Is gluconeogenesis stimulated by insulin or glucagon? (2023)

Insulin exerts direct control of gluconeogenesis by acting on the liver, but also indirectly affects gluconeogenesis by acting on other tissues. The direct effect of insulin was demonstrated in fasted dogs, where portal plasma insulin suppressed hepatic glucose production.

Gluconeogenesis supplies the needs for plasma glucose between meals. Gluconeogenesis is stimulated by the diabetogenic hormones (glucagon, growth hormone, epinephrine, and cortisol). Gluconeogenic substrates include glycerol, lactate, propionate, and certain amino acids.

Specifically, glucagon promotes hepatic conversion of glycogen to glucose (glycogenolysis), stimulates de novo glucose synthesis (gluconeogenesis), and inhibits glucose breakdown (glycolysis) and glycogen formation (glycogenesis) (Fig.

Insulin is a key hormone that inhibits gluconeogenesis, and insulin resistance is a hallmark of type 2 diabetes.

Glucagon opposes hepatic insulin action and enhances the rate of gluconeogenesis, increasing hepatic glucose output. In order to support gluconeogenesis, glucagon promotes skeletal muscle wasting to supply amino acids as gluconeogenic precursors.

Glucagon is an extremely potent hormone released by drops in blood glucose. Glucagon acts on the liver to elevate plasma glucose, an action opposite to that of insulin. Glucagon promotes hepatic glycogenolysis and increases hepatic gluconeogenesis.

Glycogenolysis is the enzymatic process of breakdown of glycogen in liver and muscles. Insulin hormone inhibits glycogenolysis in liver cells and muscles and serves as anabolic hormone. The glycogen phosphorylase or also termed s phosphorylase is mainly regulates the rate of glycogenolysis in liver and muscles.

Insulin inhibits gluconeogenesis and glycogenolysis, stimulates glycolysis and glycogenesis, stimulates uptake and incorporation of amino acids into protein, inhibits protein degradation, stimulates lipogenesis, and suppress lipolysis (Bassett, 1975. (1975).

Liver metabolic processes are tightly regulated by neuronal and hormonal systems. The sympathetic system stimulates, whereas the parasympathetic system suppresses, hepatic gluconeogenesis. Insulin stimulates glycolysis and lipogenesis, but suppresses gluconeogenesis; glucagon counteracts insulin action.

Gluconeogenesis is activated when energy is required (i.e., low ATP/AMP ratio) and inhibited if there is an excess of energy available (i.e., large ATP/AMP ratio). Gluconeogenesis is also stimulated by glucagon and inhibited by insulin (see “Phosphofructokinase-2” for the mechanism).

Insulin is the most important hormone that inhibits gluconeogenesis. It acts predominantly by suppressing the expression of the genes for the key gluconeogenic enzymes PEPCK and G-6-Pase.

Insulin secreted during the fed state promotes glucose uptake and utilization, and inhibits gluconeogenesis. In contrast, glucagon secreted during fasting stimulates gluconeogenesis and glycogenolysis.

Glycogen synthesis in skeletal muscle is under hormonal control, with a principal regulatory role being taken by insulin that acutely promotes glycogen synthesis from glucose by stimulating glucose uptake and by activating the key enzyme glycogen synthase (GS) (1).

Basically, insulin promotes anything that will decrease blood glucose levels. This can happen in two ways: either converting glucose–> pyruvate (glycolysis) or by converting glucose–>glycogen (glucogenesis). Glucagon does the opposite, it promotes any pathway that will increase blood glucose levels.

Liver metabolic processes are tightly regulated by neuronal and hormonal systems. The sympathetic system stimulates, whereas the parasympathetic system suppresses, hepatic gluconeogenesis. Insulin stimulates glycolysis and lipogenesis, but suppresses gluconeogenesis; glucagon counteracts insulin action.

When there is an excess of energy available, gluconeogenesis is inhibited. When energy is required, gluconeogenesis is activated. The conversion of pyruvate to PEP is regulated by acetyl-CoA. More specifically pyruvate carboxylase is activated by acetyl-CoA.

Glycogenolysis occurs primarily in the liver and is stimulated by the hormones glucagon and epinephrine (adrenaline).

Insulin hormone inhibits glycogenolysis in liver cells and muscles and serves as anabolic hormone. The glycogen phosphorylase or also termed s phosphorylase is mainly regulates the rate of glycogenolysis in liver and muscles.

Glucagon, epinephrine, norepinephrine, and cyclic AMP stimulated gluconeogenesis from lactate in perfused livers from fasted and fed rats.

Insulin and glucagon are the most important hormones regulating hepatic gluconeogenesis.

Insulin stimulates glycogenesis by activating and dephosphorylating glycogen synthase (GS).

In essence, the anabolic hormone insulin promotes glycogenesis and inhibits glycogenolysis via the activation of PP1, leading to the dephosphorylation of glycogen phosphorylase (inactivation) and glycogen synthase (activation), and via the activation of Akt, leading to the phosphorylation of GSK-3 (inactivation) that …

Pulse stimulation of insulin induces responses of glycolysis, gluconeogenesis and glycogenesis.

Insulin is the most important hormone that inhibits gluconeogenesis. It acts predominantly by suppressing the expression of the genes for the key gluconeogenic enzymes PEPCK and G-6-Pase.

Insulin inhibits gluconeogenesis and glycogenolysis, stimulates glycolysis and glycogenesis, stimulates uptake and incorporation of amino acids into protein, inhibits protein degradation, stimulates lipogenesis, and suppress lipolysis (Bassett, 1975. (1975).

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.