How Insulin Shuts Down Fat-Burning | MWM 2.25

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Here’s how insulin shuts down fat burning, and why it doesn’t matter for weight loss.

Insulin prevents fat-burning in part by locking fat in adipose tissue and in part by shutting down transport of fatty acids into the mitochondrion inside cells. By downregulating lipoprotein lipase (LPL) at heart and skeletal muscle and upregulating it at adipose tissue, insulin shifts dietary fat away from heart and muscle and toward adipose tissue. By downregulating hormone-sensitive lipase in adipose tissue, it prevents the release of free fatty acids from adipose tissue into the blood. At the cellular level, insulin leads to the phosphorylation and deactivation of AMPK. Since AMPK inhibits acetyl CoA carboxylase, insulin-mediated deactivation of AMPK leads to activation of acetyl CoA carboxylase and the conversion of acetyl CoA to malonyl CoA. Malonyl CoA inhibits carnitine palmitoyl transferase-1 (CPT-1) and thus blocks the transport of fatty acids into the mitochondrion. Nevertheless, all of these steps are also regulated at the most fundamental level by energy status, as covered in lesson 22. Further, insulin stimulates the burning of carbohydrate for energy, as covered in lesson 24. So, is insulin’s blockade of fat-burning sufficient to cause net fat storage, or does this critically depend on energy balance? This question will be answered in the next lesson.

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5 COMMENTS

  1. I just love all you thin guy that are not insulin resistant or carbohydrate intolerant. You sound so sure that insulin is not the problem causing obesity. Give me a break. There is tons of evidence which includes studies that show insulin to be the culprit. Yes cell energy controls substrate disposition in a perfect world without disease or problems. But add in intolerances, allergies, etc. and you have a metabolic mess. But somehow when obese people are put on a low carbohydrate diet to reduce insulin the lose weight and feel great. We are not lab rats or test tubes. I say we because I was a football player and weightlifter that worked out daily and ate the correct foods according to the nutritionists but somehow ended up obese for most of my adult life. I have worked out, gone low fat, gone hypocaloric, and still fat as fuck with whole body inflammation and pains. Then I go carnivore and lose 50 pounds and no longer have pain or inflammation. Hardly a surprise at this point. The public has been given horrible diet advice for 50 years. This shit needs to change.

  2. Dr Masterjohn – may I ask for your opinion. Low CHO/ketogenic diets (and high fat diets?) lead to increased circulating NEFA due to increased lipolysis, reduced esterification of NEFA and increased spill over of NEFA if diet is high in fat. Increased NEFA have shown to acutely cause insulin insensitivity due to insulin signalling interference whilst possible NEFA completion with glucose for oxidation leads to reduced post prandial glucose oxidation – so impaired glycaemic control. In addition, chronically, elevated fatty acids may lead to ectopic fat therefore both acute and chronically, raised NEFA may have a potent role in pathogenesis of insulin resistance. So – do you think low carb high fat diets may actually have the capacity to cause/worsen insulin resistance? Also – do you agree that acute high fat intakes and or increased NEFA does cause a temporary effect of insulin resistance post prandially?

  3. An excellent presentation which tallies with my belief that Insulin is not the main culpit behind our obesity crisis. Metabolic ward studies have shown that lowering insulin levels, in the context of matched high v low CHO diets, does not cause greater fat loss. Body composition remains similar. The reason is simple – whilst less insulin will cause increased lipolysis of adipose tissue lipolysis does not = fat oxidation. The liberated NEFA will simply circulate & if not required as fuel, will be re-esterified & re-stored as fat. Low CHO are useful dietary approaches but reducing CHO does not promote weight loss per se.

  4. Fantastically clear can't wait for the next session putting it all together & hopefully then an explanation of the prevelence of Insulin resistance

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