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Refeeding, the leucine threshold and refeeding syndrome

Also called: Breaking a fast, Hypophosphataemia

Written by Reviewed Sep 2026

Coming out of a fast is its own event, with its own rules. In a truly malnourished person, it has its own danger. That danger is not that phosphate is lost. It is that insulin drives phosphate into cells all at once.

What it is

Eating again runs the fasting signals in reverse, and it does it fast. Protein building blocks (amino acids) arrive, and the mTORC1 build switch senses them directly. Insulin arrives at the same time and works through a second route. Within minutes to tens of minutes, protein making starts to rise, autophagy is shut down, and the program that was building up the cell's digestion sacs switches off.

A meal with protein is the surest way to end the fasted state. It works better than the same calories as carbs or fat. That is because protein works through both the amino acid route and the insulin route, while fat does not strongly work through either.

This page covers two separate questions. First, how much protein, with how much leucine, does a meal need to get the most out of muscle? That matters to anyone eating in a short window. Second, what makes eating again dangerous for a badly malnourished person? That is a question about body salts, and one mineral in particular.

How it works

How the signals reverse. Leucine and arginine each lock onto their own sensor proteins (Sestrin2 and CASTOR1), which releases the brake on the build switch. Methionine raises a molecule called SAM, which locks onto a third sensor, SAMTOR. The Rag proteins then flip to "on" and pull mTORC1 onto the surface of the cell's digestion sac, where its on-switch Rheb is waiting. Sugar and amino acids both raise insulin. Insulin sets off a chain of signals that switches Rheb on too. After that, protein making starts up, the start of autophagy is blocked, and the protein TFEB is held out of the cell's control centre.

Insulin's role in muscle building is best described as allowing it, not driving it. At normal levels, insulin is needed for the full muscle-building response to amino acids. It also strongly slows protein breakdown, so the overall balance improves a lot. But pushing insulin higher, when there are already enough amino acids, does not raise protein making much more. The amount of amino acids is the limit.

The dangerous part is the same insulin doing its other jobs. Insulin drives sugar into cells, and phosphate, potassium and magnesium follow it in. Phosphate moves for an extra, stronger reason. Sugar that enters a cell gets phosphate tags added in two steps, and each one uses up phosphate and traps the sugar inside. At the same time, the cells restart burning fuel and making energy (ATP) in a rush, and red blood cells restart making a molecule called 2,3-BPG. All of that uses up phosphate. Blood phosphate can crash within 24 to 72 hours of eating again, because it is being used up and locked inside cells so fast.

What happens next follows from what phosphate does. The cells cannot remake enough ATP. And falling 2,3-BPG makes red blood cells hold onto oxygen more tightly, so less oxygen reaches the tissues. In patients, that shows up as heart rhythm problems and heart failure, weak breathing muscles, muscle breakdown, bursting red blood cells, seizures, confusion, and pins and needles. Low potassium and magnesium at the same time add to the heart rhythm risk. Low magnesium also makes low potassium hard to fix. There are two more blows. Insulin makes the body hold onto salt and water, which fills up the blood volume in someone whose heart muscle has wasted. And a sudden rush of sugar burning in someone low on vitamin B1 (thiamine) can set off a brain emergency called Wernicke's encephalopathy. That is because a key sugar-burning enzyme needs thiamine, and the demand for it jumps.

What switches it on

Amino acids, leucine most of all, and the insulin surge that carbs cause. The more sugar flows into cells on refeeding, the more phosphate gets used up. That is exactly why the carb load is the first thing hospital refeeding plans limit.

On the timing
The signal reversal is fast. In cells in a dish, the amino acid sensing steps work within minutes. Whether the real speed of autophagy in people drops within 60 minutes of a whey protein drink is the exact question one registered study was set up to answer. The only paper out so far describes the plan and has no results. The hospital timing is better known. In 62 intensive care patients fed again after 48 hours or more without food, blood phosphorus fell below 0.65 mmol/L in 21 of them. On average, that happened 1.9 days after feeding started. In 69 teenagers with anorexia nervosa, 81% hit their lowest phosphorus in the first week.

