Myth: Insulin is needed for glucose uptake

I just came across this article...

May be our other learned members suramo arunkumar Shashikantiyengar Concerned anup would like to comment..

.... As a medical student, i’ve been taught that cells need insulin to absorb glucose. Insulin causes a glucose transporter (glut) to rise to the cell surface. This transporter creates a channel for glucose to flow through. There are about 13 different gluts, and the one that needs insulin is glut4 (possibly 12, also). According to the misconception, glut4 is required for glucose uptake, and that is why insulin is necessary. Without insulin, there will be no glut4, and so we’re told that the cell cannot consume glucose, which causes glucose to build up in the blood – hyperglycemia. This is demonstrably false, as many experiments have shown. While insulin does impact absorption by doubling the glucose uptake speed, we’ll see that it is not required. 1

While it is true that glut4 is largely insulin dependent, it has almost a dozen brothers that function quite well without insulin. 2 take, for example, glut1. It’s nearly everywhere in the body, all the time, and it’s as powerful as the glut4. Glut1 is the day-to-day glucose transporter responsible for basal glucose uptake. It doesn’t need insulin. It has been hypothesized that glut1 alone can sustain an adequate uptake of glucose in muscle. 3 there mere existence of this glut1 is enough to question the notion that glucose uptake must be insulin mediated.

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17 Replies

  • Interesting. Muscles can absorb glucose without insulin but don't know whether whole body can.

  • shrisamarth

    As i have said there is active and passing transport of the substances. Muscles if developed by exercise can consume glucose even at rest without insulin. But that doesn't mean they can work independent of insulin. They also require insulin for better functioning, formation of their own glycogen and fats.

  • Question:

    Can diabetics increase glucose uptake by brain by engaging in mentally taxing activities like playing chess, solving cross word puzzles? I specifically questioned on brain as high carb proponents always find this excuse that brain alone needs 20% of total energy specifically 100gm -120gm glucose a day in order to try and defend a 60% CARBS theory to everyone.

  • Well, anup bhaiyya ...we heard PV Sindhu was of low carb/keto diet.... do we know any of our chess players/or Russian chess players on keto diet during chess matches???

  • All shishya of Gopichand are on LC :)

    Chess players and LC I am not aware.

    But LC and brain/mental faculty, here's one interesting disclosure by mother (and a registered MD herself) of her Type 1 10 year old daughter:

  • suramo et.el.

    Does this means hepatic insulin resistance is the cause....or thing to which we should focus more?

    As you also agree visceral fat is the reason for all metabolic abnormalities...

  • cure


    "Around 80% of glucose uptake is insulin independent. "

    "It has been shown quite unequivocally that insulin at concentrations that are within the normal physiological range lowers blood glucose through inhibiting hepatic glucose production (ra) without stimulating peripheral glucose uptake" unequivocally 🐒🐒🐒.

    What about dietary glucose? Why should bs rise after a meal and more so after a high sugar meal? This guy wants to rewrite the physiology in his "Unique " way. He is reading physiology in Urdu 😁😁😁. It's sugar that inhibits neoglucogenesis and not the insulin.

    "In fact, during hyperglycemia, there is more glucose inside the cell than during normoglycemia " absolutely rubbish. He doesn't explain why we are lethargic and tired out if there is enough glucose inside cells.

    "The liver is the main reason that blood sugars rise...and insulin lowers blood sugar by telling the liver to stop releasing sugar into the blood" i don't think this statement needs any clarification to this group. He talks of neo...but he doesn't explain why hyperglecemia occurs? And why is dietary glucose not cleared in our body if glucose uptake by cells is not insulin dependent?

    Almost all the substances get absorbed by two methods.

    1) passive diffusion : from higher conc to lower conc. Law of physics.

    2) active transport across the pressure gradient or to speed up the uptake or for certain physiological responses. Na+ pump to propagate impulses. Proton pump to secret more acid into the stomach. Pantaprazol : a proton pump inhibitor to treat 😳😳!! hyperacidity.😝😝😝😊😊

  • Bhai suramo

    What about dietary glucose ? Why should bs rise after a meal and more so after a high sugar meal?

    agreed....but what about fasting sugar??? raising bloodsugar level without eating anything??

