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System glucagon

Drucker DJ, Nauck MA. The incretin system glucagon-hke peptide-1 receptor agonists and dipeptidyl peptidase-4 inhibitors in type 2 diabetes. Lancet 2006 368 1696-1705. [Pg.136]

FIGURE 6.20.7 The glucose control system. Glucagon and insulin act antagonistically to maintain blood glucose level very precisely. (From Campbell, N. A. et al., Biology, 5th edn., Addison Wesley Longman, Menlo Park, CA, 1999. With permission.)... [Pg.424]

Enzymes of glycogenes Glycogen synthase system is,glycoiy T sis, and py T ruvate oxidation Insulin Insulin Glucose 6-phosphate Glucagon (cAMP) phos-phorylase, glycogen... [Pg.156]

Systemic effects of nickel exposure include hyperglycemia, increased levels of plasma glucagon, damage to the pancreatic islet cells, decreased body weight, reduced food and water intake, and hypothermia (NAS 1975 USEPA 1980 USPHS 1993). Acute administration of nickel salts caused prompt hyperglucagonemia and subsequent hyperinsulinemia in rats, rabbits, and guinea pigs (WHO... [Pg.510]

Gordienko D V, Bolton TB, Cannell MB 1998 Variability in spontaneous subcellular Ca2+ release in guinea-pig ileum smooth muscle cells. J Physiol 507 707-720 Ho R, Shao Z 1991 Axial resolution of confocal microscopes revisited. Optiik 88 147—154 Holz GG, Leech CA, Heller RS, Castonguay N, Habener JF 1999 cAMP-dependent mobilization of intracellular Ca2+ stores by activation of ryanodine receptors in pancreatic [j cells. A Ca2+ signaling system stimulated by the insulinotropic hormone glucagon-like peptide-1-(7-37). J Biol Chem 274 14147-14156 Lipsius SL, Hiiser J, Blatter LA 2001 Intracellular Ca2+ release sparks atrial pacemaker activity. News Physiol Sci 16 101-106... [Pg.173]

The next key point is to realize that each enzyme in the pathway exists in both active and inactive forms. cAMP initiates a cascade of reactions by activating protein kinase A (PK-A)," the active form of which activates the next enzyme in the sequence, and so on. At the end of the day, glycogen phosphorylase is activated and glucose or ATP is produced. This signaling pathway is a marvelous amplification system. A few molecules of glucagon or adrenaline may induce formation of many molecules of cAMP, which may activate many of PK-A, and so on. The catalytic power of enzymes is magnified in cascades of this sort. [Pg.226]

The effector systems result in changes in messenger systems that then cause the effects of the hormone. Not surprisingly, the effects of the hormone depend on which hormone is being considered. To illustrate this four hormones - insulin, cortisol, adrenaline and glucagon - are discussed. [Pg.258]

Ejfect of temperature Luisi et al. [26] reported that the temperature markedly affected the transfer of a-chymotrypsin in a chloroform-trioctyl-methylammonium chloride (TOMAQ system. By increasing the temperature from 25-40°C, about 50% higher transfer yield was realized. No appreciable transfer of glucagone took place at room temperature, whereas transfer at 37°C was possible. These results contradict work by Dekker et al. [27], who studied the back stripping (desolubilization) of a-amylase from a TOMAC/isooctane/octanol/Rewopal HV5 system by increasing the temperature. This caused a decrease in Wo with increasing temperature and, as a result, the a-amylase was expelled from the reverse micelle phase. [Pg.665]

In their report the researchers describe a culturing technique that can turn mouse embryonic stem cells into cell clusters that resemble pancreatic islets. The clusters inner cells produced insulin, while outer cells produced glucagon and somatostatin, two other proteins typically synthesized by pancreatic cells. Most important, the embryonic stem cell-derived pancreas cells produce insulin in response to glucose, the fundamental role of beta cells that regulate insulin secretion. The major shortcoming of the system at this time is the low levels of insulin production. Refinements in culture technique or drug manipulation may be needed to achieve therapeutic levels. [Pg.411]

Somatostatin, a 14-amino-acid peptide (Figure 37-2), is found in the hypothalamus, other parts of the central nervous system, the pancreas, and other sites in the gastrointestinal tract. It inhibits the release of GH, glucagon, insulin, and gastrin. [Pg.832]


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See also in sourсe #XX -- [ Pg.152 , Pg.153 ]




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