What has been measured

In people

Both halves of this page come from people. The protein work used tracers dripped into the blood, with repeated muscle samples, in living people. The refeeding danger work is from hospitals: intensive care patients, teenagers with anorexia nervosa, and one study that compared two feeding speeds head to head.

  • The biggest study, on how fast to feed. 339 intensive care adults developed refeeding syndrome within 72 hours of starting nutrition. They were split into two groups: calorie-limited feeding or standard feeding. Days alive after leaving intensive care were 44.8 against 39.9, which was not a clear difference. But more people were alive at day 60: 149 of 164 (91%) against 128 of 163 (78%). Limiting calories in people who already had low phosphate from refeeding improved survival at 60 days (Lancet Respiratory Medicine, 2015).
  • How often it happens, in teenagers with anorexia nervosa. 69 patients started at 1,200 to 1,400 calories a day, going up by 200 calories every 24 to 48 hours. Four (5.8%) had moderately low phosphate and 15 (21.7%) had mildly low phosphate. 19 (27.5%) needed phosphorus supplements. 81% hit their lowest phosphorus in the first week. The patient with the lowest phosphorus had short runs of a fast heart rhythm from the lower heart chambers (ventricular tachycardia) (Journal of Adolescent Health, 2003).
  • How often it happens, in intensive care. 62 patients were fed again after 48 hours or more without food. In 21 of 62 (34%), phosphorus fell by more than 0.16 mmol/L to below 0.65 mmol/L. In six, it fell below 0.32 mmol/L. On average, the fall came 1.9 days after feeding started (Archives of Surgery, 1996).
  • Whey protein dose, a bigger and stronger study. 48 young men who lift weights, weighing about 80 kg, ate a set high-protein breakfast, trained one leg, and then had 0, 10, 20 or 40 g of whey protein. Muscle building was measured over 4 hours. It rose 49% with 20 g and 56% with 40 g. 10 g gave no clear boost. 40 g gave no extra muscle building over 20 g, but more of the protein was burned off and turned into urea (American Journal of Clinical Nutrition, 2014).
  • Leucine on its own, apart from total protein. This is the direct test of the leucine "threshold" idea. 40 men trained one leg, then had one of five drinks: 25 g whey (3.0 g leucine); 6.25 g whey (0.75 g leucine); 6.25 g whey topped up to 3.0 g leucine; 6.25 g whey topped up to 5.0 g leucine; or 6.25 g whey topped up to 5.0 g leucine plus isoleucine and valine. From 1.5 to 4.5 hours, the biggest responses came from 25 g whey, at about 267%, and 6.25 g whey topped up to 5.0 g leucine, at about 220%. Topping up to only 3.0 g did not match. So adding leucine can bring a small protein dose closer to a much bigger one. But it took the higher leucine amount, not just matching the leucine in the 25 g dose (American Journal of Clinical Nutrition, 2014).
  • The direct challenge to the per-meal limit. 36 active young men, 12 per group, had 0, 25 or 100 g of milk protein after a full-body weight workout. 100 g gave a bigger and longer response than 25 g, lasting more than 12 hours. Muscle building was about 20% higher over 0 to 4 hours, and about 40% higher over 4 to 12 hours. Eating protein had almost no effect on whole-body protein breakdown or on how much protein was burned (Cell Reports Medicine, 2023).
