Role of Adrenergic Receptors in Glucose-Induced Insulin Secretion in Man

Cerasi, Erol; Effendic, Suad; Luft, Rolf

doi:10.1016/s0140-6736(69)90059-2

Cited by 106 publications

(27 citation statements)

References 6 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Thus during studies in which a diminished acute insulin response to glucose is observed, the acute response to secretin is increased; and conversely, when a decreased acute insulin response to secretin is observed, the subsequent acute response to glucose is increased. In addition, when epinephrine and propranolol are infused at rates which are associated with blunted glucose-stimulated insulin responses (8,9), the present data and that of others (11) indicate that the insulin responses to secretin are unimpaired. What are the possible explanations for these observations?…”

Section: Methodssupporting

confidence: 46%

“…The acute insulin responses to the four 150-U secretin pulses given at 30 min intervals progressively and significantly fell to each succeeding pulse (Table II, P < 0.05). The subsequent 5-g glucose pulse given 30 min after the final 150 U secretin pulse was associated with increased acute insulin responses (P < 0.02) and more rapid glucose disappearance rates (Table II, (4,5), it is pertinent to compare the patterns of responses during similar studies employing infusions of glucose (4), epinephrine (8), and propranolol (9). When the insulin responses to the small (15 U) secretin pulses are compared to those after a small (5 g) glucose pulse before, during, and after a glucose infusion as has been recently reported (4), important differences are readily noted.…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Studies of secretin-stimulated insulin responses in man

Lerner¹,

Porte²

1972

J. Clin. Invest.

View full text Add to dashboard Cite

A B S T R A C T Recent studies have suggested that secretin, like glucose, stimulates a rapid insulin response from a small storage pool. In order to evaluate the mechanism of the secretin-stimulated insulin response, small (15 U) rapidly administered intravenous injections (pulses) of secretin were given before, during, and after a 20 hr 300 mg/min glucose infusion. Contrary to previous studies demonstrating that the acute insulin response to a small (5 g) pulse of glucose given 45 ;min after the start of the glucose infusion was significantly diminished compared to the response to the preinfusion pulse, the acute insulin response (2-5 min Aimmuno-reactive insulin IAU/ml) to 15-U secretin pulses exhibited a greater than twofold increase (before: 31.1±15.4; during: 71.2+40.4, /LU/ml, mean ±sD, P < 0.02). The increased response to secretin was also found after 20 hr of continuous glucose infusion, but was not observed 1 hr after cessation of the infusion when plasma glucose levels returned to control values. Thus, this increased response to secretin was glucose dependent.Four 150-U secretin pulses given at 30 min intervals elicited progressively and significantly diminished acute insulin responses with each succeeding pulse, consistent with depletion of the small storage pool. Similar to the observation that the magnitude of the insulin response to secretin was glucose dependent, the glucose-stimulated output appeared to be secretin dependent. Thus the acute insulin response to 5 g glucose was increased after secretin pretreatment (presecretin: 34.9±14.8; postsecretin: 50.5+22.5 AU/ml, P < 0.02) which suggests that This work was presented in part at

show abstract

Section: Methodssupporting

confidence: 46%

Section: Methodsmentioning

confidence: 99%

Studies of secretin-stimulated insulin responses in man

Lerner¹,

Porte²

1972

J. Clin. Invest.

View full text Add to dashboard Cite

show abstract

“…The functional integrity, in B-cells of spiny mice, of the mechanisms involved in the release of insulin in response to secretory stimulation cannot be assessed on the basis of currently available data. However, in view of the apparent importance of the autonomous nervous system for the regulation of insulin release [17,2], our consistent inability to detect autonomous nerve endings in the islets of spiny mice m a y be of importance. partially purified pancreatic extracts has indicated that, similar to what is known for the rat, the pancreas of spiny mice may contain two structurally distinct insulins (Fig.…”

Section: Discussionmentioning

confidence: 79%

Metabolic state, pancreatic insulin content and B-cell morphology of normoglycemic spiny mice (acomys cahirinus): Indications for an impairment of insulin secretion

