Fusion, Fission, And Integrated Magnesium Supplementation

Majid Ali, M.D.

An Article for Professionals Concerning Integrated Magnesium Supplementation


 

Fusion, Fission, And Future of Cell Membrane Therapeutics

Why are calcium channel blockers employed commonly for unapproved use in general medical practices? Why do I commonly prescribe magnesium, potassium, and taurine for most of my patients with chronic disease in my integrative medical work? Our usual and uneasy answer is that we do so because these treatments favorably modulate cell membrane functions even though we do not know the mechanisms in play.

Zhao et al. (ref. 1) inform us their work provides the foundation and techniques for the further study of hemi-fusion and hemi-fission in live cells. We physicians look forward to that.
In 1987, I published a monograph entitled Oxidative Cell Membrane (ref. 2) in which I coined the term leaky cell membrane syndrome to draw attention to the clinical evidence for significant cell membrane permeability dysfunctions in clinicopathologic entities that are characterized by accelerated oxidative molecular injury. I encounter symptom-complexes suggestive of such dysfunctions involving nearly all cellular ecosystems that cause a broad array of clinical symptom-complexes referable to the various body organs (ref. 3,4).

A cell membrane separates internal order of a cell from its external disorder. One can imagine that evolution of cell membranes occurred with millions of steps, missteps, and counter steps. Fusions and fissions of cell membrane structures must have dominated the evolution of cell membranes, in structure and function. We wonder how fusion and fission became vital for eukaryotic life. What has primacy over the other, fusion or fission?

Zhao et al. find that dynamin-dependent fission mechanisms compete with fusion mechanisms at the hemi-fused state before full fusion occurs to counteract the transition from hemi-fusion to full fusion. Such competition is sometimes observed in real time; the sequential observation of full fusion, hemi-fission, and back to full fusion may explain the widely observed capacitance flickers that reflect repeated fusion pore opening and closure.

In 2004, I presented evidence for respiratory-to-fermentative shift (RTF shift) as the energetic-molecular basis of chronic inflammatory-immune disorders (ref 5) and recognized succinate as the Krebs metabolite of special significance. In it I noted the work of He et al. (ref.6) which established the links between Krebs metabolites with receptors for G-coupled proteins, which are the largest and most diverse group of cellular detectors transmiting extracellular information into the cytoplasm. My core findings of my Krebs cycle studies were validated by Chouchani et al (ref.7).

In 2007, I put forth my dysox model of Type 2 diabetes to focus on the centrality of respiratory-to-fermentative shift in the pathogenesis of the disease (ref.8) and to recognize the need for shift of focus from glycemic status to insulin homeostasis (ref.9). The prevailing standard of treating Type 2 diabetes is to control blood sugar levels by focusing on insulin release from beta cells of the pancreas. By contrast, based on my Krebs cycle work, I treat the disease by focusing on insulin receptor embedded in the cell membrane. Specifically, my colleagues and I implement a hyperinsulinism modification plan by which we free up the insulin receptor, so to speak, to facilitate the entry of glucose in cells and so lower blood level (ref.10). I marshaled extensive evidence for shifting focus from glycemic status to insulin homeostasis for stemming the global tides of Type 2 diabetes.

Zhao et al. provide definitive answers to some fusion-fission questions with ingenious visualization of insulin-producing cells in the pancreas using confocal and super-resolution stimulated emission depletion microscopy. They show that transition to full fusion or fission is determined by competition between fusion and calcium/dynamin-dependent fission mechanisms, and that the hemi-fused intermediate is a key structure that controls fusion and fission. I look forward to the time when future advances in cell membrane dynamics based on the work of Zhao et al. will allow clinicians like me to describe our clinical and biochemical observations and attempt to explain the underlying mechanisms in light of the foundational work of Zhao et. al.

In closing, for readers interested in patterns of hyperinsulinism modification, below I include blood glucose and insulin data of three patients. The insulin and glucose profiles were obtained with blood samples drawn at fasting and 1-hour, 2-hour, and 3-hour after a 100-gram glucose load. The insulin profile of a healthy subject with unimpaired glucose tolerance is included as a control. Insulin and glucose concentrations are expressed in uIU/mL and mg/mL respectively.


 

INSULIN AND GLUCOSE PROFILES

1.Healthy control subject: insulin levels: <2 uIU/mL, 18, uIU/mL, 4, and <2; glucose levels: 77, 168, 109, 74, 52.
2. Case One: a 75-yr-old woman with Type 2 diabetes. April 2013. Insulin: 16 uIU/mL, 59 uIU/mL, 113 uIU/mL, and 152 uIU/mL: Glucose: 112, 214, 241, 155?. April 2015. Insulin: 6.2, 42.9, 51.2, and 39.7; Glucose: 96, 193, 112, and 105.
3. Case Two: a 68-yr-old man with hepatitis C and dysautonomia. April 2105. Insulin uIU: 17, 721, 388, and 28; Glucose mg/dL: 95, 157, 87, and 42?. April 2016: Insulin: 8.1, 315.0, 15.88, and 4.8?. Glucose mg/dL: 90, 101, 24, 54.
4. Case Three: a 75-yr-old woman ? with coronary artery disease and Type 2 diabetes. June 2010. Insulin in uIU/mL: 9.8, 25, 39, 92.4; Glucose mg/dL: 112, 170, 241, 273?.May 2014. Insulin: 6.4, 58.2, 33.8, 6.4; Glucose: 99, 182, 139, 81.

References

1. Zhoa W-D, Hamid E, Shin W, et al. WHemi-fused structure mediates and controls fusion and fission in live cells. Nature.2016;534:548-552.
2. Ali M. Leaky Cell Membrane Disorder (monograph). Teaneck, NJ, 1987.
3. Ali M. Hypothesis: Chronic fatigue is a state of accelerated oxidative molecular injury. J Advancement in Medicine, 6:83-96; 1993.
4. Ali M. Ali M, Ali O: AA oxidopathy: the core pathogenic mechanism of ischemic heart disease. J Integrative Medicine 1997;1:6-112. Oxidopathy
5. Ali M. Respiratory-to-Fermentative (RTF) Shift in ATP Production in Chronic Energy Deficit States. Townsend Letter for Doctors and Patients. 2004. 253: 64-65 (2004).
6. He W, Miao F J-P, Lin D C-H, et al. Citric acid intermediates as ligands for orphan G-protein-coupled receptors. Nature. 2004;429:143-45.
7. Chouchani ET, Pel VR, Gaude E, et al. Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS. Nature;2014;515:431.
8. Ali M. Succinate Retention. In: Chouchani ET. et al. Nature;2014;515:431 (See comments at the end).
9. Ali M. The Dysox Model of Diabetes and De-Diabetization Potential. Townsend Letter-The examiner of Alternative Medicine. 2007; 286:137-145.
10. Ali M. Dr. Ali?s Plan for Reversing Diabetes. New York, Canary 21 Press. Aging Healthfully Book 2011.

 

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