  • How well the leucine threshold idea holds up overall. A review of 29 studies that measured both blood leucine and muscle building found 16 that backed the idea and 13 that did not. Of the 16 that backed it, 13 were in older adults and 14 used protein powders rather than food. The idea works best for older adults using protein powders, and much less well for protein-rich whole foods (Frontiers in Nutrition, 2021).
  • One meal does not undo everything. 8 healthy men fasted for 30 hours, with blood drawn every 20 minutes. An 800 calorie meal raised thyroid-stimulating hormone (TSH) toward midnight. It went clearly above the fasted level, but stayed clearly below their levels on a day without fasting, at the same time of day. The thyroid hormone T3 was 1.84 nmol/L fasted and 1.80 after the meal, which was no real difference. Reverse T3 tended to fall, but not clearly (Acta Endocrinologica, 1984).
  • Whole protein dose, in 6 healthy young men, each tested five times. They did leg weight training, then ate 0, 5, 10, 20 or 40 g of whole egg protein. Muscle building was measured over 4 hours. It rose with the dose, up to a top at 20 g. Albumin making also topped out at 20 g. At 20 and 40 g, more leucine was burned, meaning the protein above the top was being burned for fuel. This study had only six people (American Journal of Clinical Nutrition, 2009).
  • Why blood tests miss the risk. Six people with obesity spent 40 days on a hospital ward at 300 calories a day. That supplied 406 mg phosphorus, 7 mg magnesium and 75 mg calcium a day. Total losses in the urine beat total intake by 58% for calcium, 75% for phosphorus and 500% for magnesium. On average, they lost 104 mg calcium, 48 mg magnesium and 363 mg phosphorus a day. Yet blood phosphorus and magnesium did not change. Blood calcium fell 0.5 mg/dL. This was a fast with added protein, not a total fast, but the lesson carries over. Normal blood magnesium or phosphate during a fast does not mean the body's stores are full (American Journal of Medicine, 1981).
  • The link to refeeding danger, measured in healthy people. Healthy people had insulin dripped in, before and after a 48 hour fast. Blood phosphate fell in every one of them. The more sugar their bodies took up, the more phosphate fell. That is how refeeding drops phosphate, measured directly in healthy people. It comes from the same paper that showed fasting's selective insulin resistance (Metabolism, 1983).
  • The age comparison, and it needs its warning attached. The widely quoted figures are that older men need 0.40 g of protein per kg of body weight to get the most muscle building from a meal, against 0.24 g in younger men. That comes from the research group pooling its own older data and looking back at it, not from a new study. The paper's summary does not say how many people were included. And the main comparison fell just short of the usual bar for a real difference. Only the version based on lean body mass cleared that bar: 0.60 against 0.25 g per kg of lean mass. Resting muscle building did not differ by age, at 0.027 against 0.028% per hour (Journal of Gerontology Series A, 2015).
  • Autophagy in people after eating: responses in different types of muscle fibre were measured after an overnight fast and after a mixed meal (American Journal of Physiology: Endocrinology and Metabolism, 2022).

