Different tissues in our body can cross-talk during fasting and fed state via hormonal regulation. Two major hormones, insulin and glucagon, play an important role in regulating metabolic homeostasis by inducing different responses from tissues such as liver, adipose tissue, and muscle. During fed state, insulin promotes glucose uptake in the muscle and adipose tissue and stimulates glycogen and fatty acid synthesis in the liver. At the same time, it inhibits lipolysis and hepatic glycogenolysis and gluconeogenesis. On the other hand, glucagon during fasting state would induce the opposite responses. Low- carbohydrate diet replaced with high protein and fats such as Atkins-type diet, in essence, minimizes the release of insulin and maximizes
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This ensures that glucose uptake is predominantly done in the brain and RBCs. Additionally, the transporter allows liver to release varying concentrations of glucose during extended fasting state when the rate of gluconeogenesis is high. Secondly, glucokinase is normally insensitive to glucose due to its high Km value. During fed state when the blood glucose level is above 6mM, insulin stimulates glucokinase transcription and availability. The hormone also stimulates fatty acid synthesis in the liver mitochondria by activating acetyl-coA …show more content…
Acetyl CoA is a major hub of the metabolic system because it can be made by the oxidation of glucose or fatty acid. During low-carbohydrate diet rich in proteins and fat such as in Atkins Diet, the body relies on hepatic gluconeogenesis and ketogenesis for its source of fuel. When glycogen reservoir begins to be depleted, the body compensates by releasing glucagon, which stimulates liver gluconeogenesis and lipolysis (Pogozelski et al., 2005). As proteins are degraded, glucose-alanine cycle allows for the glucogenic amino acid, alanine, to be transported to the liver where it can be converted back to pyruvate for gluconeogenesis. Increased liver gluconeogenesis uses up available oxaloacetate, which results in the buildup of acetyl CoA. At the same time, increased beta-oxidation of fatty acids also contributes to the buildup of acetyl CoA. As a result, acetyl CoA are oxidized to acetone, acetoacetate, and D-hydroxybutyrate, which are collectively known as ketone bodies (Pogozelski et al., 2005). Generation of ketone bodies spares the utilization of glucose for obligate glucose-users such as RBCs and provide alternative fuel that is easily transportable to extra-hepatic tissues such as muscle and brain (Manninen,
This ensures that glucose uptake is predominantly done in the brain and RBCs. Additionally, the transporter allows liver to release varying concentrations of glucose during extended fasting state when the rate of gluconeogenesis is high. Secondly, glucokinase is normally insensitive to glucose due to its high Km value. During fed state when the blood glucose level is above 6mM, insulin stimulates glucokinase transcription and availability. The hormone also stimulates fatty acid synthesis in the liver mitochondria by activating acetyl-coA …show more content…
Acetyl CoA is a major hub of the metabolic system because it can be made by the oxidation of glucose or fatty acid. During low-carbohydrate diet rich in proteins and fat such as in Atkins Diet, the body relies on hepatic gluconeogenesis and ketogenesis for its source of fuel. When glycogen reservoir begins to be depleted, the body compensates by releasing glucagon, which stimulates liver gluconeogenesis and lipolysis (Pogozelski et al., 2005). As proteins are degraded, glucose-alanine cycle allows for the glucogenic amino acid, alanine, to be transported to the liver where it can be converted back to pyruvate for gluconeogenesis. Increased liver gluconeogenesis uses up available oxaloacetate, which results in the buildup of acetyl CoA. At the same time, increased beta-oxidation of fatty acids also contributes to the buildup of acetyl CoA. As a result, acetyl CoA are oxidized to acetone, acetoacetate, and D-hydroxybutyrate, which are collectively known as ketone bodies (Pogozelski et al., 2005). Generation of ketone bodies spares the utilization of glucose for obligate glucose-users such as RBCs and provide alternative fuel that is easily transportable to extra-hepatic tissues such as muscle and brain (Manninen,