Csaba Varga, PhD, Anikó Pósa, PhD, Krisztina Kedvesné Kupai: The metabolic syndrome
- The metabolic syndrome
- I. Introduction
- II. Historical survey
- III. Physiological basics
- III.1. Energy storage
- III.2. Regulation of lipid metabolism
- III.2.A. Adipose tissue distribution
- III.2.B. The endocrine function of adipose tissue
- III.2.B.a. Adiponectin
- III.2.B.b. Leptin
- III.2.B.c. Resistin
- III.2.B.d. Retinol binding protein 4 (RBP4)
- III.2.B.e. The complement system
- III.2.B.f. Interleukin-6 (IL-6)
- III.2.B.g. Monocyte chemoattractant protein-1 (MCP-1)
- III.2.B.h. Tumor necrosis factor-alpha (TNF-α)
- III.2.B.i. Plasminogen activator inhibitor type 1 (PAI-1)
- III.2.B.j. Angiotensinogen
- III.3. The glucose metabolism
- III.3.A. Transporters playing a role in Glu uptake and release
- III.3.B. Role of the pancreas
- III.3.C. Effects of catecholamines
- III.3.D. The renin-angiotensin-aldosterone system (RAAS)
- III.3.E. The effect of the growth hormone on the blood glucose level
- III.3.F. The effects of glucocorticoids
- III.3.G. The effects of thyroid hormones
- III.3.H. Regulation of the blood glucose level
- III.4. Hormonal regulation of the gastrointestinal system
- III.4.A. Gastrin
- III.4.B. Secretin
- III.4.C. Cholecystokinin (CCK)
- III.4.D. Gastric inhibitory peptide (GIP)
- III.4.E. Vasoactive intestinal peptide (VIP)
- III.4.F. Peptide histidine methionine
- III.4.G. Glucagon and enteroglucagon
- III.4.H. Pancreatic polypeptide (PP)
- III.4.I. Neuropeptide Y (NPY)
- III.4.J. Peptide tyrosine-tyrosine (PYY)
- III.4.K. Opioid peptides
- III.4.L. Motilin
- III.4.M. Metabolic effects of hormones
- III.5. The regulation of eating
- IV. Definition of the metabolic syndrome
- V. Parameters influencing the metabolic syndrome
- VI. Endothelial dysfunction in the metabolic syndrome
- VII. Cardiovascular risk factors
- VII.1. Hyperinsulinemia
- VII.2. ACE gene polymorphism
- VII.3. Microalbuminuria (MA)
- VII.4. Impaired glucose tolerance (IGT)
- VII.5. Type 2 diabetes mellitus (T2DM)
- VII. 6. Hyperlipidemia
- VII.7. Dyslipidemia
- VII.8. High cholesterol level
- VII.9. Nonalcoholic fatty liver disease (NAFLD)
- VII.10. Atherothrombosis and atherosclerosis
- VII.11. High blood pressure
- VII.12. Malnutrition
- VII.13. Lipoprotein a (Lpa)
- VII.14. Homocysteine (Hcy)
- VII.15. Hyperuricemia
- VII.16. Smoking
- VII.17. Stress
- VII.18. Depression
- VII.19. Age and sex
- VII.20. Lack of sleep
- VII.21. Obstructive sleep apnea (OSA)
- VII.22. Physical inactivity
- VIII. Cardiovascular complications
- IX. Inflammation and the metabolic syndrome
- X. The diagnostic parameters of the Metabolic syndrome
- XI. Prevention of the metabolic syndrome
- XII. Treatment of the metabolic syndrome
- XIII. Abbreviations
- XIV. References
- XV. Acknowledgments
VII.2. ACE gene polymorphism
A-I is converted to A-II by the ACE. A-II increases the BP and enhances aldosterone synthesis. It leads to a higher level of oxidative stress and the development of arteriosclerosis, and it facilitates the inflammatory pathways, coagulation (fibrosis) and apoptosis. It increases the myocardial contractility (positive inotropic effect) and heart frequency (positive chronotropic effect).
In ACE gene polymorphism, a 286 bp fragment can be found (variant I) or not (variant D) in individuals. Variant D results in an increased ACE and hence A-II level. ACE gene polymorphism may play a role in high BP, an endothelial dysfunction, heart failure and atherosclerosis too.
Készült az Új generációs sporttudományi képzés és tartalomfejlesztés, hazai és nemzetközi hálózatfejlesztés és társadalmasítás a Szegedi Tudományegyetemen c. pályázat támogatásával. Pályázati azonosító: TÁMOP-4.1.2.E-15/1/Konv-2015-0002