In animals and in cells in a dish

The amino acid sensing steps that make refeeding work at the molecule level were worked out in cells in a dish and with purified proteins. The step that switches autophagy off when food comes back was also found in cells in a dish.

  • In a dish, with cells and purified proteins: leucine locks onto Sestrin2 to release the brake (Science, 2016). Arginine locks onto CASTOR1 to do the same (Cell, 2016). SAM locks onto SAMTOR (Science, 2017). The Rag proteins grab raptor and move mTORC1 onto the digestion sac (Science, 2008).
  • In a dish: mTORC1 tags ULK1, which is the step that shuts off the start of autophagy when food comes back (Nature Cell Biology, 2011).

Why it matters

Refeeding is the half of fasting that almost nobody writes about. It holds the only reliably deadly event in the whole subject.

On protein, here is the practical reading of the tracer studies in people. In young adults, about 20 g of a fast-digesting, leucine-rich protein gets the most out of the short-term muscle-building response after exercise. Leucine content matters a lot, apart from total protein. And older adults need more. These are 4 hour measurements of muscle building in small groups of mostly young men. They are not long-term muscle growth results. They do matter for short eating windows. A person eating in a short window has fewer meals to clear whatever the per-meal bar is, and that maths gets harder with age.

On safety, it is worth knowing exactly how this works, because the usual summary gets it backwards. Refeeding syndrome is not phosphate loss. The body's total phosphate is already low from the fast while blood phosphate reads normal. Then insulin drives what is left into cells all at once. The one study that compared feeding speeds says speed matters. Limiting calories in people who already had low phosphate from refeeding improved survival at 60 days.

Refeeding syndrome happens in serious, long-lasting malnutrition. It is not a known result of a short fast in a well-fed person. The numbers on how often it happens come from hospital patients and people with eating disorders. That limit is part of the fact, not a softening of it.

A claim you will see repeated

Two things get repeated here that this page does not repeat. First, the protein figures of 0.40 against 0.24 g per kg for older against younger adults are quoted as settled. They come from one research group pooling and looking back at its own older data. The paper's summary does not say how many people were in it. And the comparison itself fell just short of the usual bar for a real difference. Only the lean body mass version cleared it. The direction is probably right, but the exact numbers should not be treated as a threshold. Second, the claim that protein above about 25 g per sitting is wasted. In 36 young men given 0, 25 or 100 g of milk protein after a full-body weight workout, 100 g gave a bigger and longer response than 25 g, lasting more than 12 hours. It had almost no effect on whole-body breakdown or on how much protein was burned. So someone eating 150 g of protein across three meals inside an 8 hour window is not, on the evidence in people, throwing the extra away. And on the hospital side: low phosphate on refeeding is often described as phosphate being lost. It is not lost on refeeding. It is used up and locked inside cells. That is why the blood number can look normal right up until feeding starts.

Sources

  1. Study in people2009
    Ingested protein dose response of muscle and albumin protein synthesis after resistance exercise in young men

    American Journal of Clinical Nutrition

    6 healthy young men did leg weights, then ate 0, 5, 10, 20 or 40 g of egg protein, one amount per visit. Muscle building peaked at 20 g, and so did the making of albumin, a blood protein. At 20 and 40 g, more leucine was burned for fuel. Several growth signal markers did not change with the protein amount.

    6 healthy young men, five trials in randomised order, leg resistance exercise then 0, 5, 10, 20 or 40 g whole egg protein, synthesis over 4 hours by primed constant leucine infusion. Muscle protein synthesis was maximally stimulated at 20 g and albumin synthesis also plateaued there. Leucine oxidation rose significantly at 20 and 40 g. Phosphorylation of p70S6K, rpS6 and eIF2B epsilon was unaffected by protein dose.

  2. Study in people2014
    Myofibrillar muscle protein synthesis rates subsequent to a meal in response to increasing doses of whey protein at rest and after resistance exercise

    American Journal of Clinical Nutrition

    48 young men who lift weights, about 80 kg each, ate a high-protein breakfast, trained one leg, then had 0, 10, 20 or 40 g of whey protein. Muscle building rose 49% with 20 g and 56% with 40 g. 10 g did not clearly raise it. 40 g built no more muscle than 20 g, but more of the protein was burned or turned into waste.

    48 resistance-trained young men of approximately 80 kg, standardised high protein breakfast then unilateral leg exercise then 0, 10, 20 or 40 g whey protein isolate, myofibrillar synthesis over 4 hours by phenylalanine infusion. The 0 g rate was 0.041 plus or minus 0.015% per hour; synthesis rose 49% with 20 g and 56% with 40 g. 10 g produced no significant stimulation. 40 g added no synthesis over 20 g but raised phenylalanine oxidation and urea production.

  3. Study in people2014
    Leucine supplementation of a low-protein mixed macronutrient beverage enhances myofibrillar protein synthesis in young men: a double-blind, randomized trial

    American Journal of Clinical Nutrition

    40 men trained one leg, then had one of five drinks with different amounts of protein and leucine. The biggest muscle building came from 25 g of whey, about 267%, and from 6.25 g of whey topped up to 5.0 g of leucine, about 220%. Topping up to only 3.0 g of leucine did not match the 25 g drink.

