Tubular reabsorption of glucose

Last updated: June 19, 2025

Tubular reabsorption of glucose

Julie-Anne's playlist

Julie-Anne's playlist

Vitamin D
Parathyroid hormone
Phosphate, calcium and magnesium homeostasis
Parathyroid disorders and calcium imbalance: Pathology review
Parathyroid conditions and calcium imbalance: Clinical
Thyroid and parathyroid gland histology
TF/Px ratio and TF/Pinulin
Measuring renal plasma flow and renal blood flow
Regulation of renal blood flow
Tubular reabsorption and secretion
Tubular secretion of PAH
Tubular reabsorption of glucose
Urea recycling
Tubular reabsorption and secretion of weak acids and bases
Proximal convoluted tubule
Loop of Henle
Distal convoluted tubule
Renin-angiotensin-aldosterone system
Sodium homeostasis
Potassium homeostasis
Osmoregulation
Antidiuretic hormone
Kidney countercurrent multiplication
Free water clearance
Erythropoietin
Physiologic pH and buffers
Buffering and Henderson-Hasselbalch equation
The role of the kidney in acid-base balance
Acid-base map and compensatory mechanisms
Respiratory acidosis
Metabolic acidosis
Plasma anion gap
Respiratory alkalosis
Metabolic alkalosis
Hypernatremia: Clinical
Hyponatremia: Clinical
Hyperkalemia: Clinical
Hypokalemia: Clinical
Metabolic and respiratory alkalosis: Clinical
Toxidromes: Clinical
Acute kidney injury: Clinical
Chronic kidney disease: Clinical
Urinary tract infections: Clinical
Nephritic and nephrotic syndromes: Clinical
Renal tubular defects: Pathology review
Renal tubular acidosis: Pathology review
Osmotic diuretics
Carbonic anhydrase inhibitors
Loop diuretics
Thiazide and thiazide-like diuretics
Potassium sparing diuretics
Diffuse parenchymal lung disease: Clinical
Restrictive lung diseases: Pathology review
Chronic obstructive pulmonary disease (COPD): Clinical
Chronic bronchitis
Obstructive lung diseases: Pathology review
Emphysema
Pulmonary hypertension
Cor pulmonale
Sympathomimetics: Direct agonists
Muscarinic antagonists
Psychomotor stimulants
Mycobacterium avium complex (NORD)
Asthma: Clinical
Bronchodilators: Beta 2-agonists and muscarinic antagonists
Bronchodilators: Leukotriene antagonists and methylxanthines
Pneumonia: Clinical
Metabolic and respiratory acidosis: Clinical
Rhinovirus

Transcript

Watch video only

Glucose is found in almost every food we eat, like bread, potatoes, or fruit. Once it’s absorbed by the body, it’s converted into a source of energy.

The body needs the plasma glucose levels to remain within a pretty narrow range, between 70 mg/dl to 110 mg/dl, when you’ve had nothing to eat and less than 140 mg/dl after a meal.

Now, the entire blood volume is about 5 liters, and the plasma volume is about 3 liters of that.

The kidneys filter the entire plasma volume 60 times a day, which means that means our kidneys filter approximately 180 liters of plasma each day!

If each liter of plasma contains about 1 g of glucose, this means about 180 g of glucose get filtered by the kidneys per single day. That’s the filtration rate of glucose.

If you had a blood glucose concentration of 1.5 g of glucose per L, you’d end up with a filtration rate of glucose of 270 g / day. Essentially, the higher the plasma glucose concentration, the more glucose will get filtered.

If we wanted to illustrate that in a graph, with plasma glucose concentration on the x axis and glucose filtration rate on the y axis, we would see that as the plasma glucose concentration increases, the filtered load of glucose increases linearly.

Now, looking at the kidney, specifically inside the kidney, there are two main parts, the outer cortex and the inner medulla.

If we zoom in, there are millions of tiny functional units called nephrons which go from the outer cortex down into the medulla and back out into the cortex again.

Each nephron is made up of the glomerulus, or a tiny clump of capillaries, where blood filtration begins.

When glucose enters the glomerulus, some of it gets filtered into the renal tubule.

Zooming in on one of these renal tubules, each one is lined by brush border cells which have two surfaces.

One is the apical surface which faces the tubular lumen and is lined with microvilli, which are tiny little projections that increase the cell’s surface area to help with solute reabsorption.

The other is the basolateral surface, which faces the peritubular capillaries, which run alongside the nephron.

Now, the body needs glucose and doesn’t want glucose getting lost in the urine, so it tries to reclaim this filtered glucose right away, in the first segment of the renal tubule, known as the proximal convoluted tubule.

Now, more than 99% of the filtered load of glucose is reabsorbed back into the circulation. But, that doesn’t just happen, there are, obviously, a couple steps to take to to accomplish this.

First, the glucose needs to crosses the apical surface of the renal tubule cells. But normally, the glucose concentration inside the cells is much higher than that inside the tubule, so for glucose to cross the apical surface requires energy.

Fortunately, the electrochemical gradient of sodium drives it to move inside the cell, and that sodium gradient is sufficient to pull glucose into the tubule cell as well.

Key Takeaways

Tubular reabsorption of glucose is an important process that occurs in the kidneys to maintain normal blood glucose levels. When blood is filtered through the glomeruli in the kidneys, glucose is freely filtered into the tubular fluid of the nephron. In a healthy individual, nearly all of this filtered glucose is reabsorbed back into the bloodstream through the proximal tubule of the nephron. The reabsorption of glucose is facilitated by glucose transporters, primarily SGLT2 and SGLT1, which move glucose from the tubular fluid into the cells and then into the bloodstream.

Sources

  1. "Medical Physiology" Elsevier (2016)
  2. "Physiology" Elsevier (2017)
  3. "Human Anatomy & Physiology" Pearson (2018)
  4. "Principles of Anatomy and Physiology" Wiley (2014)
  5. "SGLT2 Mediates Glucose Reabsorption in the Early Proximal Tubule" Journal of the American Society of Nephrology (2010)
  6. "SGK1-sensitive renal tubular glucose reabsorption in diabetes" American Journal of Physiology-Renal Physiology (2009)
  7. "SGLT2 inhibition and renal urate excretion: role of luminal glucose, GLUT9, and URAT1" American Journal of Physiology-Renal Physiology (2019)