Potassium, the hidden ally of your blood sugar levels, is an important cofactor for energy metabolism

[LucH]

Potassium, the hidden ally of your blood sugar levels, is an important cofactor for energy metabolism (to let glucose entry into cells).
Potassium, a behind-the-scenes player in carpooling and storage: Efficiency of glucose uptake
Target point
Potassium acts via the Na⁺/K⁺-ATPase pump, found on the surface of all cells, which continuously exchanges intracellular sodium for extracellular potassium.
This pump is directly stimulated by insulin, in parallel—though not at the same site or via the same mechanism—with the translocation of the GLUT4 transporter, which enables glucose to entry into the cell. In other words, insulin triggers both potassium uptake (via Na⁺/K⁺-ATPase) and glucose uptake (via GLUT4), but through two parallel pathways rather than through direct coupling to the same receptor.

1. Potassium Charges the "Cellular Battery"
Every healthy cell acts like a tiny battery. To work correctly, it must keep most potassium inside the cell and most sodium outside the cell. Low potassium hyperpolarizes the beta cell (pancreas), which reduces insulin secretion.
• This situation (potassium rather inside, sodium rather outside the cell) creates an electrical charge across the cell membrane (called the resting membrane potential).
• When you eat a bowl of pasta or rice, your pancreas releases insulin.
Note: Potassium is not really the fuel for an electrical battery. We have to go back into the tyrosine kinase pathway.
Tyrosine kinase activation => Mitochondrial ATP production => Na+/K+ exchange with cofactors. So we aren't really talking about a battery but the energy level will slow down, like a battery could do, when insulin can’t do the job correctly because of a lack. Here potassium and magnesium.

2. The Direct Link to GLUT4 (The Glucose Gates)
Insulin signals the cell to deploy specialized transport vehicles called GLUT4 receptors.
• Adequate potassium increases the efficiency of glucose uptake. When potassium is abundant, the cell can clear glucose out of the blood with far less insulin, protecting the pancreas from overworking.

3. Preventing the "Stalled Starch" Backlog
Once glucose successfully enters a muscle or liver cell, it must be instantly converted into energy or stored as glycogen in muscles (and in liver after a night shift). As established by biological rules, the body requires about 19.5 mg of potassium for every single gram of glycogen it stores.
• Potassium (K⁺) is a required cofactor for pyruvate kinase, one of the key enzymes in glycolysis (the pathway that breaks glucose down for energy). Without enough potassium, that enzyme step slows or stalls.
Where potassium/glucose do interact for real
Insulin drives glucose into cells (via GLUT4 transporters) and separately drives potassium into cells (by activating the Na⁺/K⁺-ATPase pump). These happen in parallel through the action / influence of insulin. Insulin enhances a fluent metabolism of energy then.
Mind when stopping a fast: progressiveness when feeding back is highly recommended. This is seen as a “refeeding syndrome”: reintroducing carbs after starvation spikes insulin, which shoves both glucose and potassium into cells at once, but then blood potassium could crash. Some pints of salt in water could help during a fast to avoid some side-effects.
• The Post Angle: Potassium ensures a smooth, one-way traffic flow. It enhances glucose out of the blood and immediately packs it away into the energy pathway or storage, keeping the blood “clean” and blood sugar stable.

The tyrosine kinase pathway / cascade
When insulin signal transduction fails—or when critical cofactors are missing—the whole system experiences a brownout. The metabolic engine cannot produce the power required to maintain the gradient, and the cellular voltage drops. Like a battery could do when lacking oil, but not on the same way, of course.
Schema detailing how Tyrosine Kinase activation, Mitochondrial ATP, Potassium (K+), and Magnesium (Mg2+) merge into one continuous energy pipeline.
Figure:

*) The Start of the Chain (as contributors to dysregulation)
If there is a lack of Insulin => RTK Failure
RTK = Receptor for Tyrosine Kinase (enzyme).
Phosphorylation cascade simple definition
A chain reaction inside a cell where one protein kinase enzyme activates another by adding a phosphate group, passing a signal down a line to change cell behavior. [1] A protein kinase is thus an enzyme that adds a phosphate group to target proteins, acting as a molecular switch to turn cell activities on or off.

