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DURATION OF PERFUSION, MIN

FIGURE 7-21 Typical biphasic hormone-releasing profile as seen with the isolated perfused pancreas from different species as a result of a- or /8-cell stimulation. [Reproduced with permission from Mat-schinsky F. M., Pagliara, A. A., Zawalich, W. S., and Trus, M. D. (1979). Metabolism of pancreatic islets and regulation of insulin and glucagon secretion. In "Endocrinology" (L. J. DeGroot et al, eds.), Vol. 2, p. 936. Grune & Stratton, New York.]

FIGURE 7-22 Electron micrograph and freeze-fracture study of insulin secretion. Isolated islets were exposed to a high (3.0 mg/ ml) glucose concentration, (a) Thin section of part of a /3-cell. A granule core is being discharged into the extracellular space through the opening resulting from the coalescence of the membrane limiting the granule with the plasma membrane (arrows) (X 56,000). (b) Freeze-fracture replica. On the exposed face of the plasma membrane there are several exocytotic (emiocytotic) stomata (thin arrows). The channel extending in the cytoplasm (large arrow) is possibly the result of the fusion of the membranes of several granules whose cores could be discharged through a single aperture in the plasma membrane (X 31,000). Courtesy of Dr. Lelio Orci, Geneva. [Reproduced with permission from Lacy P. E., and Greider, M. H. (1979). Anatomy and ultrastructural organization of pancreatic islets. In "Endocrinology" (L. J. DeGroot et ah, eds.), Vol. 2, p. 913. Grune & Stratton, New York.]

FIGURE 7-22 Electron micrograph and freeze-fracture study of insulin secretion. Isolated islets were exposed to a high (3.0 mg/ ml) glucose concentration, (a) Thin section of part of a /3-cell. A granule core is being discharged into the extracellular space through the opening resulting from the coalescence of the membrane limiting the granule with the plasma membrane (arrows) (X 56,000). (b) Freeze-fracture replica. On the exposed face of the plasma membrane there are several exocytotic (emiocytotic) stomata (thin arrows). The channel extending in the cytoplasm (large arrow) is possibly the result of the fusion of the membranes of several granules whose cores could be discharged through a single aperture in the plasma membrane (X 31,000). Courtesy of Dr. Lelio Orci, Geneva. [Reproduced with permission from Lacy P. E., and Greider, M. H. (1979). Anatomy and ultrastructural organization of pancreatic islets. In "Endocrinology" (L. J. DeGroot et ah, eds.), Vol. 2, p. 913. Grune & Stratton, New York.]

consequence of their uptake into the /3-cell and subsequent metabolism via intermediary metabolism. The recognition process might consist of the identification of the presence of a certain family of key metabolites or cofactors, such as NADH / NAD, ATP, and intracellular pH. This then could lead to activation of the stimulus-secretion mechanism, resulting in insulin secretion.

A third plausible model would be a combination of the two separate models described. Figure 7-24 presents a schematic working model proposed by F. Mat-schinsky to describe the coupling of the "fuel receptor" to the stimulus-secretion mechanism, which results in insulin secretion.

In terms of the biphasic secretion of insulin (Figure 7-21) then, the first acute phase of insulin secretion represents the release of insulin already stored in the granules of the /3-cell. The slower second phase of insulin release is likely supported by an initiation of de novo insulin biosynthesis.

3. Secretion of Glucagon

The principal physiological function of the pancreatic a-cell is to prevent hypoglycemia by appropriately regulating the secretion of glucagon. Glucagon secretion by the a-cells particularly is dedicated to safe guarding the delivery of fuel (usually glucose) to the cerebellum. As documented in Table 7-8, there is an array of substances that are potent modulators of glucagon secretion. In addition, there is evidence of both adrenergic and cholinergic control of glucagon secretion, which comes into play during insulin-induced hypoglycemia; this redundant neural mechanism apparently exists to combat the life-threatening situation of hypoglycemia. Glucagon release is clearly stimulated by epinephrine and blocked by the /3-adrenergic blocking agent propanolol, which indicates the presence of a /3-adrenergic receptor on the D cell membrane. Also, somatostatin can block glucagon release from the D cell. Electron micrographie studies suggest that the basic mechanism for release of the glucagon-containing granules is emiocytosis. At the present time it is not clear whether there is an involvement of a microtubule-microfilament system or whether there is a glucose receptor in the plasma membrane.

4. Integrated Secretion of Insulin and Glucagon

The overriding responsibility of insulin and glucagon is to maintain blood glucose within normal limits. Shown in Figure 7-25 are the dose-response curves of

Hormones, Second Edition

Glucose

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