Acta Scientific Medical Sciences (ISSN: 2582-0931)

E-Book Volume 4 Issue 1

Psychosomatic Molecular Mechanisms of Metabolic Syndrome and Type 2 Diabetes

András Sikter MD*

Internal Medicine, Municipal Clinic Of Szentendre, Szentendre, Hungary, Europe

*Corresponding Author: András Sikter MD, Internal Medicine, Municipal Clinic Of Szentendre, Szentendre, Hungary, Europe.

Received: December 09, 2019; Published: December 24, 2019

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Abstract

  In the first part, the author presents his cytoplasmic model, which was first published in Hungarian in 2007. He modelized the cytoplasm of the animal/human cells with three constituents: 1) Cytoplasm Builder Ions (as K+, Mg2+, Zn2+, HPO42-, and H2PO4-), 2) ATP, and 3) Functioning Proteins (enzymes). The three parts of cytoplasm are equally vital - they can only increase or decrease in unison. The author presents four models that were born at different eras and based on various logics - independently of each other, but they point in the same direction. The author’s model suggests well the relations of anabolism vs. catabolism as well as the occurrence of vicious and virtuous circles. It is presented how could this cytoplasm model be of some help in modelizing diseases and healing. Even a quick recovery from an illness can be dangerous, even deadly if the physician does not consider the hazards of instability.

  It is known the second messenger and signaling functions of almost all physiologic ions of the cell, so it is not too bold to assume that the prevailing Momentary Intracellular Ion-Pattern as a whole has an essential, perhaps the primary signaling function. It would be the so-called 'software of the cell.' It seems that H+ concentration (pHi) is the most crucial of all ions to maintain homeostasis, Therefore, regulation wants to preserve the permanence of pHi. The endeavor to keep original pHi at all costs can develop metabolic dysregulation. (See Part 2.)

  Practically essential issues such as Refeeding Syndrome are also analyzed. The author points out that there are so many errors about diagnosis and treatment in this issue because the pathogenesis does not refer to one but several disorders; therefore suggests a new terminology classification. The author also reinterprets Locus Minoris Resistance (the Place of Less Resistance) theory and declares that the occurrence of a vicious circle in biology is not random; it is a consequence of the Second Law of Thermodynamics, and such it is a frequent phenomenon. In all these issues, the cytoplasmic model guides us.

KeywordsExploitation Syndrome; Momentary Intracellular Ion-Pattern Signaling; Modelizing Of Cytoplasm; The Place Of Less Resistance; Second Law Of Thermodinamics; Utilization Syndrome

