Species difference of glucagon-like materials in the brain

Tominaga, Makoto; Ebitani, Isao; Marubashi, Seijiro; Kamimura, T.; Katagiri, Tadashi; Sasaki, Hideo

doi:10.1016/0024-3205(81)90259-9

Cited by 32 publications

(12 citation statements)

References 8 publications

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“…Although the presence of glucagon and glucagon-like peptides in brain has been reported (9)(10)(11)(12)(13)(14)(15)(16)(17), to our knowledge glucagon receptor identification and localization in the central nervous system has not been reported previously.…”

Section: Discussionmentioning

confidence: 78%

“…The regional distributions in mammalian brains of glucagon-related peptides such as vasoactive intestinal polypeptide (30), secretin (31), gastrin (32), and PHI-27 (33) differ from that for glucagon (9)(10)(11)(12)(13)(14)(15)(16)(17). hpGRF-44, which is also a member of the glucagon-secretin family of evolutionarily related peptides, did inhibit glucagon binding.…”

Section: Discussionmentioning

confidence: 99%

“…There have been several reports of glucagon and/or glucagon-like immunoreactivities in the central nervous system of rats (9)(10)(11)(12) and other mammals, including humans (13)(14)(15)(16)(17), and in the retina of goldfish, frog, and pigeon (18). We are unaware of any study identifying glucagon receptors in nervous tissue.…”

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confidence: 99%

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Identification of glucagon receptors in rat brain.

Hoosein¹,

Gurd²

1984

Proc. Natl. Acad. Sci. U.S.A.

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The binding of radiolabeled glucagon to rat brain membranes was investigated. Regional distribution studies indicate higher specific binding of l5I-labeled monoiodoglucagon to olfactory tubercule, hippocampus, anterior pituitary, and amygdala membranes, with somewhat lower binding to membranes from septum, medulla, thalamus, olfactory bulb, and hypothalamus. 1251-labeled glucagon bound to rat brain synaptic plasma membrane fractions with high affinity (KD = 2.24 nM). Specific binding was greater to synaptosomal membrane fractions relative to myelin, mitochondrial nuclear, or microsomal fractions. Inclusion of 0.1 mM GTP in the binding assay reduced the glucagon binding affinity (KD = 44.5 nM). Several neuropeptides and other neuroactive substances tested did not affect binding of labeled glucagon to brain membranes. Three different glucagon analogs inhibited labeled glucagon binding. Synthetic human pancreatic growth hormone-releasing factor, hpGRF-44, also inhibited binding, although the concentration required for half-maximal displacement was 100-fold higher than for native glucagon. Addition of glucagon to brain membranes resulted in -3-fold maximal activation of adenylate cyclase over basal levels. Glucagon at a concentration of 4.74 nM was required for half-maximal activation of pituitary membrane adenylate cyclase. These findings provide evidence for rat brain binding sites that respond to the pancreatic form of glucagon and can transduce this binding into the activation of adenylate cyclase.

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Section: Discussionmentioning

confidence: 78%

Section: Discussionmentioning

confidence: 99%

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Identification of glucagon receptors in rat brain.

Hoosein¹,

Gurd²

1984

Proc. Natl. Acad. Sci. U.S.A.

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“…In contrast to dogs, in totally depancreatized humans, there is only a negligible amount of plasma glucagon (9,20,87,135,179). We and others who detected glucagon-like peptides in the brain (80,177,181) stimulated interest in this field. It was very exciting to present these data at my Banting and Best Award and plenary lecture at the International Diabetes Federation meeting in 1985.…”

Section: Resolving the Controversy Regarding The Existence Of Extrapamentioning

confidence: 99%

Odyssey between Scylla and Charybdis through storms of carbohydrate metabolism and diabetes: a career retrospective

