Influence of Glucagon on Pancreatic Exocrine Secretion

Dyck, Walter P.; Rudick, J; Hoexter, Barton; Janowitz, Henry D.

doi:10.1016/s0016-5085(69)80162-9

Cited by 105 publications

(24 citation statements)

References 18 publications

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“…After insulin treatment, pancreatic amylase content increased, whereas trypsinogen content remained elevated. These results are in agreement with previous studies (27)(28)(29)(30)(31)(32)(33)(34)(35)(36)(37)(38)(39). The results of this and previous studies indicate that insulin plays an important role in the regulation of pancreatic enzyme synthesis as well as exocrine secretory function.…”

Section: Juice Flowsupporting

confidence: 93%

“…Serum levels and tissue contents of other islet hormones such as glucagon, somatostatin, and pancreatic polypeptide are increased by insulinopenia (34)(35)(36). These islet hormones inhibit exocrine pancreatic secretion stimulated by secretin and/or CCK (37)(38)(39). Although most of these effects have been observed in vivo, in vitro studies have shown few consistent effects on secretion (40,41).…”

Section: Juice Flowmentioning

confidence: 99%

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Secretin-Induced Exocrine Secretion in Perfused Pancreas Isolated From Diabetic Rats

Okabayashi

Ōtsuki²,

Ohki³

et al. 1988

Diabetes

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Exocrine secretory function in response to 10 pM to 10 nM synthetic secretin was evaluated in perfused pancreas isolated from control, streptozocin-induced diabetic (STZ-D), alloxan-induced diabetic (ALX-D), and insulin-treated STZ-D rats. In STZ-D rats, the basal rate of pancreatic juice flow was significantly increased (10.3 +/- 1.0 microliters/20 min) compared with control rats (4.4 +/- 0.2 microliters/20 min). The basal rate of amylase output as well as pancreatic amylase content were significantly decreased to less than 5% of control values. The basal rates of protein and trypsinogen outputs were similar in both groups. In both control and diabetic rats, secretin caused a dose-dependent increase in exocrine secretion. Secretin (10 pM to 10 nM) induced 1.1- to 11.7-fold increases in exocrine secretion in STZ-D rats. These increases were significantly lower than the 2.1- to 20.8-fold increases in control rats. Furthermore, there was no significant increase in exocrine secretion from STZ-D rats in response to 10 pM secretin, although this concentration of secretin caused a significant increase in control rats. Secretin-induced exocrine secretion in ALX-D rats was similar to that in STZ-D rats. In insulin-treated STZ-D rats, the basal rates of pancreatic secretion were not significantly different from those of control rats. These results suggest that insulin resistance in this patient was due to a circulating factor of low molecular weight that uncoupled insulin stimulation of glucose transport from receptor binding and phosphorylation. The factor appears to increase the binding activity of the alpha-subunit of the insulin receptor without affecting the kinase activity of the beta-subunit.

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Section: Juice Flowsupporting

confidence: 93%

Section: Juice Flowmentioning

confidence: 99%

Secretin-Induced Exocrine Secretion in Perfused Pancreas Isolated From Diabetic Rats

Okabayashi

Ōtsuki²,

Ohki³

et al. 1988

Diabetes

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“…Administration of glucagon to dogs with pancreatic fistulae depresses the rate of flow, volume, and enzyme concentration of pancreatic juice secreted by the pancreozymin/secretinstimulated gland (Dyck et al, 1969). These observations were confirmed by Nakajima and Magee (1970).…”

Section: Introductionmentioning

confidence: 67%

Use of Glucagon in the Treatment of Pancreatitis

Knight¹,

Condon²,

Smith³

1971

BMJ

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“…As a consequence atrophy might result. A persisting elevation of glucagon levels as observed in some diabetic patients has been suggested to contribute to exocrine damage and dysfunction [46, 47]. Somatostatin is a relevant regulator of exocrine function [48], and elevated levels, as described in streptozotocin-induced diabetes mellitus, have been shown to reduce exocrine pancreatic function [49].…”

Section: Resultsmentioning

confidence: 99%

Exocrine Pancreatic Insufficiency in Diabetes Mellitus: A Complication of Diabetic Neuropathy or a Different Type of Diabetes?

Hardt

Ewald

2011

Experimental Diabetes Research

102

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Pancreatic exocrine insufficiency is a frequently observed phenomenon in type 1 and type 2 diabetes mellitus. Alterations of exocrine pancreatic morphology can also be found frequently in diabetic patients. Several hypotheses try to explain these findings, including lack of insulin as a trophic factor for exocrine tissue, changes in secretion and/or action of other islet hormones, and autoimmunity against common endocrine and exocrine antigens. Another explanation might be that diabetes mellitus could also be a consequence of underlying pancreatic diseases (e.g., chronic pancreatitis). Another pathophysiological concept proposes the functional and morphological alterations as a consequence of diabetic neuropathy. This paper discusses the currently available studies on this subject and tries to provide an overview of the current concepts of exocrine pancreatic insufficiency in diabetes mellitus.

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Influence of Glucagon on Pancreatic Exocrine Secretion

Cited by 105 publications

References 18 publications

Secretin-Induced Exocrine Secretion in Perfused Pancreas Isolated From Diabetic Rats

Secretin-Induced Exocrine Secretion in Perfused Pancreas Isolated From Diabetic Rats

Use of Glucagon in the Treatment of Pancreatitis

Exocrine Pancreatic Insufficiency in Diabetes Mellitus: A Complication of Diabetic Neuropathy or a Different Type of Diabetes?

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