During fasting, when glycogen stores have been depleted, the body begins to synthesise glucose from

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BlackTom AI · Accepted Answer

The question asks: During fasting, when glycogen stores have been depleted, the body begins to synthesise glucose from

Option a: amino acids. This is correct because during prolonged fasting, gluconeogenesis uses non-carbohydrate precursors, primarily amino acids (especially alanine and glutamine) from muscle protein to generate glucose for tissues that depend on it, such as the brain and red blood cells.

Option b: fatty acids. Fatty acids are largely broken down to acetyl-CoA for energy via beta-oxidation and are not a primary substrate for gluconeogenesis. In mammals, acetyl-CoA derived from fatty acid oxidation cannot be converted back to pyruvate or oxaloacetate in sufficient quantities to support significant glucose production, so fatty acids do not serve as gluconeogenic substrates.

Option c: acetyl CoA. While acetyl-CoA enters the citric acid cycle to provide energy, it cannot be used directly to form glucose in gluconeogenesis because the conversion of acetyl-CoA to pyruvate or oxaloacetate is not a reversible step that yields net glucose; thus acetyl-CoA itself is not a gluconeogenic substrate.

Option d: ketone bodies. Ketone bodies are produced during prolonged fasting from acetyl-CoA to supply energy to the brain and other tissues, reducing the need for glucose. They are not substrates for gluconeogenesis; instead, they represent an alternative fuel source when glucose is scarce.

In summary, gluconeogenesis during extended fasting relies on amino acids as the principal gluconeogenic substrates, while fatty acids, acetyl-CoA, and ketone bodies serve other metabolic roles or energy pathways and do not directly supply glucose synthesis.

During fasting, when glycogen stores have been depleted, the body begins to synthesise glucose from

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