• If there is a lack of insulin, tyrosine kinase domains do not phosphorylate efficiently. Mitochondria don't get the optimal signal or fuel (glucose) to step up ATP production. As a physiological outcome, the energy pipeline slows at the source. ATP generation drops, leaving the pump underpowered.
  NB: This doesn't hold universally. Neurons, red blood cells, and the liver use insulin-independent glucose transporters (GLUT1, GLUT3), so they keep taking up glucose even without insulin.
• When there is a lack of magnesium (Mg2+) the Na+/K+ pump cannot use raw ATP. Fuel (glucose) can only become ATP when it is complexed with magnesium (Mg-ATP). Magnesium also physically stabilizes the pump's active state. Even if mitochondria make ATP, the pump cannot burn it. The engine stalls, and the cellular "battery" drains immediately.
• Without enough external potassium to exchange, the pump fails to allow an adequate bio-chemical-electrical environment. That the beginning of a falling disruptive energy level, impacting several other enzymatic cellular pathways: When energy level degrades, slowing down cellular repair, nerve conduction, and enzymatic function, a lot of problems will appear…

Sources
• Horn, R.S., Walaas, O., Walaas, E. (1973). The influence of sodium, potassium and lithium on the response of glycogen synthetase I to insulin and epinephrine in the isolated rat diaphragm. Biochim Biophys Acta, 313, 296-309.
• Hundal, H.S., Klip, A. (1993). Regulation of Glucose Transporters and the Na/K-ATPase by Insulin in Skeletal Muscle.
• Villar-Palasi, C., Guinovart, J.J. (1997). The role of glucose 6-phosphate in the control of glycogen synthase. FASEB J, 11, 544.
• Sweadner, K.J., et al. Regulation of the Na+/K+-ATPase by insulin: why and how? PubMed 9609121.
• Kreitzman, S.N., Coxon, A.Y., Szaz, K.F. (1992). Glycogen storage: illusions of easy weight loss, excessive weight regain, and distortions in estimates of body composition. Am J Clin Nutr, 56(1 Suppl), 292S-293S. (ratio de ~0,45 mmol K⁺/g glycogène, 3-4 g eau/g glycogène)

[LucH]

Which comes first — the chicken or the egg?
Various situations can arise and unfold in sequence. A single factor is not enough to disrupt homeostasis or to thwart or prevent metabolic correction (a return to an alternative equilibrium).
For example, a lack of energy (insufficient T3).
According to the "Association-Induction Hypothesis"—first developed by biophysicist Gilbert Ling and brilliantly explained by Ray Peat, PhD, on his forum:

1. A high-energy state: when cellular respiration is high (stimulated by the active thyroid hormone T3 and glucose), intracellular proteins alter their physical conformation. In this healthy state, they exhibit a high natural affinity for potassium—binding it firmly—while keeping sodium predominantly outside the cell. [1, 2]
   We can view T3 as the ultimate regulator of cellular structure and the organization of water within the cell.
2. ATP optimization: since cellular structure naturally retains potassium when energy levels are high, the cell doesn’t need to waste its precious ATP by constantly running the Na⁺/K⁺-ATPase pump to counteract leakage. This results in optimized "fueling" (available energy levels).

Source:
According to Peat (PubMed: 40272924) when a cell has optimal energy and high potassium, it naturally acts as if insulin is present. A healthy potassium buffer allows the cell to readily accept glucose and convert it into energy without needing a massive surge of insulin. Potassium literally spares the pancreas because potassium itself provides the baseline "insulin-like" cellular pull. [1, 2, 3]
In his essay Glycemia, starch, and sugar in context, Peat stated a striking deductive statistic:
"Insulin itself has been found to account for only about 8% of the 'insulin-like activity' of the blood, with potassium being probably the largest factor." [1, 2]
So a lot of waste is avoided when trying to optimize the exchanges to maintain the cellular ionic exchanges and the integrity of the membranes.

Useful link (in French, translator required):
https://mirzoune-ciboulette.forumactif.org/t2232-un-exces-de-calcium-comme-declencheur-du-stress-cellulaire-pq#31007
Excerpt:
Excess calcium is often viewed as a trigger for cellular stress. Why?
The cell maintains a strict concentration gradient between K+ and Na+. During an insult (toxicity, oxygen deprivation, inflammation), calcium channels open abnormally, causing an influx of calcium into the cytosol.
This calcium overload triggers a chain reaction of dysfunctions:

• Stress (overload and disrupted exchange);
• ROS (damage to membranes and DNA);
• Activation of destructive enzymes.

Calcium becomes an excitatory element.
To understand how calcium (Ca2+) becomes an "excitatory" agent, one must distinguish its overall chemical nature—an alkaline-earth mineral found in the diet—from its highly localized physical behavior within the cell. It is not a matter of macroscopic volume, but rather of electrical potential, molecular geometry, and pH.