    And why is dietary glucose is not cleared in our body if glucose uptake by cells is not insulin dependent ?

    is it due to continuous sugar dump by liver??

    Is it possible that body’s sugar factory is working continuously due to hepatic insulin resistance and not listening the signals given by insulin???

  • cure

    Udi baba.

    Everything has been explained in past.

    1) fasting sugar : our body has a circadian rhythm. Why do we feel sleepy at night because our body responds to the surrounding atmosphere by secreting hormones. At night when sun sets the mlatonin secretion starts pacifying our minds.

    Now in the early morning around 4 am cortisol etc secretion start to prepare for the stress of the ahead. They not only arouse your mind but provide energy for the daytime activities. Since sugar is low at that time they have to push liver - the factory of our body to produce glucose - for neoglucogenesis. Insulin is still at work of clearing the backlog can't cope with this push. Neo... at dawn is independent of bs levels.

    2) except at dawn the dependent on bs levels. Only when sugar level falls below certain level the stress hormones - cortisol, glucagon, adrenaline etc are released. Insulin has no role in liver directly.

    Bro what you know is perfect. Don't get disguised by a few who try to show their smartness. The knowledge of Physiology that we have is perfect because it satisfies all our logic.

    I have sent you the mail i sent him - dr nadeem. Let's wait for his answer. May i tell you something. The knowledge that the people like you, anup, shashi, shri and others have is perfect because we have fought back our D. Medicine is not about fantasy but facts. We are no less if not more logical than the stalwarths. And we have no "vested " interests. 👍👍👍

  • lol @udi baba

    ok...yeah I got your email...let us wait for his reply...

    between i am in dilemma ...whether to continue with metformin or stop the same....

  • cure

    If your a1c is less than 6 you can stop metformin for a few days. It's always trial and error

  • Please ask your doctor about the taking a break from the medication(s) before you do anything. Sometimes, with certain medications, it takes time for the body to build up what is needed for being in the blood stream to work correctly.

  • Here is nice explanation about insulin and glucose transport.

  • shrisamarth bit heavy lecture....:P

  • Why then was type 1 considered a death sentence pre-insulin?

    Keeping insulin/IGF-1 to a minimum may be beneficial to reduce ageing, but we do need some.


    Hepatic Insulin Resistance and Glucose Homeostasis

    With obesity and insulin resistance, hepatic glucose production after an overnight fast is normal or elevated despite the presence of hyperinsulinemia. This is because the ability of insulin to regulate hepatic glucose uptake and production is impaired (5). The defects observed in the fasted state are readily manifest during a hyperinsulinemic-euglycemic clamp, where in response to an increase in insulin infusion, hepatic glucose production fails to be suppressed. The inappropriately high rates of hepatic glucose production in the presence of hyperinsulinemia are associated with an increase in gluconeogenesis and glycogenolysis, with a greater contribution of gluconeogenesis to glucose production (6,–9).

    Hepatic glucose uptake and glycogen synthesis are also defective. Following a carbohydrate-containing meal, the liver rapidly switches from a net producer to a net consumer of glucose. A substantial portion of dietary carbohydrate is stored by the liver as glycogen (approximately one-third of the dietary glucose) and is then subsequently released during the post-absorptive state by activation of glycogenolysis (10). The magnitude of the hepatic glucose uptake is determined by the glucose and insulin concentration as well as by the route of glucose delivery (11). In addition, extrahepatic factors contribute to failed insulin suppression of hepatic glucose production. There is a failure of insulin to appropriately suppress glucagon secretion from the pancreas, as well as impaired suppression of adipose tissue lipolysis. Both of these exacerbate the impairment in liver glucose uptake in individuals with metabolic disease (12, 13). We will briefly discuss the molecular control points that contribute to the impaired hepatic glucose handling: 1) decreased glucose uptake, 2) decreased glycogen synthesis, and 3) persistent gluconeogenesis.

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