Biochemistry · MU Pleven

70. Metabolism in Renal Cortex and Medulla: Glycolysis, Gluconeogenesis, Renal Glutaminase, Buffers. Metabolism in intestines.

Explains how the renal cortex and medulla differ in oxygen supply and fuel use, with the cortex running gluconeogenesis and fatty acid oxidation while the medulla relies on anaerobic glycolysis and lactate shuttling. Goes on to renal glutaminase and ammonium-based acid excretion during acidosis, then the kidney's bicarbonate, phosphate and ammonium buffers. Closes with intestinal metabolism, covering glutamine as fuel, short-chain fatty acids from bacterial fermentation, and chylomicron packaging of dietary lipids.

Inside: 3 sections · 5 labelled pictures · 20 flashcards · 3 min

Topic 70 of 76 in the MU Pleven syllabus for Biochemistry (Medicine, Year 2). The free AceMed note covers it in 3 sections, about 419 words (3 min of reading), with 20 flashcards.

In this note

  1. Metabolism in Renal Cortex and Medulla: Glycolysis, Gluconeogenesis, Renal Glutaminase, Buffers. Metabolism in intestines.
  2. Metabolism in the Kidney
  3. Metabolism in the Intestines

Metabolism in the Kidney

The renal cortex and medulla have very different oxygen supply, energy demands and metabolic pathways.

Renal Cortex

The cortex is well oxygenated and performs energy-intensive biosynthetic work.

  • The cortex carries out gluconeogenesis, especially during fasting.
  • It uses lactate, pyruvate, glutamine, and glycerol as substrates to make glucose.
  • The glucose produced is released into the blood to help maintain blood glucose levels alongside the liver.
  • Fatty acids are also oxidized for ATP in the cortex, because oxygen is plentiful.

Renal Medulla

The medulla has low oxygen tension (hypoxic environment), so it cannot rely on oxidative phosphorylation.

  • The medulla depends mainly on anaerobic glycolysis for ATP.
  • It uses glucose from the bloodstream, converts it to lactate.
  • The lactate travels back to the liver or renal cortex to be used for gluconeogenesis (Cori-like shuttling).
  • Medulla cells also lack many enzymes needed for the TCA cycle, reinforcing glycolysis as the main pathway.

Renal Glutaminase and Acid-Base Balance

The kidney plays a crucial metabolic role in maintaining blood pH.

  • During acidosis, the kidney increases the uptake of glutamine from the blood.
  • Enzyme renal glutaminase converts glutamine → glutamate + ammonia (NH₃).
  • NH₃ binds H⁺ in the tubular lumen to form NH₄⁺, which is excreted in urine.
  • This removes acid from the body without losing Na⁺ or K⁺.
  • The remaining carbon skeleton is converted to α-ketoglutarate, which enters gluconeogenesis → glucose is returned to blood.
  • So in acidosis, kidney releases glucose and excretes acid simultaneously.

Buffer Systems in the Kidney

Kidneys regulate acid-base balance by reclaiming bicarbonate and excreting H⁺.

Buffers used in tubular fluid:

  • Bicarbonate: reabsorbed mainly in the proximal tubule.
  • Phosphate buffer (HPO₄²⁻ / H₂PO₄⁻): binds H⁺ and allows its excretion.
  • Ammonium buffer system (NH₃ / NH₄⁺): especially important in chronic acidosis and upregulated by renal glutaminase.

The ammonium buffer is the primary long-term mechanism of acid excretion.

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