Hi all, reading through this study as it possibly relates to me, can someone suggest the possible knock on effects of this?
Ive just started my peat journey of medical self education and struggle to know if im drawing any meaningful conclusion or not, as i understand v. little of the main body of these studies!
The intracellular content of K+ in thalassemia minor red blood cells is markedly reduced after incubation in autologous serum for 24 hr at 37°C. There is no compensatory increase in intracellular Na+ concentration of the cell thus reduced. This change is due to an acquired increase in selective permeability of the membrane to K+. This phenomenon follows the depletion of energy sources in the thalassemia minor cells but does not follow comparable depletion in normal cells. The loss of osmotically active intracellular contents probably accounts for the increased resistance of incubated thalassemia minor red blood cells to osmotic lysis.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC292232/pdf/jcinvest00201-0009.pdf
K+ in the cell being lost is not optimal right?
They go on to say:
an elevated internal calcium concentration can be correlated with increased potassium permeability and that ATP depletion promotes an increased intracellular calcium. The increased potassium fluxes they observed are much less than those found here in incubated thalassemia minor red cels, and whereas increased intracellular calcium causes an in creased sodium permeability, no change in the sodium rate coefficient was found in this study....The changes in pH would not appear to account for the development of selective K+ permeability in thalassemia minor.
Suggesting calcium in the cell may not be the issue in my case?
another study says:
Glucose largely prevented the K+ loss from hypochromic cells incubated either in absence or in presence of Ca2+, probably maintaining an adequate level of ATP during the incubation. EDTA only partially decreased the permeability to K+ in hypochromic cells incubated for 24 h at 37 degrees C, possibly removing Ca2+ bound to the cell membrane. The results suggest that Ca2+ does not represent the primary cause of K+ leak in hypochromic cells, but it is able to enhance a pre-existing peculiar abnormality of the cell membrane when the ATP level slows down.
Increased potassium permeability by calcium in hypochromic red blood cells - PubMed
suggesting glucose may stop this process? interestingly ive also found studies showing:
The risk of developing diabetes and insulin resistance in patients with thalassemia minor is two times greater than the general population....the inflammation noted in liver cells could be considered as the underlying cause of insulin resistance, impaired glucose tolerance and diabetes in these patients.
Relationship between beta-globin gene carrier state and insulin resistance - PubMed
Probably a thick question but will supplementing potassium help? Ive seen another post about the aldosterone relationship with Na+ and K+ ?
Thanks!
Ive just started my peat journey of medical self education and struggle to know if im drawing any meaningful conclusion or not, as i understand v. little of the main body of these studies!
The intracellular content of K+ in thalassemia minor red blood cells is markedly reduced after incubation in autologous serum for 24 hr at 37°C. There is no compensatory increase in intracellular Na+ concentration of the cell thus reduced. This change is due to an acquired increase in selective permeability of the membrane to K+. This phenomenon follows the depletion of energy sources in the thalassemia minor cells but does not follow comparable depletion in normal cells. The loss of osmotically active intracellular contents probably accounts for the increased resistance of incubated thalassemia minor red blood cells to osmotic lysis.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC292232/pdf/jcinvest00201-0009.pdf
K+ in the cell being lost is not optimal right?
They go on to say:
an elevated internal calcium concentration can be correlated with increased potassium permeability and that ATP depletion promotes an increased intracellular calcium. The increased potassium fluxes they observed are much less than those found here in incubated thalassemia minor red cels, and whereas increased intracellular calcium causes an in creased sodium permeability, no change in the sodium rate coefficient was found in this study....The changes in pH would not appear to account for the development of selective K+ permeability in thalassemia minor.
Suggesting calcium in the cell may not be the issue in my case?
another study says:
Glucose largely prevented the K+ loss from hypochromic cells incubated either in absence or in presence of Ca2+, probably maintaining an adequate level of ATP during the incubation. EDTA only partially decreased the permeability to K+ in hypochromic cells incubated for 24 h at 37 degrees C, possibly removing Ca2+ bound to the cell membrane. The results suggest that Ca2+ does not represent the primary cause of K+ leak in hypochromic cells, but it is able to enhance a pre-existing peculiar abnormality of the cell membrane when the ATP level slows down.
Increased potassium permeability by calcium in hypochromic red blood cells - PubMed
suggesting glucose may stop this process? interestingly ive also found studies showing:
The risk of developing diabetes and insulin resistance in patients with thalassemia minor is two times greater than the general population....the inflammation noted in liver cells could be considered as the underlying cause of insulin resistance, impaired glucose tolerance and diabetes in these patients.
Relationship between beta-globin gene carrier state and insulin resistance - PubMed
Probably a thick question but will supplementing potassium help? Ive seen another post about the aldosterone relationship with Na+ and K+ ?
Thanks!
