Fructose 1,6-bisphosphate dephosphorylation in gluconeogenesis

Hydrolysis of fructose 1,6-bisphosphate by fructose 1,6-bisphosphatase,found in the liver and kidneys, bypasses the irreversible phosphofructokinase-1 (PFK-1) reaction of glycolysis and provides an energetically favorable pathway for the formation of fructose 6-phosphate (Fig. 1). This reaction is an important regulatory site of gluconeogenesis.

Figure 1: Dephosphorylation of fructose 1,6-bisphosphate. AMP = adenosine monophosphate; = phosphate.

1. Regulation by intracellular energy levels: Fructose 1,6-bisphosphatase is inhibited by a rise in the adenosine monophosphate (AMP)/ATP ratio, which signals a low-energy state in the cell. Conversely, low AMP and high ATP levels stimulate gluconeogenesis, an energy-requiring pathway.
2. Regulation by fructose 2,6-bisphosphate: Fructose 1,6- bisphosphatase is inhibited by fructose 2,6-bisphosphate, an allosteric effector whose concentration is influenced by the insulin/glucagon ratio. When glucagon is high, the effector is not made by hepatic PFK-2 , and thus, the phosphatase is active (Fig. 2 ). [Note: The signals that inhibit (low energy, high fructose 2,6-bisphosphate) or activate (high energy, low fructose 2,6-bisphosphate) gluconeogenesis have the opposite effect on glycolysis, providing reciprocal control of the pathways that synthesize and oxidize glucose .]

Figure 2: Effect of elevated glucagon on the intracellular concentration of fructose 2,6-bisphosphate in the liver. AMP and ADP = adenosine mono- and diphosphates; cAMP = cyclic AMP; PFK-2 = phosphofructokinase-2; FBP-2 =fructose 2,6-bisphosphatase; FBP-1 = fructose 1,6-bisphosphatase; and =phosphate.

مواضيع ذات صلة

آلية عمل المجموعة الأولى من الهرمونات

الهرمونات وآليات الاستتباب

تدرك (تقويض) الهرمونات وتعطيلها

نقل الهرمونات في البلازما

تغاير خزن الهرمونات وإفرازها

تخليق POMC ومعالجته

The Amino Acids

Absorption & Transport of Transition Metals

Physiologic Roles of The Essential Transition Metals

تخليق الأنجيوتنسين

تخلیق PTH

تخليق الأنسولين