Glucagon is released to stop blood sugar levels dropping too low hypoglycaemia , while insulin is released to stop blood sugar levels rising too high hyperglycaemia. The release of glucagon is stimulated by low blood glucose, protein -rich meals and adrenaline another important hormone for combating low glucose. The release of glucagon is prevented by raised blood glucose and carbohydrate in meals, detected by cells in the pancreas.
For example, it encourages the use of stored fat for energy in order to preserve the limited supply of glucose. A rare tumour of the pancreas called a glucagonoma can secrete excessive quantities of glucagon.
Unusual cases of deficiency of glucagon secretion have been reported in babies. This results in severely low blood glucose which cannot be controlled without administering glucagon. Glucagon can be given by injection to restore blood glucose lowered by insulin even in unconscious patients. It can increase glucose release from glycogen stores more than insulin can suppress it. The effect of glucagon is limited, so it is very important to eat a carbohydrate meal once the person has recovered enough to eat safely.
About Contact Events News. Search Search. You and Your Hormones. One approach is the pancreatic slice preparation Huang et al. This, along with the larger glucagon granules found on E. Future studies employing the pancreas slice preparation will enable the elucidation of paracrine regulation within normal and diabetic islets.
Ideally, these clever approaches could be combined. From a clinical point of view, the mechanism whereby in T2D there is excessive response to glucagon during meals, and whether pharmacological intervention can prevent this problem. A key question is also whether it is possible to prevent hypoglycemia in insulin-treated diabetics. Patrick E. Herbert Y. Gaisano and Mladen Vranic have no financial or commercial relationships.
This work was supported by a grant to Herbert Y. Adeghate, E. Distribution of calcitonin-gene-related peptide, neuropeptide-Y, vasoactive intestinal polypeptide, cholecystokinin-8, substance P and islet peptides in the pancreas of normal and diabetic rats. Neuropeptides 33, — Altarejos, J. Cell Biol. Amatruda, J. Porte Jr. Sherwin, and A. Andersson, S.
Pflugers Arch. Barg, S. Mechanisms of exocytosis in insulin-secreting B-cells and glucagon-secreting A-cells. Tight coupling between electrical activity and exocytosis in mouse glucagon-secreting alpha-cells. Diabetes 49, — Barns, A. Ketoacidosis in pancreatectomized man. Baukrowitz, T. Science , — Boden, G. Glucagon deficiency and hyperaminoacidemia after total pancreatectomy. Bokvist, K. Bolli, G. Abnormal glucose counter-regulation in insulin-dependent diabetes mellitus.
Interaction of anti-insulin antibodies and impaired glucagon and epinephrine secretion. Diabetes 32, — Pubmed Abstract Pubmed Full Text.
Braun, M. Somatostatin release, electrical activity, membrane currents and exocytosis in human pancreatic delta cells. Diabetologia 52, — Butler, P.
Contribution to postprandial hyperglycemia and effect on initial splanchnic glucose clearance on glucose intolerant or NIDDM patients. Diabetes 40, 73— Cabrera, O.
The unique cytoarchitecture of human pancreatic islets has implications for islet cell function. Glutamate is a positive autocrine signal for glucagon release. Cell Metab. Cejvan, K. Intra-islet somatostatin regulates glucagon release via type 2 somatostatin receptors in rats. Diabetes 52, — Cryer, P. Diabetologia 4, — Per-arnt-sim PAS domain-containing protein kinase is downregulated in human islets in type 2 diabetes and regulates glucagon secretion.
Diabetologia 54, — Dagogo-Jack, S. Hypoglycemia-associated autonomic failure in insulin dependent diabetes mellitus. De Marinis, Y. Detimary, P.
The changes in adenine nucleotides measured in glucose-stimulated rodent islets occur in beta cells but not in alpha cells and are also observed in human islets. Doi, K. Identical biological effects of pancreatic glucagon and a purified moiety of canine gastric glucagon. Drucker, D. Biologic actions and therapeutic potential of the proglucagon-derived peptides. Duchen, M. Substrate-dependent changes in mitochondrial function, intracellular free calcium concentration and membrane channels in pancreatic beta-cells.
