Stimmt es, dass Kalium- und Natriummangel fettleibig machen, da die Na-K-ATPase verringert wird, und dann langsame lange Fette statt schnellen Kohlenhydraten metabolisiert werden?
Das ist nicht allzu abwegig:
Relationship between (Na + K)-ATPase activity, lipid peroxidation and fatty acid profile in erythrocytes of hypertensive and normotensive subjects - PubMed
Oxidative stress may play a role in the pathogenic mechanism of essential hypertension. Lipid peroxidation can alter the cellular structure of membrane-bound enzymes by changing the membrane phospholipids fatty acids composition. We investigated the relationship between (Na + K)-ATPase activity, lip …
https://pubmed.ncbi.nlm.nih.gov/17410406/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4848652/
Abdominal obesity is associated with potassium depletion and changes in glucose homeostasis during diuretic therapy - PubMed
The activation of the renin-angiotensin system (RAS) is an important mechanism that contributes to hypertension in obese individuals. Thiazide diuretics also activate the RAS in response to volume contraction and can lead to a decrease in serum potassium values and glucose metabolism abnormalities. …
https://pubmed.ncbi.nlm.nih.gov/18550934/
Lipid peroxides in obese patients and effects of weight loss with orlistat on lipid peroxides levels - PubMed
These results indicate that obesity is associated with increases in endogenous lipid peroxides. Our data show that the indicator of lipid peroxidation-MDA-falls markedly in association with weight loss with orlistat. The demonstration of decreased free radical generation has important implications f …
https://pubmed.ncbi.nlm.nih.gov/15467775/#:~:text=Recent%20studies%20showed%20that%20obesity,of%20plasma%20malondialdehyde%20(MDA).
Es scheint, dass man zwar zum metabolischen Syndrom kommen mag.
Ist der Na/K-Haushalt aber wegen mehr Wassereinlagerung in Fettzellen gestört, dann chronifiziert es, und keine Diät wird mehr helfen.
Außer mit Energiemetabolismus-förderndem Elektrolytausgleich.