et al. 1970

View full text Add to dashboard Cite

Summary. Plasma glucose, plasma It%I and pancreaticIt%I content were measured and B-cell morphology was studied in fasted, fed and glucose-injected normoglyeemic spiny mice of varying ages. Both high and low plasma II%I concentrations were observed at all ages, irrespective of the degree of pancreatic stimulation, In old but not in young animals, plasma II%I concentrations correlated with body weight, suggesting that accelerated weight gain was secondary to hyperinsulinemia. Pancreatic ll~I content was higher than in other strains of non-diabetic mice and increased with age but was unrelated to either plasma II~I concentrations, or to body weight individual age groups, l%elative to pancreatic IRI content, plasma II%I concentrations of spiny mice were lower than those of normal or obese-hyperglycemic mice of other strains. The B-cells showed an unusual degree of granulation. Pale granules predominated and had a characteristic tendency to fusion and confluence. With the exception of i out of 200 animals (in the islets of which emioeytosis was seen), no signs of enhanced insulin release could be observed. Nee-formation of /%granules by the Golgi complex of already well granulated cells was the only feature consistently associated with pancreatic stimulation by glucose injection. The data are in agreement with the hypothesis of a B-cell defect resulting in an impairment of insulin secretion and also suggest that the B-cells of normoglyeemie spiny mice may contain two compartments of insulin: one which is aeeessible to secretory stimulation and has a rapid turnover and one which is relatively inaccessible to stimulation and accumulates with age. Available data do not allow for the identification of the postulated defect or for the anatomical or physiological definition of the two compartments of insulin. Etat mdtabolique, contenu pancrdatique en insuline et aspect morphologique des cellules B de la souris ~ piquants (Acomys cahirgnus) normoglycdmique: Possibilitd d'une altdration de la sdcrdtion de l'insulineRdsumd. En mesurant les taux plasmatiques de glucose et de l'insuline immunor6aetive (IgI), le contenu pancrgatique en IgI, et en gtudiant ~ l'aide du microscope 61ectronique les panerdas de souris k piquants normoglyedmiques ~ jeun, nourries ou apr~s injection intrapgritondale de glucose, les rdsultats suivants out 6t6 obtenus: sans tenir eompte du degr6 de stimulation paner6atique, les animaux des diff~rents groupes d'gge out pu 8tre classgs en deux eatggories, soit ceux ayant une concentration basse ou 61evde d'IRI plasmatique. Le fair qu'une eorrglation entre le poids corporel et la concentration en II%I plasmatique peut 8tre dtablie chez les animaux adultes, mais non pus chez les jeunes, indique que l'augmentation du poids eorporel est plut6t la eonsgquenee que la cause de l'hyperinsulindmie. Par rapport d'autres espbees de souris normales ou hypergIycdmiques, le contenu pancr4atique en insuline des souris ~ piquants dtait 61evd et augmenta progressivement avee * Supported by the Fends National Suisse de la ...

show abstract

“…Possible reasons for such an anomaly in our preparation might result from changes in the basal metabolic state and the reactivity of insulin release mechanisms of pancreatic P-cells obtained from animals fasted overnight and isolated from all other tonic or facilitating influences originating elsewhere in the organism, such as humoral regulators of gastrointestinal origin (33,34,(38)(39)(40)(41), hormones originating in other endocrine glands (15,42,43), and the autonomic nervous system (28, [44][45][46][47][48][49][50][51][52]. The absence of such factors may result in failure to maintain critical concentrations of cAMP or of other as yet hypothetical cofactors required for full effectiveness of substrate stimulation.…”

Section: Resultsmentioning

confidence: 99%

Perifusion of rat pancreatic tissue in vitro: substrate modification of theophylline-induced biphasic insulin release

Burr¹,

Balant²,

Stauffacher³

et al. 1970

J. Clin. Invest.

View full text Add to dashboard Cite

A B S T R A C T The immunoreactive insulin (IRI) re-lease patterns produced by continuous theophylline stimulation of rat pancreas have been defined, using an in vitro perifusion system. In the presence of glucose, citrate, and pyruvate at concentrations which were nonstimulatory by themselves, continuous stimulation with theophylline produced a biphasic IRI release profile. In the absence of substrate, continuous theophylline stimulation produced only an abrupt and limited primary response. Of the substrates tested, only glucose significantly enhanced this primary response. With increasing theophylline concentrations, whether in the presence or absence of substrate, significant increases were noted in the primary response as estimated by either the maximum rate of IRI release attained or by the total amount of IRI released during this time. Similarly, the secondary responses to theophylline increased with theophylline concentration in the presence of either citrate or pyruvate. With glucose as substrate, however, increasing theophylline concentrations from 2.5 to 5, then 10 mM produced a progressive reduction in both indices of the secondary response, which was inversely related to the primary response. These findings suggest that cyclic AMP not only mediates IRI release in quantitative terms but is also implicated in the qualitative nature of the response pattern. They also indicate a possible metabolic basis for biphasic IRI release, the acute or primary response being dependent upon the basal state of the cell and the availability of endogenous energy sources, the secondary response upon the availability of exogenous substrate.

show abstract

Role of Adrenergic Receptors in Glucose-Induced Insulin Secretion in Man

Cited by 106 publications

References 6 publications

Studies of secretin-stimulated insulin responses in man

Studies of secretin-stimulated insulin responses in man

Metabolic state, pancreatic insulin content and B-cell morphology of normoglycemic spiny mice (acomys cahirinus): Indications for an impairment of insulin secretion

Perifusion of rat pancreatic tissue in vitro: substrate modification of theophylline-induced biphasic insulin release

Contact Info

Product

Resources

About