Vranić

2010

American Journal of Physiology-Endocrinology and Metabolism

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Vranic M. Odyssey between Scylla and Charybdis through storms of carbohydrate metabolism and diabetes: a career retrospective. Am J Physiol Endocrinol Metab 299: E849 -E867, 2010. First published September 7, 2010; doi:10.1152/ajpendo.00344.2010.-This research perspective allows me to summarize some of my work completed over 50 years, and it is organized in seven sections. 1) The treatment of diabetes concentrates on the liver and/or the periphery. We quantified hormonal and metabolic interactions involved in physiology and the pathogenesis of diabetes by developing tracer methods to separate the effects of diabetes on both. We collaborated in the first tracer clinical studies on insulin resistance, hypertriglyceridemia, and the Cori cycle.2) Diabetes reflects insulin deficiency and glucagon abundance. Extrapancreatic glucagon changed the prevailing dogma and permitted precise exploration of the roles of insulin and glucagon in physiology and diabetes. 3) We established the critical role of glucagon-insulin interaction and the control of glucose metabolism during moderate exercise and of catecholamines during strenuous exercise. Deficiencies of the release and effects of these hormones were quantified in diabetes. We also revealed how acute and chronic hyperglycemia affects the expression of GLUT2 gene and protein in diabetes. 4) We outlined molecular and physiological mechanisms whereby exercise training and repetitive neurogenic stress can prevent diabetes in ZDF rats. 5) We and others established that the indirect effect of insulin plays an important role in the regulation of glucose production in dogs. We confirmed this effect in humans and demonstrated that in type 2 diabetes it is mainly the indirect effect. 6) We indicated that the muscle and the liver protected against glucose changes. 7) We described molecular mechanisms responsible for increased HPA axis in diabetes and for the diminished responses of HPA axis, catecholamines, and glucagon to hypoglycemia. We proposed a new approach to decrease the threat of hypoglycemia. exercise; stress; diabetes pathogenesis; hypoglycemia SCYLLA AND CHARYBDIS are two sea monsters in Greek mythology described by Homer. They were located close enough to each other that they posed an inescapable threat to passing sailors, including Odysseus. Avoiding Charybdis meant passing too close to Scylla and vice versa. Substitute Scylla for granting agencies and Charybdis for high-impact journals. There is a feedback relationship between problems with granting agencies and the acceptance of papers in important journals. The storms (originality) require the strength of Odysseus to sail safely toward acceptance of a new and original hypothesis.I am very indebted to Amira Klip (the first non-U.S. editor of the American Journal of Physiology -Endocrinology and Metabolism), who invited me to write a review related to my research endeavors over the past half-century. Since this is a personal history rather than a general review, I have focused primarily on my laboratory work as well ...

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“…Radioimmunoassay was performed by the method described previously [11]. The values measured by radioimmunoassay with C-terminal specific antibody 30K (Texas University, Dallas, Texas, USA) [12] or OAL123 (Otsuka Assay Laboratory, Tokushima, Japan) [13] are referred to as immunoreactive glucagon (IRG), and those measured with central portion reactive antibody K4023 (Nova, Copenhagen, Denmark) [14] or OAL196 (Otsuka Assay Laboratory, Tokushima, Japan) [15] are referred to as glucagon-like immunoreactivity (GLI) in this text.…”

Section: Radioimmunoassaymentioning

confidence: 99%

125I-glucagon-degrading activity in acid-saline extracts of rat salivary gland

et al. 1984

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Summary. The antibody-binding ability of the glucagon-like substance in rat submaxillary gland acid saline extract was examined by affinity chromatography, and the biological activity studied using the isolated liver perfusion method. We found that the glucagon-like substances in acid saline extract could not be bound to anti-glucagon antibody and that the gel-filtration peak on ultrogel AcA 54 could increase neither glucose nor cyclic AMP output from isolated perfused rat liver. Furthermore, the radioactivity peak of 125I-glucagon on Bio Gel P-6 column chromatography moved from its original position and eluted in later fractions after incubation with an acid saline extract of the submaxillary gland. In consequence, there was 125I-glucagon degrading activity in the submaxillary gland, but no glucagon-related peptide. Therefore, it is suggested that the glucagon-like substance, which has been reported in acid saline extract of the rat salivary gland, may be an artifact due to tracer degrading activity.

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Species difference of glucagon-like materials in the brain

Cited by 32 publications

References 8 publications

Identification of glucagon receptors in rat brain.

Identification of glucagon receptors in rat brain.

Odyssey between Scylla and Charybdis through storms of carbohydrate metabolism and diabetes: a career retrospective

125I-glucagon-degrading activity in acid-saline extracts of rat salivary gland

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