A few weeks ago, I had a patient come in with uncontrolled type 2 diabetes, despite a strict diet and medications.. Her fasting glucose was high, but interestingly, her post-meal sugars spiked even more. This got me thinking, are we overlooking how glucose is absorbed and reabsorbed in the body?
In this video, I will explain how the key glucose transporters SGLT-1 and SGLT-2 influence blood sugar control. Understanding their function helps us appreciate how our body absorbs glucose and how certain medications can effectively treat diabetes by targeting these pathways.
While both transporters move glucose across cell membranes, they operate in different tissues and serve distinct physiological functions. Sodium-glucose co-transporters are proteins responsible for actively transporting glucose along with sodium across cell membranes.
SGLT-1 is predominantly located in the small intestine, where it absorbs dietary glucose and galactose. It’s also present in the kidney, but to a lesser extent. When we consume carbohydrates, they are broken down into glucose molecules that need to be absorbed into our bloodstream. This is where SGLT-1 has a role. It actively transports glucose from the intestinal lumen into our intestinal cells, coupled with sodium ions. This transporter has a high affinity for glucose but a low capacity, meaning it binds glucose molecules tightly but can only transport a limited amount.
Individuals with a deficiency or inhibition of SGLT-1 tend to have blunted post-meal glucose spikes. That’s why partial SGLT-1 inhibition is being explored to reduce postprandial hyperglycaemia in type 2 diabetes. When patients have genetic variations affecting SGLT-1 function, they often present with glucose-galactose malabsorption, resulting in severe diarrhoea after carbohydrate consumption. This underscores SGLT-1’s critical role in nutrient absorption.
On the other hand, SGLT-2 is located in the kidneys, and it reabsorbs glucose from the urine back into the bloodstream. So SGLT-1 determines how much glucose enters the blood from the gut, while SGLT-2 controls how much glucose stays in the body through the kidneys. SGLT-2 is responsible for reabsorbing around 90% of the filtered glucose in the kidneys. In Diabetes, this reabsorption can worsen hyperglycaemia by retaining excess glucose.
SGLT-2 inhibitors, such as empagliflozin or canagliflozin, block this transporter, allowing glucose to be excreted in the urine. This results in lowering the fasting and overall glucose levels, and even benefits like weight loss and reduced risk of cardiovascular disease.
The differential expression and function of the transporters highlight the body’s glucose management system. When this system falters, as in diabetes, understanding these molecular mechanisms allows us to intervene more accurately.
I have seen how targeting these specific transporters has transformed outcomes for many. It not only improves glycaemic control but also offers unexpected benefits for heart failure and kidney protection.
Kripa, is a Specialist Dietitian at The London Obesity & Endocrine Clinic. She has helped many patients overcome weight management barriers. ©Simplyweight
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