    40 men, unilateral resistance exercise then one of five drinks varying total protein and total leucine, myofibrillar synthesis by phenylalanine infusion with serial biopsies in a rested and an exercised leg. Over 1.5 to 4.5 hours the greatest responses were 25 g whey at approximately 267% and 6.25 g whey topped to 5.0 g total leucine at approximately 220%, P = 0.002. Topping only to 3.0 g total leucine did not match the 25 g dose.

  4. Study in people2015
    Protein ingestion to stimulate myofibrillar protein synthesis requires greater relative protein intakes in healthy older versus younger men

    Journal of Gerontology Series A: Biological Sciences and Medical Sciences

    This pooled the group's own older studies again, and the number of people is not given. Older men seemed to need more protein per kg of body weight than younger men to max out muscle building, 0.40 against 0.24 g, but that gap was not clear enough to be sure. Per kg of lean mass the gap was clear: 0.60 against 0.25 g. Resting muscle building was the same at both ages.

    A retrospective pooled reanalysis of the group's own prior datasets, not a new prospective trial; total participant count is not stated in the abstract. The plateau was reached at 0.40 plus or minus 0.19 g/kg body mass in older men versus 0.24 plus or minus 0.06 in younger men, p = 0.055, which is not statistically significant. Only the lean-body-mass comparison cleared significance, 0.60 plus or minus 0.29 versus 0.25 plus or minus 0.13 g/kg lean mass, p < 0.01. Basal fractional synthetic rate did not differ by age, 0.027 versus 0.028% per hour, p = 0.53.

  5. Study in people2023
    The anabolic response to protein ingestion during recovery from exercise has no upper limit in magnitude and duration in vivo in humans

    Cell Reports Medicine

    36 active young men, 12 per group, had 0, 25 or 100 g of milk protein after a full-body weight workout. 100 g gave a bigger and longer muscle-building response than 25 g, lasting more than 12 hours. Muscle building was roughly 20% higher in the first 4 hours and roughly 40% higher from 4 to 12 hours. Protein barely changed how much body protein was broken down or burned.

    36 recreationally active young men, 12 per group, given 0, 25 or 100 g of intrinsically labelled milk protein after 60 minutes of whole-body resistance exercise. 100 g produced a greater and more prolonged response than 25 g, lasting beyond 12 hours, with myofibrillar synthesis roughly 20% higher over 0 to 4 hours and roughly 40% higher over 4 to 12 hours. Protein ingestion had negligible effect on whole-body protein breakdown or amino acid oxidation rates.

  6. Review of studies2021
    Evaluating the Leucine Trigger Hypothesis to Explain the Post-prandial Regulation of Muscle Protein Synthesis in Young and Older Adults: A Systematic Review

    Frontiers in Nutrition

    A review of 29 studies that measured both blood leucine and muscle building. 16 backed the idea that a leucine spike triggers muscle building, and 13 did not. Of the 16, 13 were in older adults and 14 used isolated proteins. So the idea fits older adults eating isolated protein best, and fits protein-rich whole foods much less well.

    Of 29 eligible studies measuring both blood leucine and muscle protein synthesis, 16 supported the leucine trigger hypothesis and 13 did not. Of the 16 supportive studies, 13 were in older adults and 14 used isolated proteins, so the concept applies best to older adults eating isolated protein and much less well to protein-rich whole foods.

  7. Study in people2022
    Muscle fiber type-specific autophagy responses following an overnight fast and mixed meal ingestion in human skeletal muscle

    American Journal of Physiology: Endocrinology and Metabolism

    Researchers looked at muscle recycling in different muscle fibre types, after an overnight fast and after a mixed meal. This entry does not say what they found.

    Autophagy responses measured by muscle fibre type in human skeletal muscle after an overnight fast and after mixed meal ingestion.