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References

  1. Chow LS., et al. “Mechanism of insulin's anabolic effect on muscle: measurements of muscle protein synthesis and breakdown using aminoacyl-tRNA and other surrogate measures”. American Journal of Physiology Endocrinology and Metabolism 291.4 (2006): E729-E736. 
  2. Hayflick L. “Entropy explains aging, genetic determinism explains longevity, and undefined terminology explains misunderstanding both”. PLoS Genetics 3.12 (2007): e220.
  3. Sikter A., et al. “New aspects in the pathomechanism of diseases of civilization, particularly psychosomatic disorders. Part 1. Theoretical background of a hypothesis”. Neuropsychopharmacologia Hungarica 9.2 (2017): 95-105.
  4. Das AM. “Regulation of the mitochondrial ATP-synthase in health and disease”. Molecular Genetics and Metabolism 79 (2003): 71-82.
  5. Farber E. “ATP and cell integrity”. Federation Proceedings 32 (1973): 1534-1539.
  6. Kyle U G., et al. “Age-related differences in fat-free mass, skeletal muscle, body cell mass and fat mass between 18 and 94 years”. European Journal of Clinical Nutrition 55.8 (2001): 663-672.
  7. Hoffer LJ. “Clinical nutrition: 1. Protein-energy malnutrition in the inpatient”. Canadian Medical Association Journal 165.10 (2001): 1345-1349.
  8. Calder WA. “Body size, mortality, and longevity”. Journal of Theoretical Biology 102.1 (1983): 135-144.
  9. Relman AS. “Metabolic consequences of acid-base disorders”. Kidney International 1.5 (1972): 347-359.
  10. Cuthbertson KS and Cobbold PH. “Phorbol ester and sperm activate mouse oocytes by inducing sustained oscillations in cell Ca2+”. Nature 316.6028 (1985): 541-542.
  11. Nair A., et al. “Conceptual Evolution of Cell Signaling”. International Journal of Molecular Sciences 20.13 (2019): E3292. 
  12. Elkinton JR. editorial. “Hyponatremia: clinical state or biochemical sign?” Circulation 14 (1956): 1027-1034.
  13. Iseri LT., et al. “Water and electrolyte content of cardiac and skeletal muscle in heart failure and myocardial infarction”. American Heart Journal 43 (1952): 215-222.
  14. Cunningham JNJr, et al. “Resting transmembrane potential difference of skeletal muscle in normal subjects and severely ill patients”. Journal of Clinical Investigation 50.1 (1971): 49-59.
  15. Knochel JP., et al. “The muscle cell in chronic alcoholism. The possible role of phosphate depletion in alcoholic myopathy”. Annals of the New York Academy of Sciences 252 (1975): 274-286.
  16. Cronin RE., et al. “Skeletal muscle injury after magnesium depletion in the dog”. American Journal of Physiology 243 (1982): F113-F120.
  17. Heggtveit HA., et al. “Cardiac necrosis and calcification in experimental magnesium deficiency”. American Journal of Pathology 45 (1964): 757-782.
  18. Pesta DH., et al. “Hypophosphatemia promotes lower rates of muscle ATP synthesis”. FASEB Journal 30.10 (2016): 3378-3387.
  19. Quamme GA. “Renal magnesium handling: New insight in understanding old problems”. Kidney International 52 (1997): 1180-1195.
  20. Wacker WEC and Williams RJP. “Magnesium/calcium balances and steady states of biological systems”. Journal of Theoretical Biology 20.1 (1968): 65-78.
  21. Moore FD., et al. “The Body Cell Mass and Its Supporting Enviroment,” Philadelphia, PA, Saunders (1963).
  22. Sikter A. “[Ionokról, elektrolitokról egy belgyógyász-kardiológus szemével”.] ”Ions, electrolytes, through the eyes of an internist and cardiologist”. (In Hungarian) Cardiologia Hungarica 37 B (2007): B3-B47.
  23. Golden BE and Golden MH. “Effect of zinc on lean tissue synthesis during recovery from malnutrition”. European Journal of Clinical Nutriton 46.10 (1992): 697-706.
  24. Golden MH. “The nature of nutritional deficiency in relation to growth failure and poverty”. Acta Paediatrica Scandinavica 374 (1991): 95-110.
  25. Golden MHN and Golden BE. “Effect of zinc supplementation on the dietary intake, rate of weight gain, and energy cost of tissue deposition in children recovering from severe malnutrition”. American Journal of Clinical Nutrition 34 (1981): 900-908.
  26. Mehanna HM., et al. “Refeeding syndrome: what it is, and how to prevent and treat it”. British Medical Journal 336 (2008): 1495-1498.
