagon, Insulin-like Growth Factors, Thyroid Hormones, and Glucose Concentrations in Chick Embryos and Hatched Chicks [14].
• Glucagon was isolated from a side fraction generated during the preparation of insulin and the new pancreatic peptide, avian pancreatic polypeptide from chicken pancreas [15].
• The hypothalamus is involved in the anorexic effect of glucagon-like peptide-1 in chicks [17].
• ICV injection of GLP-1 stimulated the expression of Fos-like immunoreactive (FLI) cells in the ventromedial hypothalamic nucleus (VMN) [17].
• The prolonged accumulation of cyclic AMP due to glucagon in chicken fat cells was primarily intracellular [18].

Associations of GCG with chemical compounds

• Developmental hormonal changes in Cobb 500 chick embryos and hatched chicks were determined by measuring plasma insulin, glucagon, insulin-like growth factor (IGF)-I, IGF-II, triiodothyronine, thyroxine, and glucose concentrations at different ages of embryogenesis and posthatch development [14].
• The amino acid composition of chicken glucagon indicates that it contains 1 more serine residue than the porcine hormone and 1 less aspartic acid (asparagine) residue [15].
• The amino acid sequence of chicken glucagon was HSQGTFTSDYSKYLDSRRAQDFVQWLMST, which was contained in the 151-amino acid long precursor, being preceded by a signal sequence and an amino-terminal peptide (NH2-peptide) and followed by an intervening peptide and a glucagon-like peptide I (GLP-I) [19].
• Our data suggest that GCG and GCC codons play a key role in polyalanine-coding sequence appearance and polymorphism [20].
• Labeling experiments with chicken liver cell monolayers and suspensions show that glucagon and N6, O2-dibutyryladenosine 3':5'-cyclic monophosphate (dibutyryl cyclic AMP) block fatty acid synthesis from acetate without appreciably affecting cholesterogenesis from acetate or acylglyceride synthesis from palmitate [9].

Physical interactions of GCG

• These results suggest that central GLP-1 may interact with NPY and may be the most potent inhibitor of food intake in the chicken [21].

Regulatory relationships of GCG

• Thus, glucagon regulates fatty acid synthase by controlling the concentration of its mRNA [22].
• The mechanisms by which triiodothyronine (T3), glucose, insulin, and glucagon regulate acetyl-CoA carboxylase expression in primary cultures of chick embryo hepatocytes have been investigated [23].
• Influence of fasting and neuropeptide Y on the suppressive food intake induced by intracerebroventricular injection of glucagon-like peptide-1 in the neonatal chick [21].
• Glucagon-induced hyperglycaemia suppressed the level of GH in the plasma and stimulated that of prolactin [24].
• Insulin stimulates somatostatin and inhibits glucagon secretion from the perfused chicken pancreas-duodenum [25].

Other interactions of GCG

• The percentage carcass protein for ad libitum-fed breeders was positively correlated to IGF-I, T4, T3, insulin/glucagon M ratio, and insulin [26].
• Carcass percentage protein for feed-restricted breeders was positively correlated to IGF-I, IGF-II, T4, and glucagon [26].
• In chick embryo hepatocytes in culture, the stimulatory effect of feeding on fatty acid synthase activity is mimicked by adding triiodothyronine and insulin; the inhibitory effect of starvation is mimicked by adding glucagon or cyclic AMP [27].
• These results suggest an important role for c-Fos and ATF-2 in glucagon-mediated inhibition of transcription of the malic enzyme gene [28].
• The recovery of adenylosuccinase activity is equally rapid after refeeding a balanced diet, or corn oil, or glucose, and is not inhibited by injection of glucagon, in contrast to malic enzyme activity [29].

Analytical, diagnostic and therapeutic context of GCG

• Microinjection of GLP-1 into the (LHA) also inhibited feeding in chicks, although ICV injection of GLP-1 did not stimulate FLI expression in the brain area [17].
• The level of the GLP-1 mRNA was evaluated by RT-PCR 24 h after transfection [30].
• Coculture assay of the GLP-1 plasmid-transfected cells with isolated rat islet cells demonstrated that GLP-1 increased insulin secretion by twofold, compared to controls during a hyperglycemic challenge [30].
• Immunoreactive glucagon and immunoreactive vasoactive intestinal polypeptide (VIP) have been demonstrated in neuronal elements in the retina of a number of species by immunohistochemistry [31].
• Finally, it was shown that retinal glucagon mRNA content increased after treatment with positive lenses [32].

References