  8. Review of studies2022
    The Break-Fast study protocol: a single arm pre-post study to measure the effect of a protein-rich breakfast on autophagic flux in fasting healthy individuals

    BMC Nutrition

    This is a plan for a study, not results. It will test whether a whey protein drink slows cell recycling within 60 minutes in healthy adults who fasted overnight. It is often cited as if it had results. It does not.

    A registered trial protocol, not a results paper. It is designed to test whether a whey protein drink suppresses autophagic flux within 60 minutes in overnight-fasted healthy adults. It is listed here because it is frequently cited as though it contained results. It does not.

  9. Study in people1983
    Insulin action during acute starvation: evidence for selective insulin resistance in normal man

    Metabolism

    6 lean people were given insulin at four levels, before and after a 48 hour fast, while blood sugar was held steady. Blood phosphate fell during insulin in everyone. The more sugar their bodies took in, the more phosphate dropped. This is how low phosphate after refeeding happens, measured directly in healthy people.

    6 lean subjects, sequential euglycaemic clamps at four insulin infusion rates before and after a 48 hour fast. Serum phosphate fell during insulin infusion in all subjects (P < 0.001) and the magnitude correlated with glucose disposal rate at r = 0.76, P < 0.005. This is the mechanism of refeeding hypophosphataemia measured directly in healthy humans: the greater the glucose flux, the greater the phosphate consumption.

  10. Study in people1981
    Adverse effects of liquid protein fast on the handling of magnesium, calcium and phosphorus

    American Journal of Medicine

    6 obese people spent 40 days in a hospital research ward on a 300 calorie liquid protein diet. They lost more minerals in urine than they took in: 58% more calcium, 75% more phosphorus and 500% more magnesium. Blood phosphorus and magnesium did not change, and blood calcium fell 0.5 mg/dL. This diet included protein, so it was not a total fast.

    6 obese subjects, 40 days on a metabolic ward at 300 kcal per day supplying 75 mg calcium, 406 mg phosphorus, 7 mg magnesium, 33 mEq potassium and 11.5 g nitrogen daily. Cumulative urinary losses exceeded cumulative intake by 58% for calcium, 75% for phosphorus and 500% for magnesium. Mean daily balances were minus 104 mg calcium, minus 48 mg magnesium and minus 363 mg phosphorus. Serum phosphorus and magnesium did not change; serum calcium fell 0.5 mg/dL, p < 0.05. This is a protein-supplemented fast rather than a total fast.

  11. Study in people1996
    Refeeding hypophosphatemia in critically ill patients in an intensive care unit. A prospective study

    Archives of Surgery

    62 intensive care patients started eating again after 48 hours or more without food. In 21 of them (34%), blood phosphorus dropped to a low level. In six, it fell very low. The drop came about 1.9 days after feeding started, on average.

    62 intensive care patients refed after 48 hours or more of starvation. Serum phosphorus fell more than 0.16 mmol/L to below 0.65 mmol/L in 21 of 62 (34%), and below 0.32 mmol/L in six patients. Mean time to the fall was 1.9 plus or minus 1.1 days after feeding started.

  12. Study in people2003
    Hypophosphatemia during nutritional rehabilitation in anorexia nervosa: implications for refeeding and monitoring

    Journal of Adolescent Health

    69 teenagers with anorexia started at 1,200 to 1,400 calories a day, going up 200 calories every 24 to 48 hours. Four (5.8%) got moderately low phosphorus and 15 (21.7%) mildly low. 19 (27.5%) needed phosphorus supplements. 81% hit their lowest level in the first week. The patient with the lowest phosphorus had short bursts of a dangerous fast heart rhythm.

    69 adolescents with anorexia nervosa started at 1,200 to 1,400 kcal per day advancing 200 kcal every 24 to 48 hours. Four (5.8%) developed moderate hypophosphataemia, 15 (21.7%) mild, and 19 (27.5%) required phosphorus supplementation. 81% reached their phosphorus nadir within the first week. The patient with the lowest phosphorus had short runs of ventricular tachycardia.