Change in electrical charge (the trigger for excitation)
At rest, the interior of a muscle cell is negatively charged relative to the exterior. Calcium (Ca²⁺) carries two positive charges.

• Electrical excitation: When a nerve signal commands the muscle to contract, channels open. Ca²⁺ rushes into the cell, attracted by the internal negative charge.* => Concentration gradient and appropriate Ca²⁺ polarization.
• Depolarization: This massive influx locally reverses or nullifies the membrane's electrical voltage. It is this change in electrical charge (the action potential) that propagates the excitation signal throughout the muscle fiber.
  NB*: In electricity, opposite poles attract.

As the Ca2+ ion rushes into the cell, it introduces positive charges (electrical charge), reverses the membrane polarity (action potential), and triggers the mechanical response of structural proteins ("coiled proteins").
It is the disruption of equilibrium caused by this influx—followed by the energy cost (ATP) required to pump the calcium back out of the cell—that ultimately disturbs the cell's internal metabolism and balance. Thus, it is the demands placed on the system to restore equilibrium that consume energy...

You can find more information on the "War of the Pumps" at the link previously provided. You will then be able to connect the dots regarding the lack of energy and potassium; subsequently, if you still lack energy, you can look into optimizing T3 levels—but you must do so correctly, not the way I’ve often seen with synthetic hormones. The problem lies not in the synthetic nature but in the lack of cofactors.

[LucH]

Deiodinase enzyme roles
The thyroid's key roles
In situations of stress or prolonged insult (whether physical, mental, or environmental), the body seeks to reduce the energy expenditure associated with maintenance in order to focus on cellular survival (species protection). This braking mechanism is activated at the level of peripheral conversion through an enzymatic shift between the deiodinase enzymes DIO2/D2 (activation) and D3 (inactivation). [1]

1. https://pmc.ncbi.nlm.nih.gov/articles/PMC3670672/
   D3 does not merely serve an inactivating function. It acts as a modulator by adding or removing an iodine atom from an enzyme, depending on whether activation (T4 to T3) or inactivation is required. And I assume D2 is not always inert, either.
   D1 (Type 1 deiodinase). D1 is the only "mixed" enzyme capable of cleaving either the inner or the outer ring, thereby activating or inactivating the hormone depending on the metabolic context.

Roles of deiodinases
Deiodinases are enzymes that control energy metabolism by activating or inactivating thyroid hormones at the tissue level, directly determining the local availability of the biologically active hormone T3.

What Are Deiodinases?
Deiodinases are a family of three enzymes (D1, D2, and D3) containing selenocysteine that remove iodine atoms from thyroid hormones: [1]
NB: D1 = DIO1 = Deiodinase-1 = desodinase-1.
• Type 1 (D1): double function (add or remove a ring)
D1 converts inactive T4 (thyroxine) into active T3, and clears reverse T3 (rT3) from the blood. Found mostly in the liver, kidneys, and thyroid. [1, 2, 3, 4]
• Type 2 (D2): remove a ring (T4 => T3)
D2 exclusively activates T4 into T3 inside specific tissues, providing local intracellular T3 surges. Found in brown adipose tissue (BAT), skeletal muscle, brain, and pituitary gland. [1, 2, 3]
• Type 3 (D3): Inactivates both T4 and T3 by converting them into inactive metabolites (like rT3). Acts as a physiological brake on thyroid signaling. [1, 2, 3]

Role in Energy Metabolism
Deiodinases customize energy expenditure and metabolic rate independently of baseline circulating hormone levels: [1, 2, 3, 4]
• Thermogenesis (Heat Production): In brown adipose tissue, D2 activates T4 to T3 locally. This T3 binds to nuclear receptors to trigger mitochondrial uncoupling proteins (like UCP1) and PGC1α, ramping up calorie burning to generate heat. [1, 2]
• Energy Expenditure: High D2 activity in tissues like skeletal muscle and fat accelerates cellular respiration and energy usage. [1, 2]
• Metabolic Adaptation: During fasting or calorie restriction, D2 and D1 activity often drop while D3 rises, lowering active T3 levels to conserve energy and slow down the metabolic rate. Nutrient excess has the opposite effect, boosting activation. [1]

Impact on T3 Levels
• Local vs. Systemic T3: More than 80% of intracellular T3 does not come directly from the thyroid gland, but is generated locally inside tissues via D1 and D2 acting on circulating T4. [1]
• Tissue-Specific Control: Even if blood levels of T3 look normal, local changes in D2 or D3 expression can create high-T3 or low-T3 environments inside individual organs (like the liver or muscle), dictating how fast or slow those specific cells burn energy. [1, 2, 3]