Dufer, M. Methyl pyruvate stimulates pancreatic beta-cells by a direct effect on KATP channels, and not as a mitochondrial substrate. Dunning, B. Alpha cell function in health and disease: influence of glucagon-like peptide Diabetologia 48, — The role of alpha-cell dysregulation in fasting and postprandial hyperglycemia in type 2 diabetes and therapeutic implications.
Fanelli, C. Long-term recovery from unawareness, deficient counterregulation and lack of cognitive dysfunction during hypoglycemia following institution of rational intensive therapy in IDDM. Diabetologia 37, — Franklin, I. Beta-cell secretory products activate alpha-cell ATP-dependent potassium channels to inhibit glucagon release.
Diabetes 54, — GABA in the endocrine pancreas: its putative role as an islet cell paracrine-signalling molecule. Fu, A. Role of AMPK in pancreatic beta cell function. PMID: Gaisano, H. Pancreatic islet alpha-cell commands itself: secrete more glucagon! Gauthier, B. Synaptotagmins bind calcium to release insulin. Gerich, J. Glucose counterregulation and its impact on diabetes mellitus. Diabetes 37, — Lack of glucagon response to hypoglycaemia in diabetes: evidence for an intrinsic pancreatic alpha cell defect.
Gopel, S. Gromada, J. Alpha-cells of the endocrine pancreas: 35 years of research but the enigma remains. Somatostatin inhibits exocytosis in rat pancreatic alpha-cells by G i2 -dependent activation of calcineurin and depriming of secretory granules.
Diabetes 53, S—S Gupta, V. The defective glucagon response from transplanted intrahepatic pancreatic islets during hypoglycemia is transplantation site-determined. Diabetes 46, 28— Gustavsson, N.
Hatton, T. Glucagon-like immunoreactants in extracts of the rat hypothalamus. Endocrinology , — Biosynthesis of glucagon IRG in canine gastric mucosa. Diabetes 34, 38— Hauge-Evans, A. Diabetes 58, — Hayashi, M. Vesicular inhibitory amino acid transporter is present in glucagon-containing secretory granules in alphaTC6 cells, mouse clonal alpha-cells, and alpha-cells of islets of Langerhans. Heimberg, H. The glucose sensor protein glucokinase is expressed in glucagon producing alpha cells.
Henquin, J. Hierarchy of the beta-cell signals controlling insulin secretion. Hocart, S. Highly potent cyclic disulfide antagonists of somatostatin. Holst, J. Circulating glucagon after total pancreatectomy in man.
Diabetologia 25, — Hope, K. Diabetes 53, — Huang, Y. Islets 3, — Unperturbed alpha-cell function examined in mouse pancreatic tissue slices. In situ electrophysiological examination of pancreatic alpha-cells in the streptozotocin-induced diabetes model revealing the cellular basis of glucagon hypersecretion. Diabetes in press.
Inouye, K. Effects of recurrent hyperinsulinemia with and without hypoglycemia on counterregulation in diabetic rats. Ishihara, H. Islet beta-cell secretion determines glucagon release from neighbouring alpha-cells. Ito, A. Adhesion molecule CADM1 contributes to gap junctional communication among pancreatic islet alpha-cells and prevents their excessive secretion of glucagon.
Islets 4. Kanno, T. Cellular function in multicellular system for hormone-secretion: electrophysiological aspect of studies on alpha-, beta- and delta-cells of the pancreatic islet. Kawamori, D. Insulin signaling in alpha cells modulates glucagon secretion in vivo.
Kim, A. Islet architecture: a comparative study. Islets 1, — Le Marchand, S. It is not clear whether this reflects a direct effect of glucose on the alpha cell, or perhaps an effect of insulin, which is known to dampen glucagon release.
Another hormone well known to inhibit glucagon secretion is somatostatin. Diseases associated with excessively high or low secretion of glucagon are rare. Cancers of alpha cells glucagonomas are one situation known to cause excessive glucagon secretion. These tumors typically lead to a wasting syndrome and, interestingly, rash and other skin lesions. Although insulin deficiency is clearly the major defect in type 1 diabetes mellitus, there is considerable evidence that aberrant secretion of glucagon contributes to the metabolic derangements seen in this important disease.
For example, many diabetic patients with hyperglycemia also have elevated blood concentrations of glucagon, but glucagon secretion is normally suppressed by elevated levels of blood glucose.
0コメント