  13. Study in people2015
    Restricted versus continued standard caloric intake during the management of refeeding syndrome in critically ill adults: a randomised, parallel-group, multicentre, single-blind controlled trial

    Lancet Respiratory Medicine

    339 adults in intensive care developed refeeding syndrome within 72 hours of starting nutrition. They were put on fewer calories or kept on standard feeding. Days alive after leaving intensive care did not clearly differ, 44.8 against 39.9. But more people on fewer calories were alive at day 60: 91% against 78%.

    339 intensive care adults who developed refeeding syndrome within 72 hours of starting nutrition, randomised to caloric restriction or standard feeding. Days alive after intensive care discharge 44.8 versus 39.9, not significant at p = 0.19, but more patients alive at day 60: 149 of 164 (91%) versus 128 of 163 (78%), p = 0.002.

  14. Study in people1984
    Rapid adaptations of serum thyrotrophin, triiodothyronine and reverse triiodothyronine levels to short-term starvation and refeeding

    Acta Endocrinologica

    8 healthy men fasted 30 hours, then ate 800 calories, with blood taken every 20 minutes. Fasting pushed the thyroid signal TSH below 1 and wiped out its night-time peak. The thyroid hormone T3 fell from 2.30 to 1.84 nmol/L, and reverse T3 rose. Eating raised TSH, but not back to normal. The 800 calories did not change T3. Cortisol was the same throughout.

    8 healthy male volunteers fasted 30 hours then refed 800 kcal, with blood sampled at 20 minute intervals. Starvation lowered TSH below 1 mU/L and abolished the nocturnal peak; serum T3 fell from 2.30 plus or minus 0.06 to 1.84 plus or minus 0.03 nmol/L (P < 0.01) and reverse T3 rose. Refeeding raised TSH significantly above the starved state but it remained significantly below never-starved values, and 800 kcal did not measurably change T3 (1.80 plus or minus 0.05 nmol/L, not significant). Serum cortisol did not differ across conditions.

  15. Review of studies2008
    Refeeding syndrome: what it is, and how to prevent and treat it

    BMJ

    A review of refeeding syndrome. When insulin rises after a fast, phosphate, potassium and magnesium move into cells and blood levels drop. It covers who is at risk and how to prevent and treat it.

    The standard clinical account of refeeding syndrome: the intracellular shift of phosphate, potassium and magnesium on insulin release, the risk groups, and the prevention and treatment framework.

  16. Review of studies2020
    ASPEN Consensus Recommendations for Refeeding Syndrome

    Nutrition in Clinical Practice

    Expert guidelines from ASPEN, a clinical nutrition group, on refeeding syndrome. It is diagnosed by a drop in blood phosphorus, potassium or magnesium. Check those levels before feeding starts, and hold back calories in people with very low levels until they are fixed.

    Current consensus diagnostic criteria, based on a decrease in serum phosphorus, potassium and/or magnesium, together with risk stratification and a management framework including checking those electrolytes before initiating nutrition and delaying calories in patients with severely low values until corrected.

  17. Lab (cells in a dish)2016
    Sestrin2 is a leucine sensor for the mTORC1 pathway

    Science

    In a dish. Leucine sticks to Sestrin2 and makes it release GATOR2. That is the first step by which a meal with protein turns the mTORC1 growth switch back on and ends the fasting state.

    Cultured cells and purified proteins. Leucine binds Sestrin2 directly and releases GATOR2, which is the first step by which a protein-containing meal reactivates mTORC1 and therefore ends the fasted signalling state.

  18. Lab (cells in a dish)2011
    AMPK and mTOR regulate autophagy through direct phosphorylation of Ulk1

    Nature Cell Biology

    In a dish. mTORC1 tags ULK1 at one spot to stop cell recycling from starting. This is the step that switches recycling off when food comes back.

    Cultured cells. mTORC1 phosphorylates ULK1 at serine 757 to suppress autophagy initiation, which is the step that switches recycling off when food returns.