  27. Roelofs SM. “Hyperventilation, anxiety, craving for alcohol: a subacute alcohol withdrawal syndrome”. Alcohol 2.3 (1985): 501-505.
  28. Keys A., et al. “The biology of human starvation”. Minneapolis, MN: University of Minnesota Press, Volum I.-II. (1950)
  29. Schnitker MA., et al. “A clinical study of malnutrition in Japanese prisoners of war”. Annals of Internal Medicine 35 (1951): 69-96.
  30. Baquerizo A., et al. “Phosphorus as an early predictive factor in patients with acute liver failure”. Transplantation 75.12 (2003): 207-214. 
  31. Matz R. “Parallels between treated uncontrolled diabetes and the refeeding syndrome with emphasis on fluid and electrolyte abnormalities”. Diabetes Care 17.10 (1994): 1209-1213. 
  32. Henry Y., et al. “Influence of the level of dietary phosphorus on the voluntary intake of energy and metabolic utilization of nutrients in the growing rat”. The British Journal of Nutrition 42.1 (1979): 127-137. 
  33. Mitch WE., et al. “Metabolic acidosis stimulates muscle protein degradation by activating the adenosine triphosphate-dependent pathway involving ubiquitin and proteasomes”. The Journal of Clinical Investigation 93.5 (1994): 2127-2133. 
  34. Storm TL. “Severe hypophosphataemia during recovery from acute respiratory acidosis”. British Medical Journal (Clinical Research Edit) 289.6443 (1984): 456-457.
  35. Knochel JP. “The pathophysiology and clinical characteristics of severe hypophosphatemia”. Archives of Internal Medicine 137.2 (1977): 203-220.
  36. Zipf WB., et al. “Hypocalcemia, hypomagnesemia, and transient hypoparathyroidism during therapy with potassium phosphate in diabetic ketoacidosis”. Diabetes Care 2.3 (1979): 265-268. 
  37. Faure P., et al. “Lipid peroxidation and trace element status in diabetic ketotic patients: Influence of insulin therapy”. Clinical Chemistry 39.5 (1993): 789-793. 
  38. Gaasbeek A and Meinders AE. “Hypophosphatemia: An update on its etiology and treatment”. The American Journal of Medicine 118.10 (2005): 1094-1101.
  39. Poldeman KH and Girbes AR. “Severe electrolyte disorders following cardiac surgery: a prospective controlled observational study”. Critical Care 8.6 (2004): R459-R466.
  40. Zazzo JF., et al. “High incidence of hypophosphatemia in surgical intensive care patients: efficacy of phosphorus therapy on myocardial function”. Intensive Care Medicine 21.10 (1995): 826-831. 
  41. Muth L. “Hospital experience of total parenteral nutrition with 3-litre containers (big bags)”. Acta Anaethesiologica Scandinavica 82 (1985): 76-80. 
  42. Ham BJ and Choi IG. “Psychiatric implications of nutritional deficiencies in alcoholism”. Psychiatry Investigation 2.2 (2005): 44-59.
  43. Biery JR., et al. “Alcohol craving in rehabilitation: assessment of nutrition therapy”. Journal of the American Dietetic Association 91.4 (1991): 463-466.
  44. Jahnen-Dechent W and Ketteler M. “Magnesium basics”. Clinical Kidney Journal 5.1 (2012): i3-i14. 
  45. He FJ and MacGregor GA. “Fortnightly review: Beneficial effects of potassium”. British Medical Journal 323.7311 (2001): 497-501.
  46. Nielsen FH and Lukaski HC. “Update on the relationship between magnesium and exercise”. Magnesium Research 19.3 (2006): 180-189.
  47. Lo Schiavo A., et al. “Locus minoris resistentiae: An old but still valid way of thinking in medicine”. Clinics in Dermatology 32.5 (2014): 553-556. 
  48. Bachrach LK. et al. “Recovery from Osteopenia in Adolescent Girls with Anorexia Nervosa”. The Journal of Clinical Endocrinology and Metabolism 72.3 (1991): 602-606.
  49. Laurin D., et al. “Physical activity and risk of cognitive impairment and dementia in elderly persons”. Archives of Neurology 58.3 (2001): 498-504.
  50. Newsholme EA and Crabtree B. “Substrate cycles in metabolic regulation and in heat generation”. Biochemical Society Symposium 41 (1976): 61-109.
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Citation

Citation: András Sikter. “Psychosomatic Molecular Mechanisms of Metabolic Syndrome and Type 2 Diabetes. Part 1. A Theory for Modelizing the Cytoplasm and Diseases". Acta Scientific Medical Sciences 4.1 (2020): 124-140.



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