As a counterregulatory hormone for insulin, glucagon plays a critical role in maintaining glucose homeostasis in vivo in both animals and humans. To increase blood glucose, glucagon promotes hepatic glucose output by increasing glycogenolysis and gluconeogenesis and by decreasing glycogenesis and glycolysis in a concerted fashion via multiple mechanisms. Compared with healthy subjects, diabetic patients and animals have abnormal secretion of not only insulin but also glucagon. Hyperglucagonemia and altered insulin-to-glucagon ratios play important roles in initiating and maintaining pathological hyperglycemic states. Not surprisingly, glucagon and glucagon receptor have been pursued extensively in recent years as potential targets for the therapeutic treatment of diabetes.

Glucagon and regulation of glucose metabolism

Anti-hyperglycemic effect of Eugenia jambolana and Tinospora cordifolia in experimental diabetes and their effects on key metabolic enzymes involved in carbohydrate metabolism.

It was in 1909 that Young, in the laboratory of Harden, isolated from fermenting yeast the fructose bisphosphate (the Harden and Young ester) that was later identified by Levene & Raymond (1928) as fructose 1,6-bisphosphate. Some 71 years elapsed until a second fructose bisphosphate was isolated from living cells and identified as fructose 2,6bisphosphate (Van Schaftingen et al., 1980c). In contrast with its elder brother, Fru-2,6-P2 is not an intermediary metabolite of glycolysis, but its most potent regulator. In the present review, we will summarize the work that led to its discovery and we will try to delineate its potential role in the control of metabolism in various organisms.

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Fructose 2,6-bisphosphate 2 Years After its Discovery

Fructose 2,6-bisphosphate.

The low-molecular-weight stimulator of phosphofructokinase [Van Schaftingen, Hue & Hers (1980) Biochem. J. 192, 887-895] has been purified from rat liver. It was completely destroyed upon incubation with 0.01 M-HCl for 10 min at 20 degrees C and fructose 6-phosphate and a reducing power equivalent in amount to the acid-labile organic phosphate were formed. It was therefore tentatively identified as fructose 2,6-bisphosphate.

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J E Felíu

Papers

Inactivation of phosphofructokinase by glucagon in rat hepatocytes.